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Microbiome—Microbial Metabolome—Cancer Cell Interactions in Breast Cancer—Familiar, but Unexplored

Edit Mikó, Tünde Kovács, Éva Sebő and 7 more

Cells · 2019 · Review · CC BY

Abstract

Breast cancer is a leading cause of death among women worldwide. Dysbiosis, an aberrant composition of the microbiome, characterizes breast cancer. In this review we discuss the changes to the metabolism of breast cancer cells, as well as the composition of the breast and gut microbiome in breast cancer. The role of the breast microbiome in breast cancer is unresolved, nevertheless it seems that the gut microbiome does have a role in the pathology of the disease. The gut microbiome secretes bioactive metabolites (reactivated estrogens, short chain fatty acids, amino acid metabolites, or secondary bile acids) that modulate breast cancer. We highlight the bacterial species or taxonomical units that generate these metabolites, we show their mode of action, and discuss how the metabolites affect mitochondrial metabolism and other molecular events in breast cancer. These metabolites resemble human hormones, as they are produced in a “gland” (in this case, the microbiome) and they are subsequently transferred to distant sites of action through the circulation. These metabolites appear to be important constituents of the tumor microenvironment. Finally, we discuss how bacterial dysbiosis interferes with breast cancer treatment through interfering with chemotherapeutic drug metabolism and availability.

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From PubMed Central, U.S. National Library of Medicine, as current on Oct 21, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Breast Cancer, a Leading Cause of Death among Women

1Breast cancer is the most common cancer among women, with the estimated age-adjusted annual incidence of breast cancer in Europe in 2012 being 94.2/100,000, with similar numbers in the United States (US) or the United Kingdom (UK). The estimated age-adjusted annual mortality is 23.1/100,000 for breast cancer in Europe. In 2019, in the US, the number of newly diagnosed invasive breast cancer cases is estimated to be 268,000, while the newly diagnosed in situ cases are estimated to be around 62,930. In 2019, 41,760 women out of these numbers are expected to die of breast cancer in the US. The five year survival of breast cancer is over 80% in developed countries due to screening programs and the consequent early detection.

2Several risk factors for breast cancer had been described, nevertheless the majority of the newly diagnosed women have no obvious risk factors. The risk for breast cancer increases over the age. The majority of the patients are diagnosed after menopause, after the age of 50. The incidence rates for in situ breast cancer in the UK were the highest in people that were aged 65–69 (2013–2015). Extended female hormone exposure by the use of hormone-replacement therapy or early menarche or late menopause also increases the risk for breast cancer. Mutations in the BRCA1 and BRCA2 genes represent a predisposing factor for breast cancer, similarly to a family history of breast cancer or personal history of neoplastic diseases or breast cancer Finally, dense breast is an independent risk factor of breast cancer. Physical activity, successful pregnancies, and lactation are protective factors.

3In Western countries there are organized screening programs from the age of 40–45 to 65 years of age for women with bi-annual intervals. The first step in screening is mammography, followed by ultrasonography in breast cancer-suspect individuals. The final diagnosis is based on needle biopsy. Breast cancer screening does not reach the whole target population, for example, in Hungary only around 50% of the target population undergoes screening.

4The treatment schemes for breast cancer include the surgical procedures, chemotherapy, targeted therapy, endocrine-, and radiotherapy. Chemotherapy regimens contain anthracyclines, cyclophosphamides, taxanes, antimetabolites (5-fluorouracil, gemcitabine, capecitabine), and navelbine that targets mitotic tubules. Targeted therapy in breast cancer is used in the management of HER2 positive cases and it involves monoclonal antibodies against the HER2 receptor (trastuzumab, pertuzumab, and trastuzumab-emtansine, in which the humanized HER2 antibody is conjugated to DM1, a tubulin toxin) and the tyrosine kinase inhibitor lapatinib. Endocrine therapy, which involves selective estrogen receptor modulators (SERMs), aromatase inhibitors, and gonadotropin-releasing hormone (GNRH)-analogs, is the standard treatment for hormone-receptor positive breast cancer. There are new inhibitors with potential use in breast cancer therapy, such as poly(ADP-ribose) polymerase (PARP) inhibitors or the inhibitors of CDK4/6 (cyclin-dependent kinases).

5For further information regarding the clinico-pathology of breast cancer, we refer the Readers to the relevant guidelines and draw the attention of the Readers to use the most up-to-date version of the guidelines.

2. The Dysregulation of Metabolism in Breast Cancer

6Breast cancer cells show characteristic pathological changes in metabolism and, in line with that, the pathological metabolism of the host (e.g., obesity, metabolic syndrome, type II diabetes) increases breast cancer risk that we discuss below briefly; for comprehensive reviews, see and Table 1.

7Originally, Otto Warburg suggested that cancer cells switch for “aerobic glycolysis” that are characterized by increased glycolytic flux and decreased mitochondrial oxidation that supports the high proliferative capacity of cancer cells. Indeed, breast cancer cells were shown to exert features of Warburg metabolism, and in line with that, reverting Warburg metabolism can slow down the proliferation of breast cancer cells or declutch cell death, too. Later, besides changes to glycolysis and mitochondrial oxidation, other metabolic pathways were shown to be upregulated in breast cancer, such as glutamine metabolism, lipid and fatty acid, glutamine-serine pathway, protein translation, or cholesterol metabolism. These changes are the consequences of a complex rearrangement of the cellular energy sensor web, such as the activation of hypoxia-inducible factors (HIFs), mammalian target of rapamcyin (mTOR), estrogen-related receptors, estrogen receptors, phosphatidyl-inositol-3 kinase (PI3 kinase), AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor cofactor-1α and β (PGC1α and PGC1β), or nuclear respiratory factor 1 (NRF1).

8Metabolic changes have important pathological roles, as these changes have important roles in supporting proliferation, angiogenesis, or epithelial-to-mesenchymal transition (EMT). It is also very likely that two risk factors of breast cancer, obesity or type II diabetes, at least in part, increase risk through predisposing for changes towards pathological metabolism in (cancer) cells. Breast cancer metabolism is an attractive new target for chemotherapeutic interventions; furthermore, changes to metabolism in breast cancer can be used to monitor the efficiency of chemotherapy and changes to cancer cell metabolism can be exploited to overcome chemotherapy resistance.

9There are four molecular (intrinsic) subtypes of breast cancer: luminal A (ER+, low proliferative capacity), luminal B (ER+, high proliferative capacity), HER2-enriched (ER−, HER2+), and basal-type (triple negative breast cancer, TNBC). All of the subtypes have metabolic alterations and there is compelling evidence that it is possible to discriminate between the intrinsic subtypes as a function of changes to metabolism (see Table 1). These results also highlight the strong contribution of pathological metabolism of breast cancer cells to proliferative capacity and aggressiveness.

10The discovery of differences between the metabolism of cell types of breast cancer makes the landscape of the metabolic changes more complex. Namely, cancer stroma cells (dubbed non-tumorigenic cancer cells) or cancer-associated fibroblasts indeed rely on Warburg metabolism; however, the metabolism of cancer stem cells is dominated by mitochondrial oxidation. Cancer stem cells in breast cancer have two different forms, the mesenchymal-like cancer stem cells are CD44+/CD24−, while the epithelial-like cancer stem cells are aldehyde dehydrogenase 1 family, member A1 (ALDH1) positive. The inhibition of mitochondrial oxidation can increase the proportions of cancer stroma to stem cells, facilitating the efficiency of conventional chemotherapy that primarily targets stromal cells. Larger proportions of stem cells than ER+ positive cancers characterize TNBCs. In support of that observation, the TCA cycle is more active in TNBC as compared to the ER+ cases. There is accumulating evidence that the metabolism of circulating cancer cells change to a more oxidative phosphorylation-dependent metabolism.

11The actual shape of cancer cell metabolism is sharply regulated by the tumor microenvironment: the abundance of collagen, the circulating cytokines, or the adipocytes surrounding the tumor are all major determinants of cancer cell metabolism. In this review, we add a new component to this list, bacterial metabolites, which are produced by the gut microbiome.

3. Microbiome Dysbiosis in Breast Cancer

12Dysbiosis denotes an abnormal composition or maladaptation of the microbial community (the microbiome) of a given organism or a given compartment of the organism. Dysbiosis disrupts the normal function of the microbial community through hampering the symbiotic relationships in the community (e.g., cross-feeding). Dysbiosis can occur when the composition or the bacterial biomass changes (i.e., the proportions of certain species change within the community). Dysbiosis characterizes several neoplastic diseases, including breast cancer. Although the largest microbial community of the human body resides in the gastrointestinal tract, when discussing dysbiosis in breast cancer, the breast’s own microbiome also has to be taken into account. This, yet, ill-characterized, bacterial community that is found in the milk-ducts of the breast also exhibits dysbiosis in breast cancer. Studies have shown dysbiosis in the breast microbiome (Table 2) and in the fecal microbiome (Table 3).

13Obtaining nipple aspirate fluid or sterile biopsy are starting materials for the analysis of the breast microbiome that is then subjected to next-generation sequencing. The biomass of the breast microbiome decreases in breast cancer patients. One explanation for the variability could be that the geographical difference creates notable changes in the composition of the microbiome, as pointed out in. Changes to the breast microbiome are in correlation with the molecular subtype (hormone receptor+, HER2+, or triple negative), where the microbiome composition of the triple negative cases differs from other types. Furthermore, the breast microbiome change as a function of the grade and aggressivity of the disease. These changes are translated into functional changes, as in the breast microbiome glycerophospholipid biosynthesis and ribosome biosynthesis processes are upregulated, while the flavonoid biosynthesis decreased as the grade of the disease increases. It is of note that there are also characteristic changes to the virome and fungome of the breast.

14The fecal microbiome is also characterized by changes in breast cancer patients. The group of James J. Goedert published a series of studies illustrating that the diversity of the gut microbiome decreases in breast cancer patients as compared to healthy controls and the relative abundance of Clostridiales increase in patients. Using the biobank set-up by the Goedert group, Miko and co-workers and Kovacs and colleagues assessed a subset of bacterial species and showed that the most drastic decreases were observed in early stage breast cancer (stage 0 and stage 1). These observations are supported be the observations of Luu and colleagues; the log10 equivalent number/g stool of all Bacteroidetes, Clostridium coccoides, Clostridium leptum, Faecalibacterium prausnitzii, and Blautia species increased in stage II and III patients as compared to the stage 0 and I patients. In contrast to that, Zhu and co-workers showed that the diversity of the gut microbiome changes differently in the pre- and postmenopausal breast cancer patients, furthermore the diversity of the gut microbiome increases in patients when compared to healthy controls.

15There are correlative studies showing that antibiotic consumption, which decreases the diversity of the microbiome, increases the risk and recurrence of breast cancer. Despite the non-mechanistic nature of these studies and the chance for uncontrolled confounding, these studies strengthen the observations that the decreases in the diversity of the microbiome increase the risk for breast cancer. Importantly, a recent murine study showed that the use of a cephalosporin antibiotic (Cephalexin) accentuated the decrease in microbiome diversity that was induced by the tumor itself and induced tumor formation, suggesting a causative relationship between antibiotic use and breast cancer incidence, as well as strengthening the hypothesis of the reduced bacterial diversity in breast cancer. Cephalexin reduced the abundance of Odoribacter and Anaeotruncus (both are butyrate-producing bacterial groups), while increasing the abundance of Bacteroides.

4. Interactions between Microbiome and Breast Cancer Cells—Metabolites in Action

16There are multifaceted bidirectional interactions between the host and the microbiome. The host regulates the composition of its microbiome through its innate immune system or its feeding or hygiene behavior, but, in turn, as recent research strongly argues, the microbiome can also fine tune the (patho)physiology of the host. A major pathway in microbiome-to-host signaling is the secretion of bacterial metabolites that enter the circulation and reach their target cells. In that respect, the function of these bacterial metabolites is similar to human hormones, which are synthesized in an organ or gland (in this case, it is the microbiome) and they are transferred to other anatomical locations, where they exert their biological effects. Such blood-borne microbial metabolites were shown to modulate the behavior of breast cancer, lithocholic acid (LCA), short chain fatty acids (SCFA), cadaverine, or deconjugated estrogens. These bacterial metabolites have profound impact on mitochondrial metabolism, nevertheless it is of note that metabolites also regulate other metabolic processes (e.g., lipid metabolism) (For overview, please see Table 4 and Figure 1).

4.1. Estrogen Deconjugation and Reuptake

17The group of James J. Goedert showed that, in men and postmenopausal women, the gut microbiome is a key determinant of estrogen metabolism. The microbiome has a vital role in estrogen metabolism, as bacteria can deconjugate excreted estrogens enabling their reuptake, in line with that, the urinary estrogen levels showed correlation with the richness of the fecal flora in men and in postmenopausal women. Bacterial β-glucuronidases are responsible for the deconjugation of conjugated estrogens that are coded by the gus and BG genes. gus is widespread among gut bacteria, being more common among Firmicutes, while BG is more widespread, being present in Bacteroidetes and Firmicutes. The following bacterial genuses were shown to express β-glucuronidases: Collinsella, Edwardsiella, Alistipes, Bacteroides, Bifidobacterium, Citrobacter, Clostridium, Dermabacter, Escherichia, Faecalibacterium, Lactobacillus, Marvinbryantia, Propionibacterium, Roseburia, and Tannerella. Goedert and colleagues have provided strong functional evidence for the role of Clostridiales in estrogen reactivation and showed that the relative abundance of Clostridiales increases in breast cancer patients. Feeding regimes can modulate β-glucuronidase expression in the gut. (Reactivated) estrogens act through estrogen receptors, and hence promote the progression of ER+ breast cancer through multiple pathways (Table 1).

18Reactivation of estrogens enable their reuptake and increase serum estrogen levels, estrogen-evoked changes in the expression of mitochondrial genes were suggested to contribute to estrogen-induced carcinogenesis. In line with that, both estrogen receptors (ER), ERα and ERβ, reside on the surface of mitochondria and the ER-responsive sites were suggested to be present in mitochondrial DNA. ERβ is directly involved in the expression of nuclear-coded mitochondrial proteins. Endocrine-resistant tumors have higher mitochondrial respiration when compared to the tumors that are sensitive for endocrine therapy, which is due to the increased expression of NRF1 and TFAM1. Increased oxidative phosphorylation was shown to contribute to tamoxifen-resistance and general therapy failure, support metastasis, and render the tumors more aggressive. The flip-side of the induction of mitochondrial oxidation is the increased mitochondrial production of free radicals that is cytostatic and is dependent on ERβ. When taken together, bacterial estrogen deconjugation can promote breast cancer progression.

4.2. Short-Chain Fatty Acid Production

19The microbiome by the saccharolytic fermentation of non-digestible carbohydrates generate short-chain fatty acids (SCFAs, acetate, propionate, butyrate). Fermentation of the non-digestible carbohydrates yield formate, acetate, propionate, butyrate, and lactate. A relatively small proportion of SCFAs are produced through amino acid degradation; the degradation of branched chain amino acids yield branched-chain fatty acids; nevertheless, the amount of branched-chain fatty acids is extremely low.

20The capability for acetate production is widespread among bacteria, while the production of other metabolites is more restricted to certain species. Akkermansia muciniphila is a key player in propionate production from mucin, while Lachnospiraceae, Ruminococcus obeum, and Roseburia inulinivorans are responsible for the degradation of deoxy sugars (e.g., fucose, rhamnose) and hexoses by Bacteroidetes and Negativicutes sp. to produce propionate. The majority of butyrate production is bound to Faecalibacterium prausnitzii, Eubacterium rectale, Roseburia faecis, Eubacterium hallii, and an unnamed cultured species SS2/1, as well as the genera Odoribacter and Anaeotruncus. It is also of note that the application of Cephalexin, which is an antibiotic that is frequently used as a pre-surgery premedication to breast cancer patients, reduced the abundance of Odoribacter and Anaeotruncus that are butyrate producer bacteria. The abundance of Akkermansia muciniphila, which is a cross-feeder and propionate producer species, was associated with the richness of the gut microbiome in breast cancer patients.

21The serum concentration of the total SCFAs fall into the 10–100 µM range, wherein acetate, propionate, isobutyrate, and butyrate make up the bulk. SCFAs modulate numerous cancer hallmarks, such as cell proliferation, apoptosis, cell invasion, gene expression, metabolism, among others, in breast cancer. The main receptors of SCFAs are the free fatty acid receptors (FFARs) that are only situated on the cancer cells, but also on stromal cells (e.g., adipocytes). The effects of SCFAs can have positive (e.g.,) and negative (e.g.,) effects in breast cancer as a function of the context.

22The knowledge on role of SCFAs in mediating metabolism in breast cancer cells is very limited. In breast cancer cells, even-chain short fatty acids, acetate, butyrate, or lactate can be directly utilized as energy substrates, in line with that, sodium-butyrate induces oxygen consumption in breast cancer cell lines and the inhibition of the lactate metabolism sharply reduces the viability of breast cancer cells. Furthermore, butyrate can induce apoptosis through inducing mitochondrial ROS generation. SCFAs, most notably, butyrate, are histone deacetylase inhibitors that are a key feature for their anticancer activity.

4.3. Secondary Bile Acid Metabolism

23Lithocholic acid is secondary bile acid that is synthesized from chenodeoycholic acid (CDCA) and ursodeoxycholic acid (UDCA), by the dehydroxylation at position 7. The genes that are involved in the degradation of secondary bile acids can be found in the bile acid-inducible operon (bai operon). The enzyme catalyzing the formation of lithocholic acid that is cytostatic in breast cancer is 7α/β-hydroxysteroid dehydroxylase (baiH). Anaerobic bacteria, mostly the Clostridiales, are responsible for bile acid transformation. The bile acids in the breast are of the gut origin.

24The capacity of the human body and the microbiome to synthesize LCA is largely reduced in breast cancer, which is the most dominant in early stages (stages 0 and 1). Serum lithocholic acid levels negatively correlate with Ki67 labelling index in breast cancer. LCA, in concentrations corresponding to its serum or breast tissue concentrations (30–50 nM or < 1 µM, respectively), exerts antineoplastic effects on breast cancer cells by inhibiting epithelial-to-mesenchymal transition, vascular endothelial growth factor (VEGF) production, metastasis formation, induced antitumor immunity, and elicited changes in metabolism. In supraphysiological concentrations (>1 µM), LCA inhibits fatty acid biosynthesis, induces induced multidrug resistance proteins, and induces cell death. LCA did not exert antiproliferative effects in its tissue reference concentrations on non-transformed primary fibroblasts. A exert its antineoplastic effects through the G protein-coupled bile acid receptor 1 (TGR5) and in supraphysiological concentrations through Farnesoid X receptor (FRX). Other secondary bile acids, deoxycholic acid (DCA) or ursodeoxycholic acid (UDCA), had no effect on breast cancer cells in the reference concentration.

25Bile acid-induced activation of TGR5 was shown to induce OXPHOS in metabolic models, in good accordance with that, LCA can elicit anti-Warburg effects in breast cancer models. In breast cancer cells, LCA induces mitochondrial biogenesis through NRF1, AMPK, and PGC-1β; the same effectors are also induced in murine breast cancer models upon LCA feeding. The induction of these energy sensors declutch transcription programs that induced the expression of mitochondrial proteins (cytochrome c, atp5g1, ndufb5) and consequently enhanced mitochondrial activity. both when, the TCA cycle was fed on acetate or on glucose suggesting enhanced glycolytic flux, too. In parallel, oxygen consumption rates were also induced suggesting improved terminal oxidation. Besides the regulation of oxidative phosphorylation, LCA induced mesenchymal-to-epithelial transition, antitumor immune response, and inhibited proliferation and metastasis formation (see Table 1).

4.4. Amino Acid Degradation

26Cadaverine is synthesized from lysine by the bacterial enzymes LdcC and CadA. Human cells are also capable of synthesizing cadaverine; however, it seems that bacterial cadaverine production is dominant over human biosynthesis. Shigella flexneri, Shigella sonnei, Escherichia coli, and Streptococci were shown to express cadaverine biosynthetic enzymes.

27Cadaverine in concentrations corresponding to its serum reference concentrations (100–800 nM) inhibited cell proliferation, epithelial-to-mesenchymal transition, cell movement and invasion, and tumor infiltration to the surrounding tissues. Moreover, cadaverine changed metabolism in breast cancer cells and it reduced the proportion of ALDH1+ cancer stem cells in 4T1 murine breast cancer cells. Cadaverine exerted its effects through the trace amine-associated receptor-1, 2, 3, 5, 8, 9 (TAAR1, 2, 3, 5, 8, 9), of which TAAR1 was already associated with the inhibition of breast cancer growth. The capacity of the microbiome to synthesize cadaverine is suppressed in breast cancer, most dominantly in early stage breast cancer (stages 0 and 1). Putrescine had no effect on breast cancer cells; furthermore, cadaverine was not effective on primary, untransformed cells.

28Cadaverine has been shown to reduce cellular oxygen consumption that is a readout of OXPHOS activity, rendering the cells more glycolytic. The molecular mechanisms bringing about that phenotype has not yet been elucidated. In line with the more glycolytic phenotype of cells, the percentage of cancer stem cells was reduced upon cadaverine treatment. In addition to these, cadaverine inhibited migration, invasion, and metastasis formation, as well as induced mesenchymal-to-epithelial transition.

5. Interference of the Microbiome and Anticancer Treatment

29Bacteria of the microbiome can interfere with chemo- and radiotherapy in cancer treatment and management, which is also true for breast cancer. There are several aspects to the interactions between the microbiome and anticancer treatment; the microbiome can metabolize the chemotherapeutic drugs, inactivating or activating them, can modulate the immune system, can interfere with the side-effects of therapy, or the therapy can modulate the microbiome. Alexander and colleagues suggested a framework, called TIMER (from Translocation, Immunomodulation, Metabolism, Enzymatic degradation, and Reduced diversity and ecological variation), to support a coordinated description of the interactions between the microbiome and cancer drugs. Below, we discuss the drugs that are relevant for breast cancer treatment.

30Anthracyclines are synthesized by Streptomyces strains and can hence modulate the composition of the microbiome, for example, anthracyclines can be bacteriostatic on Acinetobacter species. Several bacteria can metabolize anthracyclines (i.e., detoxify them); Streptomyces WAC04685 can deglycosylate and inactivate doxorubicin. Streptomycetes can be found with a low prevalence in the human gut, making it likely that the microbiome can interfere with the bioavailability and pharmacokinetics and the pharmacodynamics of anthracyclines. Furthermore, upon anthracycline treatment, certain bacteria can cross the intestinal barrier to enter secondary lymphoid organs.

31Cyclophosphamides cause damage to the gut mucosa and, thereby, attenuate the barrier function that makes the gut leaky and gut bacteria can enter. Rich microbiome is protective against cyclophospmamide-induced mucosal injury; in fact, strains of Lactobacillus plantarum as a probiotic was shown to be protective against mucosal injury. Bacteria (usually Gram-positive microorganisms, such as Lactobacillus johnsonii, L. murinus, Barnesiella intestinihominis, and Enterococcus hirae) can enter secondary lymphoid organs and thereby shape the anticancer immune response of the host. Lactobacillus plantarum HY7712 can ameliorate cyclophosphamide-induced immunosuppression in mice.

32Selective estrogen receptor modulators (SERMs) (Tamoxifen, Raloxifen) tamoxifen can modulate the composition of the microbiome. SERMs can be toxic for Pseudomonas aeruginosa, Klebsiella pneumoniae, Acinetobacter baumannii, Porphyromonas gingivalis, Streptococcus mutans, Enterococcus faecium, and Bacillus stearothermophilus. To date, no bacterial drug metabolism was related to SERMs. Tamoxifen resistance was shown to be a reason of changes to cancer cell metabolism, which can be modulated by the microbiome.

33Taxanes can be a subject to bacterial metabolism. Moreover, taxanes may interfere with bacterial LPS in activating the immune system. Finally, taxanes can interfere with the composition of the microbiome.

34Antimetabolites, 5-fluorouracil (5FU), and gemcitabine were shown to interact with the microbiome. Both of the drugs are metabolized by the microbiome. Bacterial enzymes can activate both drugs; nevertheless, the bacterial deactivation of the active metabolites is equally important. Although, studies in breast cancer or its models had not been performed, it is known that the bacterial metabolism of 5FU can influence the treatment efficacy of colorectal cancer. Intratumoral bacteria (Gammaproteobacteria) were shown to be the key players in deactivating gemcitabine in colorectal cancer that was alleviated by the eradication of Gammaproteobacteria by ciprofloxacin. A loss of gemcitabine cytotoxicity was also observed in Mycoplasma-infected cells in culture. Geller and Straussman identified Gammaproteobacteria in human pancreatic ductal adenocarcinoma tumors in elevated numbers than in healthy pancreas tissue that can regulate gemcitabine availability. This observation can be extended for breast cancer, as it is also a solid tumor inside the human body. Cytidine deaminase was shown to be responsible for gemcitabine inactivation. Both 5FU and gemcitabine have bactericide properties and, therefore, they modulate the composition of the microbiome. Capecitabine was not toxic on E. coli and its effects on the microbiome is largely uncharacterized. 5FU-induced dysbiosis contributes to the severity of the 5FU-induced mucositis that can be corrected by the use of probiotics. 5FU mucositis can induce bacterial translocation through the intestinal barrier.

35PARP inhibitors, which are drugs likely to be used in the future in breast cancer treatment, were shown to increase the diversity of the gut microbiome. To date, there is no literature on the interplay between aromatase inhibitors, navelbine, GNRH-analogs, and the microbiome. It is of note that bacteria can also interfere with biological therapies; nevertheless, no interactions were found with the antibodies used in breast cancer targeted therapy. Finally, the microbiome can modulate the severity of radiation-induced mucositis and can protect against radiation-induced toxicity.

6. Applicability and Future Directions

36Bacterial dysbiosis characterizes breast cancer, both in the breast tissue and in the gut. Both the gut and breast microbiome sharply responds to the disease and display changes as a function of the histological variants, grade, or stage of the disease. The role of the breast microbiome in carcinogenesis is unresolved, in contrast to that, the gut microbiome was shown to produce or modify metabolites (e.g., LCA, cadaverine, SCFAs, estrogens), which, through the circulation, get to distant sites, such as the breast, where they modulate cancer cell function. In that sense, these metabolites resemble human hormones, as they are produced in a “gland” (in this case, the microbiome) and are subsequently transferred to distant sites of action through the circulation. These metabolites appear to be important constituents of the tumor microenvironment.

37All known bacterial metabolites have pleiotropic effects on breast cancer cells; nevertheless, almost all of them modulate mitochondrial metabolism. However, the actual effects are rather variable and there are inducers (e.g., estrogens or LCA) and inhibitors (e.g., cadaverine) of mitochondrial metabolism. Changes to mitochondrial metabolism is a double-edged sword in breast cancer. Switching for an anti-Warburg mitochondrial metabolism, comprising the upregulation of mitochondrial oxidation, can slow the proliferation of cancer cells and sensitize stromal cell for chemotherapy; however, in parallel, the induction of mitochondrial oxidation can tune cancer cells into cancer stem cells. An example for that is cadaverine, which represses mitochondrial oxidation and, hence, reduces the percentage of cancer stem cells. It is also of note that the substrate availability and substrate preference of cancer cells can also drive a switch between cancer stroma and cancer stem cells. Consequently, a good understanding of metabolite-induced changes can enable us to use these metabolites in combatting breast cancer, either as stand-alone drugs or in combination with other chemotherapy regimens or mitochondrial drugs.

38There is an intricate connection with feeding regimes and breast cancer risk, suggesting that it may be possible to create feeding regimes that maintain a “cytostatic microbiome”—probiotics and changes to diet can influence SCFA serum levels. Finally, there are natural dietary compounds (e.g., polyphenols) that can also modulate the microbiome and mitochondrial metabolism. Maintaining the microbiome in good shape can be also vital in the successful completion of chemotherapeutic regime in breast cancer treatment.

39The microbiome may also have indirect effects on breast cancer. For example, the white adipose tissue has aromatase activity and, therefore, it can synthesize estrogen and thereby promote breast cancer. Pathological composition of the microbiome is also associated with obesity and increases in the body mass index (BMI) are a risk factor of breast cancer. There are other drivers of dysbiosis, apart from antibiotics or obesity, such as aging or diseases (e.g., type II diabetes, polycystic ovary syndrome, non-alcoholic fatty liver disease, etc.), which may explain the association of cancer events with these diseases. Bacteria in the microbiome can serve as sources of immunogenicity, similarly to the appearance of the counter-antibodies of the AB0 blood group system, and through that could modulate the activity of the immune system. Finally, cachexia is also associated with dysbiosis.

40We are still scratching the surface in understanding the role of dysbiosis in breast cancer. Nevertheless, there seems to be a meaningful, complex, and deep molecular network, below which can be exploited in the combat against cancer.

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Tan J., Le A. Breast Cancer Metabolism. Adv. Exp. Med. Biol. 2018;1063:83-93.
Not in our library10.1007/978-3-319-77736-8_6
19.
Metabolic Reprogramming in Breast Cancer and Its Therapeutic Implications · 2019
No notice
20.
Martinez-Outschoorn U.E., Peiris-Pages M., Pestell R.G., Sotgia F., Lisanti M.P. Cancer metabolism: A therapeutic perspective. Nat. Rev. Clin. Oncol. 2017;14:11-31.
Not in our library10.1038/nrclinonc.2016.60
21.
Kulkoyluoglu-Cotul E., Arca A., Madak-Erdogan Z. Crosstalk between Estrogen Signaling and Breast Cancer Metabolism. Trends Endocrinol. Metab. 2019;30:25-38.
Not in our library10.1016/j.tem.2018.10.006
22.
Warburg O., Wind F., Negelein E. The Metabolism of Tumors in the Body. J. Gen. Physiol. 1927;8:519-530.
Not in our library10.1085/jgp.8.6.519
23.
Isidoro A., Casado E., Redondo A., Acebo P., Espinosa E., Alonso A.M., Cejas P., Hardisson D., Fresno Vara J.A., Belda-Iniesta C., et al. Breast carcinomas fulfill the Warburg hypothesis and provide metabolic markers of cancer prognosis. Carcinogenesis. 2005;26:2095-2104.
Not in our library10.1093/carcin/bgi188
24.
Fodor T., Szanto M., Abdul-Rahman O., Nagy L., Der A., Kiss B., Bai P. Combined Treatment of MCF-7 Cells with AICAR and Methotrexate, Arrests Cell Cycle and Reverses Warburg Metabolism through AMP-Activated Protein Kinase (AMPK) and FOXO1. PLoS ONE. 2016;11:e0150232.
Not in our library10.1371/journal.pone.0150232
25.
Elia I., Schmieder R., Christen S., Fendt S.M. Organ-Specific Cancer Metabolism and Its Potential for Therapy. Handb. Exp. Pharmacol. 2016;233:321-353.
Not in our library10.1007/164_2015_10
26.
Amino Acid Transporters and Glutamine Metabolism in Breast Cancer · 2018
No notice
27.
Poulose N., Mills I.G., Steele R.E. The impact of transcription on metabolism in prostate and breast cancers. Endocr. Relat. Cancer. 2018;25:R435-R452.
Not in our library10.1530/erc-18-0048
28.
Saavedra-Garcia P., Nichols K., Mahmud Z., Fan L.Y., Lam E.W. Unravelling the role of fatty acid metabolism in cancer through the FOXO3-FOXM1 axis. Mol. Cell Endocrinol. 2018;462:82-92.
Not in our library10.1016/j.mce.2017.01.012
29.
Obesity and Breast Cancer: Current Insights on the Role of Fatty Acids and Lipid Metabolism in Promoting Breast Cancer Growth and Progression · 2017
No notice
30.
Thakur S.B., Horvat J.V., Hancu I., Sutton O.M., Bernard-Davila B., Weber M., Oh J.H., Marino M.A., Avendano D., Leithner D., et al. Quantitative in vivo proton MR spectroscopic assessment of lipid metabolism: Value for breast cancer diagnosis and prognosis. J. Magn. Reson. Imaging. 2019.
Not in our library10.1002/jmri.26622
31.
Cha Y.J., Kim H.M., Koo J.S. Expression of Lipid Metabolism-Related Proteins Differs between Invasive Lobular Carcinoma and Invasive Ductal Carcinoma. Int. J. Mol. Sci. 2017;18.
Not in our library10.3390/ijms18010232
32.
Possemato R., Marks K.M., Shaul Y.D., Pacold M.E., Kim D., Birsoy K., Sethumadhavan S., Woo H.K., Jang H.G., Jha A.K., et al. Functional genomics reveal that the serine synthesis pathway is essential in breast cancer. Nature. 2011;476:346-350.
Not in our library10.1038/nature10350
33.
van Geldermalsen M., Quek L.E., Turner N., Freidman N., Pang A., Guan Y.F., Krycer J.R., Ryan R., Wang Q., Holst J. Benzylserine inhibits breast cancer cell growth by disrupting intracellular amino acid homeostasis and triggering amino acid response pathways. BMC Cancer. 2018;18:689.
Not in our library10.1186/s12885-018-4599-8
34.
Du T., Zhu L., Levine K.M., Tasdemir N., Lee A.V., Vignali D.A.A., Houten B.V., Tseng G.C., Oesterreich S. Invasive lobular and ductal breast carcinoma differ in immune response, protein translation efficiency and metabolism. Sci. Rep. 2018;8:7205.
Not in our library10.1038/s41598-018-25357-0
35.
Schito L., Rey S. Hypoxic pathobiology of breast cancer metastasis. Biochim. Biophys. Acta Rev. Cancer. 2017;1868:239-245.
Not in our library10.1016/j.bbcan.2017.05.004
36.
Nie C., Lv H., Bie L., Hou H., Chen X. Hypoxia-inducible factor 1-alpha expression correlates with response to neoadjuvant chemotherapy in women with breast cancer. Medicine (Baltimore). 2018;97:e13551.
Not in our library10.1097/md.0000000000013551
37.
Craze M.L., Cheung H., Jewa N., Coimbra N.D.M., Soria D., El-Ansari R., Aleskandarany M.A., Wai Cheng K., Diez-Rodriguez M., Nolan C.C., et al. MYC regulation of glutamine-proline regulatory axis is key in luminal B breast cancer. Br. J. Cancer. 2018;118:258-265.
Not in our library10.1038/bjc.2017.387
38.
Kim S., Kim D.H., Jung W.H., Koo J.S. Expression of glutamine metabolism-related proteins according to molecular subtype of breast cancer. Endocr. Relat. Cancer. 2013;20:339-348.
Not in our library10.1530/erc-12-0398
39.
El Ansari R., McIntyre A., Craze M.L., Ellis I.O., Rakha E.A., Green A.R. Altered glutamine metabolism in breast cancer; subtype dependencies and alternative adaptations. Histopathology. 2018;72:183-190.
Not in our library10.1111/his.13334
40.
Maiese K. Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer. Curr. Neurovasc. Res. 2017;14:299-304.
Not in our library10.2174/1567202614666170718092010
41.
Ranhotra H.S. The estrogen-related receptors in metabolism and cancer: Newer insights. J. Recept Signal. Transduct. Res. 2018;38:95-100.
Not in our library10.1080/10799893.2018.1456552
42.
Raphael J., Desautels D., Pritchard K.I., Petkova E., Shah P.S. Phosphoinositide 3-kinase inhibitors in advanced breast cancer: A systematic review and meta-analysis. Eur. J. Cancer. 2018;91:38-46.
Not in our library10.1016/j.ejca.2017.12.010
43.
Keegan N.M., Gleeson J.P., Hennessy B.T., Morris P.G. PI3K inhibition to overcome endocrine resistance in breast cancer. Expert Opin. Investig. Drugs. 2018;27:1-15.
Not in our library10.1080/13543784.2018.1417384
44.
Histological evaluation of AMPK signalling in primary breast cancer · 2009
No notice
45.
Laderoute K.R., Calaoagan J.M., Chao W.R., Dinh D., Denko N., Duellman S., Kalra J., Liu X., Papandreou I., Sambucetti L., et al. 5′-AMP-activated protein kinase (AMPK) supports the growth of aggressive experimental human breast cancer tumors. J. Biol. Chem. 2014;289:22850-22864.
Not in our library10.1074/jbc.m114.576371
46.
Sotgia F., Whitaker-Menezes D., Martinez-Outschoorn U.E., Salem A.F., Tsirigos A., Lamb R., Sneddon S., Hulit J., Howell A., Lisanti M.P. Mitochondria “fuel” breast cancer metabolism: Fifteen markers of mitochondrial biogenesis label epithelial cancer cells, but are excluded from adjacent stromal cells. Cell Cycle. 2012;11:4390-4401.
Not in our library10.4161/cc.22777
47.
Fuchinoue F., Hirotani Y., Nakanishi Y., Yamaguchi H., Nishimaki H., Noda H., Tang X.Y., Iizuka M., Amano S., Sugitani M., et al. Overexpression of PGC1alpha and accumulation of p62 in apocrine carcinoma of the breast. Pathol. Int. 2015;65:19-26.
Not in our library10.1111/pin.12235
48.
Lim S., Liu H., Madeira da Silva L., Arora R., Liu Z., Phillips J.B., Schmitt D.C., Vu T., McClellan S., Lin Y., et al. Immunoregulatory Protein B7-H3 Reprograms Glucose Metabolism in Cancer Cells by ROS-Mediated Stabilization of HIF1alpha. Cancer Res. 2016;76:2231-2242.
Not in our library10.1158/0008-5472.can-15-1538
49.
Migneco G., Whitaker-Menezes D., Chiavarina B., Castello-Cros R., Pavlides S., Pestell R.G., Fatatis A., Flomenberg N., Tsirigos A., Howell A., et al. Glycolytic cancer associated fibroblasts promote breast cancer tumor growth, without a measurable increase in angiogenesis: Evidence for stromal-epithelial metabolic coupling. Cell Cycle. 2010;9:2412-2422.
Not in our library10.4161/cc.9.12.11989
50.
Huang R., Zong X. Aberrant cancer metabolism in epithelial-mesenchymal transition and cancer metastasis: Mechanisms in cancer progression. Crit. Rev. Oncol. Hematol. 2017;115:13-22.
Not in our library10.1016/j.critrevonc.2017.04.005
51.
Kondaveeti Y., Guttilla Reed I.K., White B.A. Epithelial-mesenchymal transition induces similar metabolic alterations in two independent breast cancer cell lines. Cancer Lett. 2015;364:44-58.
Not in our library10.1016/j.canlet.2015.04.025
52.
Choi J., Cha Y.J., Koo J.S. Adipocyte biology in breast cancer: From silent bystander to active facilitator. Prog. Lipid Res. 2018;69:11-20.
Not in our library10.1016/j.plipres.2017.11.002
53.
Hidayat K., Yang C.M., Shi B.M. Body fatness at a young age, body fatness gain and risk of breast cancer: Systematic review and meta-analysis of cohort studies. Obes. Rev. 2018;19:254-268.
Not in our library10.1111/obr.12627
54.
Martin S.D., McGee S.L. Metabolic reprogramming in type 2 diabetes and the development of breast cancer. J. Endocrinol. 2018;237:R35-R46.
Not in our library10.1530/joe-18-0037
55.
Association between changes in body fat and disease progression after breast cancer surgery is moderated by menopausal status · 2017
Not checked
56.
Sun H., Zou J., Chen L., Zu X., Wen G., Zhong J. Triple-negative breast cancer and its association with obesity. Mol. Clin. Oncol. 2017;7:935-942.
Not in our library10.3892/mco.2017.1429
57.
Avgerinos K.I., Spyrou N., Mantzoros C.S., Dalamaga M. Obesity and Cancer Risk: Emerging biological mechanisms and perspectives. Metabolism. 2018;13:30232-30234.
Not in our library10.1016/j.metabol.2018.11.001
58.
Dennison J.B., Molina J.R., Mitra S., González-Angulo A.M., Balko J.M., Kuba M.G., Sanders M.E., Pinto J.A., Gómez H.L., Arteaga C.L., et al. Lactate dehydrogenase B: A metabolic marker of response to neoadjuvant chemotherapy in breast cancer. Clin. Cancer Res. 2013;19:3703-3713.
Not in our library10.1158/1078-0432.ccr-13-0623
59.
The Influence of Metabolism on Drug Response in Cancer · 2018
No notice
60.
Targeting Breast Cancer Stem Cells to Overcome Treatment Resistance · 2018
No notice
61.
Sinn H.P., Kreipe H. A Brief Overview of the WHO Classification of Breast Tumors, 4th Edition, Focusing on Issues and Updates from the 3rd Edition. Breast Care (Basel). 2013;8:149-154.
Not in our library10.1159/000350774
62.
Warner M., Gustafsson J.A. On estrogen, cholesterol metabolism, and breast cancer. N. Engl. J. Med. 2014;370:572-573.
Not in our library10.1056/nejmcibr1315176
63.
Association of tamoxifen resistance and lipid reprogramming in breast cancer · 2018
No notice
64.
Munir M.T., Ponce C., Powell C.A., Tarafdar K., Yanagita T., Choudhury M., Gollahon L.S., Rahman S.M. The contribution of cholesterol and epigenetic changes to the pathophysiology of breast cancer. J. Steroid Biochem. Mol. Biol. 2018;183:1-9.
Not in our library10.1016/j.jsbmb.2018.05.001
65.
McDonnell D.P., Park S., Goulet M.T., Jasper J., Wardell S.E., Chang C.Y., Norris J.D., Guyton J.R., Nelson E.R. Obesity, cholesterol metabolism, and breast cancer pathogenesis. Cancer Res. 2014;74:4976-4982.
Not in our library10.1158/0008-5472.can-14-1756
66.
Nelson E.R., Chang C.Y., McDonnell D.P. Cholesterol and breast cancer pathophysiology. Trends Endocrinol. Metab. 2014;25:649-655.
Not in our library10.1016/j.tem.2014.10.001
67.
Wu Q., Ishikawa T., Sirianni R., Tang H., McDonald J.G., Yuhanna I.S., Thompson B., Girard L., Mineo C., Brekken R.A., et al. 27-Hydroxycholesterol promotes cell-autonomous, ER-positive breast cancer growth. Cell Rep. 2013;5:637-645.
Not in our library10.1016/j.celrep.2013.10.006
68.
Mokarram P., Alizadeh J., Razban V., Barazeh M., Solomon C., Kavousipour S. Interconnection of Estrogen/Testosterone Metabolism and Mevalonate Pathway in Breast and Prostate Cancers. Curr. Mol. Pharmacol. 2017;10:86-114.
Not in our library10.2174/1874467209666160112125631
69.
Chen W., Zhu L., Yu X., Fu Q., Xu W., Wang P. Quantitative assessment of metabolic tumor burden in molecular subtypes of primary breast cancer with FDG PET/CT. Diagn. Interv. Radiol. 2018;24:336-341.
Not in our library10.5152/dir.2018.17367
70.
Lee S.J., Chung M.S., Shin S.J., Choi Y.Y. Correlation of tumor uptake on breast-specific gamma imaging and fluorodeoxyglucose PET/CT with molecular subtypes of breast cancer. Medicine (Baltimore). 2018;97:e12840.
Not in our library10.1097/md.0000000000012840
71.
Incoronato M., Grimaldi A.M., Cavaliere C., Inglese M., Mirabelli P., Monti S., Ferbo U., Nicolai E., Soricelli A., Catalano O.A., et al. Relationship between functional imaging and immunohistochemical markers and prediction of breast cancer subtype: A PET/MRI study. Eur. J. Nucl. Med. Mol. Imaging. 2018;45:1680-1693.
Not in our library10.1007/s00259-018-4010-7
72.
Mullarky E., Lairson L.L., Cantley L.C., Lyssiotis C.A. A novel small-molecule inhibitor of 3-phosphoglycerate dehydrogenase. Mol. Cell Oncol. 2016;3:e1164280.
Not in our library10.1080/23723556.2016.1164280
73.
Choi J., Kim E.S., Koo J.S. Expression of Pentose Phosphate Pathway-Related Proteins in Breast Cancer. Dis. Markers. 2018;2018:9369358.
Not in our library10.1155/2018/9369358
74.
Kim S.K., Jung W.H., Koo J.S. Differential expression of enzymes associated with serine/glycine metabolism in different breast cancer subtypes. PLoS ONE. 2014;9:e101004.
Not in our library10.1371/journal.pone.0101004
75.
Kalhan S.C., Hanson R.W. Resurgence of serine: An often neglected but indispensable amino Acid. J. Biol. Chem. 2012;287:19786-19791.
Not in our library10.1074/jbc.r112.357194
76.
Bostner J., Alayev A., Berman A.Y., Fornander T., Nordenskjold B., Holz M.K., Stal O. Raptor localization predicts prognosis and tamoxifen response in estrogen receptor-positive breast cancer. Breast Cancer Res. Treat. 2018;168:17-27.
Not in our library10.1007/s10549-017-4508-x
77.
Shea M.P., O’Leary K.A., Wegner K.A., Vezina C.M., Schuler L.A. High collagen density augments mTOR-dependent cancer stem cells in ERalpha+ mammary carcinomas, and increases mTOR-independent lung metastases. Cancer Lett. 2018;433:1-9.
Not in our library10.1016/j.canlet.2018.06.025
78.
Schettini F., Buono G., Trivedi M.V., De Placido S., Arpino G., Giuliano M. PI3K/mTOR Inhibitors in the Treatment of Luminal Breast Cancer. Why, When and to Whom? Breast Care (Basel). 2017;12:290-294.
Not in our library10.1159/000481657
79.
Pavlides S., Whitaker-Menezes D., Castello-Cros R., Flomenberg N., Witkiewicz A.K., Frank P.G., Casimiro M.C., Wang C., Fortina P., Addya S., et al. The reverse Warburg effect: Aerobic glycolysis in cancer associated fibroblasts and the tumor stroma. Cell Cycle. 2009;8:3984-4001.
Not in our library10.4161/cc.8.23.10238
80.
Bonuccelli G., Whitaker-Menezes D., Castello-Cros R., Pavlides S., Pestell R.G., Fatatis A., Witkiewicz A.K., Vander Heiden M.G., Migneco G., Chiavarina B., et al. The reverse Warburg effect: Glycolysis inhibitors prevent the tumor promoting effects of caveolin-1 deficient cancer associated fibroblasts. Cell Cycle. 2010;9:1960-1971.
Not in our library10.4161/cc.9.10.11601
81.
Mitochondrial biogenesis is required for the anchorage-independent survival and propagation of stem-like cancer cells · 2015
No notice
82.
Choi J., Kim D.H., Jung W.H., Koo J.S. Metabolic interaction between cancer cells and stromal cells according to breast cancer molecular subtype. Breast Cancer Res. 2013;15:R78.
Not in our library10.1186/bcr3472
83.
Kim S., Kim D.H., Jung W.H., Koo J.S. Metabolic phenotypes in triple-negative breast cancer. Tumour Biol. 2013;34:1699-1712.
Not in our library10.1007/s13277-013-0707-1
84.
Feng W., Gentles A., Nair R.V., Huang M., Lin Y., Lee C.Y., Cai S., Scheeren F.A., Kuo A.H., Diehn M. Targeting unique metabolic properties of breast tumor initiating cells. Stem Cells. 2014;32:1734-1745.
Not in our library10.1002/stem.1662
85.
Fiorillo M., Peiris-Pagès M., Sanchez-Alvarez R., Bartella L., Di Donna L., Dolce V., Sindona G., Sotgia F., Cappello A.R., Lisanti M.P. Bergamot natural products eradicate cancer stem cells (CSCs) by targeting mevalonate, Rho-GDI-signalling and mitochondrial metabolism. Biochim. Biophys. Acta. 2018;4:30061-30066.
Not in our library10.1016/j.bbabio.2018.03.018
86.
Ozsvari B., Fiorillo M., Bonuccelli G., Cappello A.R., Frattaruolo L., Sotgia F., Trowbridge R., Foster R., Lisanti M.P. Mitoriboscins: Mitochondrial-based therapeutics targeting cancer stem cells (CSCs), bacteria and pathogenic yeast. Oncotarget. 2017;8:67457-67472.
Not in our library10.18632/oncotarget.19084
87.
Fiorillo M., Lamb R., Tanowitz H.B., Cappello A.R., Martinez-Outschoorn U.E., Sotgia F., Lisanti M.P. Bedaquiline, an FDA-approved antibiotic, inhibits mitochondrial function and potently blocks the proliferative expansion of stem-like cancer cells (CSCs). Aging (Albany NY). 2016;8:1593-1607.
Not in our library10.18632/aging.100983
88.
Zhou Y., Xu Z., Quan D., Zhang F., Zhang H., Xiao T., Hou S., Qiao H., Harismendy O., Wang J.Y.J., et al. Nuclear respiratory factor 1 promotes spheroid survival and mesenchymal transition in mammary epithelial cells. Oncogene. 2018.
Not in our library10.1038/s41388-018-0349-2
89.
Rabinovich I., Sebastiao A.P.M., Lima R.S., Urban C.A., Junior E.S., Anselmi K.F., Elifio-Esposito S., De Noronha L., Moreno-Amaral A.N. Cancer stem cell markers ALDH1 and CD44+/CD24− phenotype and their prognosis impact in invasive ductal carcinoma. Eur J. Histochem. 2018;62.
Not in our library10.4081/ejh.2018.2943
90.
Rycaj K., Tang D.G. Cell-of-Origin of Cancer versus Cancer Stem Cells: Assays and Interpretations. Cancer Res. 2015;75:4003-4011.
Not in our library10.1158/0008-5472.can-15-0798
91.
Cadaverine, a metabolite of the microbiome, reduces breast cancer aggressiveness through trace amino acid receptors · 2019
No notice
92.
Ozsvari B., Sotgia F., Lisanti M.P. A new mutation-independent approach to cancer therapy: Inhibiting oncogenic RAS and MYC, by targeting mitochondrial biogenesis. Aging (Albany NY). 2017;9:2098-2116.
Not in our library10.18632/aging.101304
93.
Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: Treating cancer like an infectious disease · 2015
No notice
94.
Metabolic profiling of triple-negative breast cancer cells reveals metabolic vulnerabilities · 2017
No notice
95.
Winnike J.H., Stewart D.A., Pathmasiri W.W., McRitchie S.L., Sumner S.J. Stable Isotope-Resolved Metabolomic Differences between Hormone-Responsive and Triple-Negative Breast Cancer Cell Lines. Int. J. Breast Cancer. 2018;2018:2063540.
Not in our library10.1155/2018/2063540
96.
Morris B.A., Burkel B., Ponik S.M., Fan J., Condeelis J.S., Aguirre-Ghiso J.A., Castracane J., Denu J.M., Keely P.J. Collagen Matrix Density Drives the Metabolic Shift in Breast Cancer Cells. EBioMedicine. 2016;13:146-156.
Not in our library10.1016/j.ebiom.2016.10.012
97.
Gao D., Fish E.N. Chemokines in breast cancer: Regulating metabolism. Cytokine. 2018;109:57-64.
Not in our library10.1016/j.cyto.2018.02.010
98.
Jones F.A. Physiology of the Gastrointestinal Tract. 2018.
Not in our library
99.
Chen J., Domingue J.C., Sears C.L. Microbiota dysbiosis in select human cancers: Evidence of association and causality. Semin. Immunol. 2017;32:25-34.
Not in our library10.1016/j.smim.2017.08.001
100.
Mima K., Nakagawa S., Sawayama H., Ishimoto T., Imai K., Iwatsuki M., Hashimoto D., Baba Y., Yamashita Y.I., Yoshida N., et al. The microbiome and hepatobiliary-pancreatic cancers. Cancer Lett. 2017;402:9-15.
Not in our library10.1016/j.canlet.2017.05.001
101.
Mao Q., Jiang F., Yin R., Wang J., Xia W., Dong G., Ma W., Yang Y., Xu L., Hu J., et al. Interplay between the lung microbiome and lung cancer. Cancer Lett. 2018;415:40-48.
Not in our library10.1016/j.canlet.2017.11.036
102.
Bai J., Behera M., Bruner D.W. The gut microbiome, symptoms, and targeted interventions in children with cancer: A systematic review. Support. Care Cancer. 2018;26:427-439.
Not in our library10.1007/s00520-017-3982-3
103.
Biragyn A., Ferrucci L. Gut dysbiosis: A potential link between increased cancer risk in ageing and inflammaging. Lancet Oncol. 2018;19:e295-e304.
Not in our library10.1016/s1470-2045(18)30095-0
104.
Potgens S.A., Brossel H., Sboarina M., Catry E., Cani P.D., Neyrinck A.M., Delzenne N.M., Bindels L.B. Klebsiella oxytoca expands in cancer cachexia and acts as a gut pathobiont contributing to intestinal dysfunction. Sci. Rep. 2018;8:12321.
Not in our library10.1038/s41598-018-30569-5
105.
Microbial Dysbiosis Is Associated with Human Breast Cancer · 2014
No notice
106.
The Microbiota of Breast Tissue and Its Association with Breast Cancer · 2016
No notice
107.
Banerjee S., Wei Z., Tan F., Peck K.N., Shih N., Feldman M., Rebbeck T.R., Alwine J.C., Robertson E.S. Distinct microbiological signatures associated with triple negative breast cancer. Sci. Rep. 2015;5:15162.
Not in our library10.1038/srep15162
108.
Characterization of the microbiome of nipple aspirate fluid of breast cancer survivors · 2016
No notice
109.
The Microbiome of Aseptically Collected Human Breast Tissue in Benign and Malignant Disease · 2016
No notice
110.
Urbaniak C., Cummins J., Brackstone M., Macklaim J.M., Gloor G.B., Baban C.K., Scott L., O’Hanlon D.M., Burton J.P., Francis K.P., et al. Microbiota of human breast tissue. Appl. Environ. Microbiol. 2014;80:3007-3014.
Not in our library10.1128/aem.00242-14
111.
Breast tissue, oral and urinary microbiomes in breast cancer · 2017
No notice
112.
A comprehensive analysis of breast cancer microbiota and host gene expression · 2017
No notice
113.
Distinct Microbial Signatures Associated With Different Breast Cancer Types · 2018
No notice
114.
Costantini L., Magno S., Albanese D., Donati C., Molinari R., Filippone A., Masetti R., Merendino N. Characterization of human breast tissue microbiota from core needle biopsies through the analysis of multi hypervariable 16S-rRNA gene regions. Sci. Rep. 2018;8:16893.
Not in our library10.1038/s41598-018-35329-z
115.
Study of Microbiomes in Aseptically Collected Samples of Human Breast Tissue Using Needle Biopsy and the Potential Role of in situ Tissue Microbiomes for Promoting Malignancy · 2018
No notice
116.
Fecal microbial determinants of fecal and systemic estrogens and estrogen metabolites: a cross-sectional study · 2012
No notice
117.
Fuhrman B.J., Feigelson H.S., Flores R., Gail M.H., Xu X., Ravel J., Goedert J.J. Associations of the fecal microbiome with urinary estrogens and estrogen metabolites in postmenopausal women. J. Clin. Endocrinol. Metab. 2014;99:4632-4640.
Not in our library10.1210/jc.2014-2222
118.
Goedert J.J., Jones G., Hua X., Xu X., Yu G., Flores R., Falk R.T., Gail M.H., Shi J., Ravel J., et al. Investigation of the association between the fecal microbiota and breast cancer in postmenopausal women: A population-based case-control pilot study. J. Natl, Cancer Inst. 2015;107:djv147.
Not in our library10.1093/jnci/djv147
119.
Goedert J.J., Hua X., Bielecka A., Okayasu I., Milne G.L., Jones G.S., Fujiwara M., Sinha R., Wan Y., Xu X., et al. Postmenopausal breast cancer and oestrogen associations with the IgA-coated and IgA-noncoated faecal microbiota. Br. J. Cancer. 2018;23:435.
Not in our library10.1038/bjc.2017.435
120.
Miko E., Vida A., Kovácsm T., Ujlakim G., Trencsényim G., Márton J., Sári Z., Kovács P., Boratkó A., Hujber Z., et al. Lithocholic acid, a bacterial metabolite reduces breast cancer cell proliferation and aggressiveness. Biochim. Biophys. Acta. 2018;1859:958-974.
Not in our library10.1016/j.bbabio.2018.04.002
121.
Luu T.H., Michel C., Bard J.M., Dravet F., Nazih H., Bobin-Dubigeon C. Intestinal Proportion of Blautia sp. is Associated with Clinical Stage and Histoprognostic Grade in Patients with Early-Stage Breast Cancer. Nutr. Cancer. 2017;69:267-275.
Not in our library10.1080/01635581.2017.1263750
122.
Breast cancer in postmenopausal women is associated with an altered gut metagenome · 2018
No notice
123.
Robinson K.M., Crabtree J., Mattick J.S., Anderson K.E., Dunning Hotopp J.C. Distinguishing potential bacteria-tumor associations from contamination in a secondary data analysis of public cancer genome sequence data. Microbiome. 2017.
Not in our library10.1186/s40168-016-0224-8
124.
Noguti J., Lee D.J. Association of microbes with breast cancer. Microbiome and Cancer. 2019;123-149.
Not in our library
125.
Fruge A.D., Van der Pol W., Rogers L.Q., Morrow C.D., Tsuruta Y., Demark-Wahnefried W. Fecal Akkermansia muciniphila Is Associated with Body Composition and Microbiota Diversity in Overweight and Obese Women with Breast Cancer Participating in a Presurgical Weight Loss Trial. J. Acad. Nutr. Diet. 2018;9:164.
Not in our library10.1016/j.jand.2018.08.164
126.
Velicer C.M., Heckbert S.R., Lampe J.W., Potter J.D., Robertson C.A., Taplin S.H. Antibiotic use in relation to the risk of breast cancer. JAMA. 2004;291:827-835.
Not in our library10.1001/jama.291.7.827
127.
Velicer C.M., Heckbert S.R., Rutter C., Lampe J.W., Malone K. Association between antibiotic use prior to breast cancer diagnosis and breast tumour characteristics (United States). Cancer Causes Control. 2006;17:307-313.
Not in our library10.1007/s10552-005-0445-9
128.
Friedman G.D., Oestreicher N., Chan J., Quesenberry C.P., Udaltsova N., Habel L.A. Antibiotics and risk of breast cancer: Up to 9 years of follow-up of 2.1 million women. Cancer Epidemiol. Biomarkers Prev. 2006;15:2102-2106.
Not in our library10.1158/1055-9965.epi-06-0401
129.
Wirtz H.S., Buist D.S.M., Gralow J.R., Barlow W.E., Gray S., Chubak J., Yu O., Bowles E.J.A., Fujii M., Boudreau D.M. Frequent antibiotic use and second breast cancer events. Cancer Epidemiol. Biomarkers Prev. 2013;22:1588-1599.
Not in our library10.1158/1055-9965.epi-13-0454
130.
Tamim H.M., Hanley J.A., Hajeer A.H., Boivin J.F., Collet J.P. Risk of breast cancer in relation to antibiotic use. Pharmacoepidemiol. Drug Saf. 2008;17:144-150.
Not in our library10.1002/pds.1512
131.
Satram-Hoang S., Moran E.M., Anton-Culver H., Burras R.W., Heimann T.M., Boggio I., Dykstra-Long G.R., Wood P.A., Zulka R., Hufnagel G., et al. A pilot study of male breast cancer in the Veterans Affairs healthcare system. J. Environ. Pathol. Toxicol. Oncol. 2010;29:235-244.
Not in our library10.1615/jenvironpatholtoxicoloncol.v29.i3.60
132.
Kirkup B., McKee A., Makin K., Paveley J., Caim S., Alcon-Giner C., Leclaire C., Dalby M., Le Gall G., Andrusaite A., et al. Perturbation of the gut microbiota by antibiotics results in accelerated breast tumour growth and metabolic dysregulation. BioRxiv. 2019.
Not in our library10.1101/553602
133.
Miko E., Vida A., Bai P. Translational aspects of the microbiome-to be exploited. Cell Biol. Toxicol. 2016;32:153-156.
Not in our library10.1007/s10565-016-9320-6
134.
Tao J., Li S., Gan R.Y., Zhao C.N., Meng X., Li H.B. Targeting gut microbiota with dietary components on cancer: Effects and potential mechanisms of action. Crit. Rev. Food Sci. Nutr. 2019;11:1-13.
Not in our library10.1080/10408398.2018.1555789
135.
Di Ciaula A., Wang D.Q., Molina-Molina E., Lunardi Baccetto R., Calamita G., Palmieri V.O., Portincasa P. Bile Acids and Cancer: Direct and Environmental-Dependent Effects. Ann. Hepatol. 2017;16:s87-s105.
Not in our library10.5604/01.3001.0010.5501
136.
Wikoff W.R., Anfora A.T., Liu J., Schultz P.G., Lesley S.A., Peters E.C., Siuzdak G. Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. Proc. Natl. Acad. Sci. USA. 2009;106:3698-3703.
Not in our library10.1073/pnas.0812874106
137.
Dumas M.E. The microbial-mammalian metabolic axis: Beyond simple metabolism. Cell Metab. 2011;13:489-490.
Not in our library10.1016/j.cmet.2011.04.005
138.
Burcelin R., Serino M., Chabo C., Garidou L., Pomie C., Courtney M., Amar J., Bouloumie A. Metagenome and metabolism: The tissue microbiota hypothesis. Diabetes Obes. Metab. 2013;15:61-70.
Not in our library10.1111/dom.12157
139.
Puertollano E., Kolida S., Yaqoob P. Biological significance of short-chain fatty acid metabolism by the intestinal microbiome. Curr. Opin. Clin. Nutr. Metab. Care. 2014;2:2.
Not in our library10.1097/mco.0000000000000025
140.
Goldberg A.A., Beach A., Davies G.F., Harkness T.A., Leblanc A., Titorenko V.I. Lithocholic bile acid selectively kills neuroblastoma cells, while sparing normal neuronal cells. Oncotarget. 2011;2:761-782.
Not in our library10.18632/oncotarget.338
141.
Goldberg A.A., Titorenko V.I., Beach A., Sanderson J.T. Bile acids induce apoptosis selectively in androgen-dependent and -independent prostate cancer cells. PeerJ. 2013;1:e122.
Not in our library10.7717/peerj.122
142.
Gafar A.A., Draz H.M., Goldberg A.A., Bashandy M.A., Bakry S., Khalifa M.A., AbuShair W., Titorenko V.I., Sanderson J.T. Lithocholic acid induces endoplasmic reticulum stress, autophagy and mitochondrial dysfunction in human prostate cancer cells. PeerJ. 2016;4:e2445.
Not in our library10.7717/peerj.2445
143.
Luu T.H., Bard J.M., Carbonnelle D., Chaillou C., Huvelin J.M., Bobin-Dubigeon C., Nazih H. Lithocholic bile acid inhibits lipogenesis and induces apoptosis in breast cancer cells. Cell Oncol. (Dordr). 2018;41:13-24.
Not in our library10.1007/s13402-017-0353-5
144.
Thirunavukkarasan M., Wang C., Rao A., Hind T., Teo Y.R., Siddiquee A.A., Goghari M.A.I., Kumar A.P., Herr D.R. Short-chain fatty acid receptors inhibit invasive phenotypes in breast cancer cells. PLoS ONE. 2017;12:e0186334.
Not in our library10.1371/journal.pone.0186334
145.
Dabek M., McCrae S.I., Stevens V.J., Duncan S.H., Louis P. Distribution of beta-glucosidase and beta-glucuronidase activity and of beta-glucuronidase gene gus in human colonic bacteria. FEMS Microbiol. Ecol. 2008;66:487-495.
Not in our library10.1111/j.1574-6941.2008.00520.x
146.
McIntosh F.M., Maison N., Holtrop G., Young P., Stevens V.J., Ince J., Johnstone A.M., Lobley G.E., Flint H.J., Louis P. Phylogenetic distribution of genes encoding beta-glucuronidase activity in human colonic bacteria and the impact of diet on faecal glycosidase activities. Environ. Microbiol. 2012;14:1876-1887.
Not in our library10.1111/j.1462-2920.2012.02711.x
147.
Gloux K., Berteau O., El Oumami H., Beguet F., Leclerc M., Dore J. A metagenomic beta-glucuronidase uncovers a core adaptive function of the human intestinal microbiome. Proc. Natl. Acad. Sci. USA. 2011;108:4539-4546.
Not in our library10.1073/pnas.1000066107
148.
Radde B.N., Ivanova M.M., Mai H.X., Salabei J.K., Hill B.G., Klinge C.M. Bioenergetic differences between MCF-7 and T47D breast cancer cells and their regulation by oestradiol and tamoxifen. Biochem. J. 2015;465:49-61.
Not in our library10.1042/bj20131608
149.
Radde B.N., Ivanova M.M., Mai H.X., Alizadeh-Rad N., Piell K., Van Hoose P., Cole M.P., Muluhngwi P., Kalbfleisch T.S., Rouchka E.C., et al. Nuclear respiratory factor-1 and bioenergetics in tamoxifen-resistant breast cancer cells. Exp. Cell Res. 2016;347:222-231.
Not in our library10.1016/j.yexcr.2016.08.006
150.
Sotgia F., Lisanti M.P. Mitochondrial mRNA transcripts predict overall survival, tumor recurrence and progression in serous ovarian cancer: Companion diagnostics for cancer therapy. Oncotarget. 2017;8:66925-66939.
Not in our library10.18632/oncotarget.19963
151.
Zacksenhaus E., Shrestha M., Liu J.C., Vorobieva I., Chung P.E.D., Ju Y., Nir U., Jiang Z. Mitochondrial OXPHOS Induced by RB1 Deficiency in Breast Cancer: Implications for Anabolic Metabolism, Stemness, and Metastasis. Trends Cancer. 2017;3:768-779.
Not in our library10.1016/j.trecan.2017.09.002
152.
Maximov P.Y., Abderrahman B., Curpan R.F., Hawsawi Y.M., Fan P., Jordan V.C. A unifying biology of sex steroid-induced apoptosis in prostate and breast cancers. Endocr. Relat. Cancer. 2018;25:R83-R113.
Not in our library10.1530/erc-17-0416
153.
Al-Howail H.A., Hakami H.A., Al-Otaibi B., Al-Mazrou A., Daghestani M.H., Al-Jammaz I., Al-Khalaf H.H., Aboussekhra A. PAC down-regulates estrogen receptor alpha and suppresses epithelial-to-mesenchymal transition in breast cancer cells. BMC Cancer. 2016;16:540.
Not in our library10.1186/s12885-016-2583-8
154.
Bouris P., Skandalis S.S., Piperigkou Z., Afratis N., Karamanou K., Aletras A.J., Moustakas A., Theocharis A.D., Karamanos N.K. Estrogen receptor alpha mediates epithelial to mesenchymal transition, expression of specific matrix effectors and functional properties of breast cancer cells. Matrix Biol. 2015;43:42-60.
Not in our library10.1016/j.matbio.2015.02.008
155.
Derrien M., Vaughan E.E., Plugge C.M., de Vos W.M. Akkermansia muciniphila gen. nov., sp. nov., a human intestinal mucin-degrading bacterium. Int. J. Syst. Evol. Microbiol. 2004;54:1469-1476.
Not in our library10.1099/ijs.0.02873-0
156.
Louis P., Young P., Holtrop G., Flint H.J. Diversity of human colonic butyrate-producing bacteria revealed by analysis of the butyryl-CoA:acetate CoA-transferase gene. Environ. Microbiol. 2010;12:304-314.
Not in our library10.1111/j.1462-2920.2009.02066.x
157.
Reichardt N., Duncan S.H., Young P., Belenguer A., McWilliam Leitch C., Scott K.P., Flint H.J., Louis P. Phylogenetic distribution of three pathways for propionate production within the human gut microbiota. ISME J. 2014;8:1323-1335.
Not in our library10.1038/ismej.2014.14
158.
Rodrigues M.F., Carvalho E., Pezzuto P., Rumjanek F.D., Amoedo N.D. Reciprocal modulation of histone deacetylase inhibitors sodium butyrate and trichostatin A on the energy metabolism of breast cancer cells. J. Cell Biochem. 2015;116:797-808.
Not in our library10.1002/jcb.25036
159.
Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment · 2017
No notice
160.
Arpaia N., Campbell C., Fan X., Dikiy S., van der Veeken J., deRoos P., Liu H., Cross J.R., Pfeffer K., Coffer P.J., et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Nature. 2013;504:451-455.
Not in our library10.1038/nature12726
161.
Tan J., McKenzie C., Potamitis M., Thorburn A.N., Mackay C.R., Macia L. The role of short-chain Fatty acids in health and disease. Adv. Immunol. 2014;121:91-119.
Not in our library10.1016/b978-0-12-800100-4.00003-9
162.
Yu X., Shahir A.M., Sha J., Feng Z., Eapen B., Nithianantham S., Das B., Karn J., Weinberg A., Bissada N.F., et al. Short Chain Fatty Acids From Periodontal Pathogens Suppress HDACs, EZH2, and SUV39H1 to Promote Kaposi’s Sarcoma-Associated Herpesvirus Replication. J. Virol. 2014;5:5.
Not in our library10.1128/jvi.03326-13
163.
The Short Chain Fatty Acid Butyrate Imprints an Antimicrobial Program in Macrophages · 2019
No notice
164.
Bile salt biotransformations by human intestinal bacteria · 2006
Not checked
165.
Ridlon J.M., Harris S.C., Bhowmik S., Kang D.J., Hylemon P.B. Consequences of bile salt biotransformations by intestinal bacteria. Gut Microbes. 2016;7:22-39.
Not in our library10.1080/19490976.2015.1127483
166.
Swales K.E., Korbonits M., Carpenter R., Walsh D.T., Warner T.D., Bishop-Bailey D. The farnesoid X receptor is expressed in breast cancer and regulates apoptosis and aromatase expression. Cancer Res. 2006;66:10120-10126.
Not in our library10.1158/0008-5472.can-06-2399
167.
A joint analysis of metabolomics and genetics of breast cancer · 2014
No notice
168.
Baker J.M., Al-Nakkash L., Herbst-Kralovetz M.M. Estrogen-gut microbiome axis: Physiological and clinical implications. Maturitas. 2017;103:45-53.
Not in our library10.1016/j.maturitas.2017.06.025
169.
Kwa M., Plottel C.S., Blaser M.J., Adams S. The Intestinal Microbiome and Estrogen Receptor-Positive Female Breast Cancer. J. Natl. Cancer Inst. 2016;108:djw029.
Not in our library10.1093/jnci/djw029
170.
Chen J.Q., Yager J.D. Estrogen’s effects on mitochondrial gene expression: Mechanisms and potential contributions to estrogen carcinogenesis. Ann. N. Y. Acad. Sci. 2004;1028:258-272.
Not in our library10.1196/annals.1322.030
171.
Chen J.Q., Delannoy M., Cooke C., Yager J.D. Mitochondrial localization of ERalpha and ERbeta in human MCF7 cells. Am. J. Physiol. Endocrinol. Metab. 2004;286:E1011-E1022.
Not in our library10.1152/ajpendo.00508.2003
172.
Chen J.Q., Russo P.A., Cooke C., Russo I.H., Russo J. ERbeta shifts from mitochondria to nucleus during estrogen-induced neoplastic transformation of human breast epithelial cells and is involved in estrogen-induced synthesis of mitochondrial respiratory chain proteins. Biochim. Biophys. Acta. 2007;1773:1732-1746.
Not in our library10.1016/j.bbamcr.2007.05.008
173.
Sansone P., Savini C., Kurelac I., Chang Q., Amato L.B., Strillacci A., Stepanova A., Iommarini L., Mastroleo C., Daly L., et al. Packaging and transfer of mitochondrial DNA via exosomes regulate escape from dormancy in hormonal therapy-resistant breast cancer. Proc. Natl. Acad. Sci. USA. 2017;114:E9066-E9075.
Not in our library10.1073/pnas.1704862114
174.
Sastre-Serra J., Valle A., Company M.M., Garau I., Oliver J., Roca P. Estrogen down-regulates uncoupling proteins and increases oxidative stress in breast cancer. Free Radic. Biol. Med. 2010;48:506-512.
Not in our library10.1016/j.freeradbiomed.2009.11.025
175.
Sastre-Serra J., Nadal-Serrano M., Pons D.G., Valle A., Garau I., Garcia-Bonafe M., Oliver J., Roca P. The oxidative stress in breast tumors of postmenopausal women is ERalpha/ERbeta ratio dependent. Free Radic. Biol. Med. 2013;61:11-17.
Not in our library10.1016/j.freeradbiomed.2013.03.005
176.
Formation of short chain fatty acids by the gut microbiota and their impact on human metabolism · 2016
No notice
177.
Clausen M.R., Mortensen P.B., Bendtsen F. Serum levels of short-chain fatty acids in cirrhosis and hepatic coma. Hepatology. 1991;14:1040-1045.
Not in our library10.1002/hep.1840140616
178.
Jakobsdottir G., Bjerregaard J.H., Skovbjerg H., Nyman M. Fasting serum concentration of short-chain fatty acids in subjects with microscopic colitis and celiac disease: No difference compared with controls, but between genders. Scand. J. Gastroenterol. 2013;48:696-701.
Not in our library10.3109/00365521.2013.786128
179.
Ktsoyan Z.A., Mkrtchyan M.S., Zakharyan M.K., Mnatsakanyan A.A., Arakelova K.A., Gevorgyan Z.U., Sedrakyan A.M., Hovhannisyan A.I., Arakelyan A.A., Aminov R.I. Systemic Concentrations of Short Chain Fatty Acids Are Elevated in Salmonellosis and Exacerbation of Familial Mediterranean Fever. Front. Microbiol. 2016;7:776.
Not in our library10.3389/fmicb.2016.00776
180.
Hopkins M.M., Meier K.E. Free Fatty Acid Receptors and Cancer: From Nutrition to Pharmacology. Handb. Exp. Pharmacol. 2017;236:233-251.
Not in our library10.1007/164_2016_48
181.
Yonezawa T., Kobayashi Y., Obara Y. Short-chain fatty acids induce acute phosphorylation of the p38 mitogen-activated protein kinase/heat shock protein 27 pathway via GPR43 in the MCF-7 human breast cancer cell line. Cell Signal. 2007;19:185-193.
Not in our library10.1016/j.cellsig.2006.06.004
182.
Bindels L.B., Porporato P., Dewulf E.M., Verrax J., Neyrinck A.M., Martin J.C., Scott K.P., Buc Calderon P., Feron O., Muccioli G.G., et al. Gut microbiota-derived propionate reduces cancer cell proliferation in the liver. Br. J. Cancer. 2012;107:1337-1344.
Not in our library10.1038/bjc.2012.409
183.
Ivan J., Major E., Sipos A., Kovacs K., Horvath D., Tamas I., Bay P., Dombradi V., Lontay B. The Short-Chain Fatty Acid Propionate Inhibits Adipogenic Differentiation of Human Chorion-Derived Mesenchymal Stem Cells Through the Free Fatty Acid Receptor 2. Stem Cells Dev. 2017;26:1724-1733.
Not in our library10.1089/scd.2017.0035
184.
Huang C.K., Chang P.H., Kuo W.H., Chen C.L., Jeng Y.M., Chang K.J., Shew J.Y., Hu C.M., Lee W.H. Adipocytes promote malignant growth of breast tumours with monocarboxylate transporter 2 expression via beta-hydroxybutyrate. Nat. Commun. 2017;8:14706.
Not in our library10.1038/ncomms14706
185.
Martinez-Outschoorn U.E., Lisanti M.P., Sotgia F. Catabolic cancer-associated fibroblasts transfer energy and biomass to anabolic cancer cells, fueling tumor growth. Semin. Cancer Biol. 2014;25:47-60.
Not in our library10.1016/j.semcancer.2014.01.005
186.
Long S.L., Gahan C.G.M., Joyce S.A. Interactions between gut bacteria and bile in health and disease. Mol. Aspects Med. 2017;56:54-65.
Not in our library10.1016/j.mam.2017.06.002
187.
Javitt N.B., Budai K., Miller D.G., Cahan A.C., Raju U., Levitz M. Breast-gut connection: Origin of chenodeoxycholic acid in breast cyst fluid. Lancet. 1994;343:633-635.
Not in our library10.1016/s0140-6736(94)92635-2
188.
Raju U., Levitz M., Javitt N.B. Bile acids in human breast cyst fluid: The identification of lithocholic acid. J. Clin. Endocrinol. Metab. 1990;70:1030-1034.
Not in our library10.1210/jcem-70-4-1030
189.
Watanabe M., Houten S.M., Mataki C., Christoffolete M.A., Kim B.W., Sato H., Messaddeq N., Harney J.W., Ezaki O., Kodama T., et al. Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation. Nature. 2006;439:484-489.
Not in our library10.1038/nature04330
190.
Thomas C., Gioiello A., Noriega L., Strehle A., Oury J., Rizzo G., Macchiarulo A., Yamamoto H., Mataki C., Pruzanski M., et al. TGR5-mediated bile acid sensing controls glucose homeostasis. Cell Metab. 2009;10:167-177.
Not in our library10.1016/j.cmet.2009.08.001
191.
Lefebvre P., Cariou B., Lien F., Kuipers F., Staels B. Role of bile acids and bile acid receptors in metabolic regulation. Physiol. Rev. 2009;89:147-191.
Not in our library10.1152/physrev.00010.2008
192.
Martinot E., Sedes L., Baptissart M., Lobaccaro J.M., Caira F., Beaudoin C., Volle D.H. Bile acids and their receptors. Mol. Aspects Med. 2017;56:2-9.
Not in our library10.1016/j.mam.2017.01.006
193.
Miller-Fleming L., Olin-Sandoval V., Campbell K., Ralser M. Remaining Mysteries of Molecular Biology: The Role of Polyamines in the Cell. J. Mol. Biol. 2015;427:3389-3406.
Not in our library10.1016/j.jmb.2015.06.020
194.
Seiler N. Catabolism of polyamines. Amino Acids. 2004;26:217-233.
Not in our library10.1007/s00726-004-0070-z
195.
de las Rivas B., Marcobal A., Carrascosa A.V., Munoz R. PCR detection of foodborne bacteria producing the biogenic amines histamine, tyramine, putrescine, and cadaverine. J. Food Prot. 2006;69:2509-2514.
Not in our library10.4315/0362-028x-69.10.2509
196.
Loser C., Folsch U.R., Paprotny C., Creutzfeldt W. Polyamine concentrations in pancreatic tissue, serum, and urine of patients with pancreatic cancer. Pancreas. 1990;5:119-127.
Not in our library10.1097/00006676-199003000-00001
197.
Loser C., Folsch U.R., Paprotny C., Creutzfeldt W. Polyamines in colorectal cancer. Evaluation of polyamine concentrations in the colon tissue, serum, and urine of 50 patients with colorectal cancer. Cancer. 1990;65:958-966.
Not in our library10.1002/1097-0142(19900215)65:4<958::aid-cncr2820650423>3.0.co;2-z
198.
Vattai A., Akyol E., Kuhn C., Hofmann S., Heidegger H., von Koch F., Hermelink K., Wuerstlein R., Harbeck N., Mayr D., et al. Increased trace amine-associated receptor 1 (TAAR1) expression is associated with a positive survival rate in patients with breast cancer. J. Cancer Res. Clin. Oncol. 2017;143:1637-1647.
Not in our library10.1007/s00432-017-2420-8
199.
Bashiardes S., Tuganbaev T., Federici S., Elinav E. The microbiome in anti-cancer therapy. Semin. Immunol. 2017;32:74-81.
Not in our library10.1016/j.smim.2017.04.001
200.
Roy S., Trinchieri G. Microbiota: A key orchestrator of cancer therapy. Nat. Rev. Cancer. 2017;17:271-285.
Not in our library10.1038/nrc.2017.13
201.
Manepalli S., Gandhi J.A., Ekhar V.V., Asplund M.B., Coelho C., Martinez L.R. Characterization of a cyclophosphamide-induced murine model of immunosuppression to study Acinetobacter baumannii pathogenesis. J. Med. Microbiol. 2013;62:1747-1754.
Not in our library10.1099/jmm.0.060004-0
202.
Viaud S., Saccheri F., Mignot G., Yamazaki T., Daillère R., Hannani D., Enot D.P., Pfirschke C., Engblom C., Pittet M.J., et al. The intestinal microbiota modulates the anticancer immune effects of cyclophosphamide. Science. 2013;342:971-976.
Not in our library10.1126/science.1240537
203.
Alexander J.L., Wilson I.D., Teare J., Marchesi J.R., Nicholson J.K., Kinross J.M. Gut microbiota modulation of chemotherapy efficacy and toxicity. Nat. Rev. Gastroenterol. Hepatol. 2017;14:356-365.
Not in our library10.1038/nrgastro.2017.20
204.
Cox G., Koteva K., Wright G.D. An unusual class of anthracyclines potentiate Gram-positive antibiotics in intrinsically resistant Gram-negative bacteria. J. Antimicrob. Chemother. 2014;69:1844-1855.
Not in our library10.1093/jac/dku057
205.
McCarron A.J., Armstrong C., Glynn G., Millar B.C., Rooney P.J., Goldsmith C.E., Xu J., Moore J.E. Antibacterial effects on acinetobacter species of commonly employed antineoplastic agents used in the treatment of haematological malignancies: An in vitro laboratory evaluation. Br. J. Biomed. Sci. 2012;69:14-17.
Not in our library10.1080/09674845.2012.11669916
206.
Parajuli P., Pandey R.P., Nguyen T.H.T., Dhakal D., Sohng J.K. Substrate Scope of O-Methyltransferase from Streptomyces peucetius for Biosynthesis of Diverse Natural Products Methoxides. Appl. Biochem. Biotechnol. 2018;184:1404-1420.
Not in our library10.1007/s12010-017-2603-4
207.
Dhakal D., Lim S.K., Kim D.H., Kim B.G., Yamaguchi T., Sohng J.K. Complete genome sequence of Streptomyces peucetius ATCC 27952, the producer of anticancer anthracyclines and diverse secondary metabolites. J. Biotechnol. 2018;267:50-54.
Not in our library10.1016/j.jbiotec.2017.12.024
208.
Zabala D., Brana A.F., Florez A.B., Salas J.A., Mendez C. Engineering precursor metabolite pools for increasing production of antitumor mithramycins in Streptomyces argillaceus. Metab. Eng. 2013;20:187-197.
Not in our library10.1016/j.ymben.2013.10.002
209.
Westman E.L., Canova M.J., Radhi I.J., Koteva K., Kireeva I., Waglechner N., Wright G.D. Bacterial inactivation of the anticancer drug doxorubicin. Chem. Biol. 2012;19:1255-1264.
Not in our library10.1016/j.chembiol.2012.08.011
210.
Bolourian A., Mojtahedi Z. Streptomyces, shared microbiome member of soil and gut, as ’old friends’ against colon cancer. FEMS Microbiol. Ecol. 2018;94.
Not in our library10.1093/femsec/fiy120
211.
Yang J., Liu K.X., Qu J.M., Wang X.D. The changes induced by cyclophosphamide in intestinal barrier and microflora in mice. Eur. J. Pharmacol. 2013;714:120-124.
Not in our library10.1016/j.ejphar.2013.06.006
212.
Liu T., Wu Y., Wang L., Pang X., Zhao L., Yuan H., Zhang C. A More Robust Gut Microbiota in Calorie-Restricted Mice Is Associated with Attenuated Intestinal Injury Caused by the Chemotherapy Drug Cyclophosphamide. MBio. 2019;10.
Not in our library10.1128/mbio.02903-18
213.
Xie J.H., Fan S.T., Nie S.P., Yu Q., Xiong T., Gong D., Xie M.Y. Lactobacillus plantarum NCU116 attenuates cyclophosphamide-induced intestinal mucosal injury, metabolism and intestinal microbiota disorders in mice. Food Funct. 2016;7:1584-1592.
Not in our library10.1039/c5fo01516b
214.
Daillere R., Vétizou M., Waldschmitt N., Yamazaki T., Isnard C., Poirier-Colame V., Duong C.P.M., Flament C., Lepage P., Roberti M.P., et al. Enterococcus hirae and Barnesiella intestinihominis Facilitate Cyclophosphamide-Induced Therapeutic Immunomodulatory Effects. Immunity. 2016;45:931-943.
Not in our library10.1016/j.immuni.2016.09.009
215.
Salva S., Marranzino G., Villena J., Aguero G., Alvarez S. Probiotic Lactobacillus strains protect against myelosuppression and immunosuppression in cyclophosphamide-treated mice. Int. Immunopharmacol. 2014;22:209-221.
Not in our library10.1016/j.intimp.2014.06.017
216.
Hussein M.H., Schneider E.K., Elliott A.G., Han M., Reyes-Ortega F., Morris F., Blastovich M.A.T., Jasim R., Currie B., Mayo M., et al. From Breast Cancer to Antimicrobial: Combating Extremely Resistant Gram-Negative “Superbugs” Using Novel Combinations of Polymyxin B with Selective Estrogen Receptor Modulators. Microb. Drug Resist. 2017;23:640-650.
Not in our library10.1089/mdr.2016.0196
217.
Scott S.A., Spencer C.T., O’Reilly M.C., Brown K.A., Lavieri R.R., Cho C.H., Jung D.I., Larock R.C., Brown H.A., Lindsley C.W. Discovery of desketoraloxifene analogues as inhibitors of mammalian, Pseudomonas aeruginosa, and NAPE phospholipase D enzymes. ACS Chem. Biol. 2015;10:421-432.
Not in our library10.1021/cb500828m
218.
Ho Sui S.J., Lo R., Fernandes A.R., Caulfield M.D., Lerman J.A., Xie L., Bourne P.E., Baillie D.L., Brinkman F.S. Raloxifene attenuates Pseudomonas aeruginosa pyocyanin production and virulence. Int. J. Antimicrob. Agents. 2012;40:246-251.
Not in our library10.1016/j.ijantimicag.2012.05.009
219.
Gerits E., Defraine V., Vandamme K., De Cremer K., De Brucker K., Thevissen K., Cammue B.P.A., Beullens S., Fauvart M., Verstraeten N., et al. Repurposing Toremifene for Treatment of Oral Bacterial Infections. Antimicrob. Agents Chemother. 2017;61.
Not in our library10.1128/aac.01846-16
220.
Jacobs A.C., Didone L., Jobson J., Sofia M.K., Krysan D., Dunman P.M. Adenylate kinase release as a high-throughput-screening-compatible reporter of bacterial lysis for identification of antibacterial agents. Antimicrob. Agents Chemother. 2013;57:26-36.
Not in our library10.1128/aac.01640-12
221.
Luxo C., Jurado A.S., Custodio J.B., Madeira V.M. Toxic effects of tamoxifen on the growth and respiratory activity of Bacillus stearothermophilus. Toxicol. In Vitro. 2001;15:303-305.
Not in our library10.1016/s0887-2333(01)00024-8
222.
Poirot M., Silvente-Poirot S., Weichselbaum R.R. Cholesterol metabolism and resistance to tamoxifen. Curr. Opin. Pharmacol. 2012;12:683-689.
Not in our library10.1016/j.coph.2012.09.007
223.
Dou T.Y., Luan H.W., Liu X.B., Li S.Y., Du X.F., Yang L. Enzymatic hydrolysis of 7-xylosyltaxanes by an extracellular xylosidase from Cellulosimicrobium cellulans. Biotechnol. Lett. 2015;37:1905-1910.
Not in our library10.1007/s10529-015-1867-4
224.
Zhou D.J., Pan J., Yu H.L., Zheng G.W., Xu J.H. Target-oriented discovery of a new esterase-producing strain Enterobacter sp. ECU1107 for whole cell-catalyzed production of (2S,3R)-3-phenylglycidate as a chiral synthon of Taxol. Appl. Microbiol. Biotechnol. 2013;97:6293-6300.
Not in our library10.1007/s00253-012-4435-z
225.
Byrd C.A., Bornmann W., Erdjument-Bromage H., Tempst P., Pavletich N., Rosen N., Nathan C.F., Ding A. Heat shock protein 90 mediates macrophage activation by Taxol and bacterial lipopolysaccharide. Proc. Natl. Acad. Sci. USA. 1999;96:5645-5650.
Not in our library10.1073/pnas.96.10.5645
226.
Oelschlaeger T.A., Tall B.D. Invasion of cultured human epithelial cells by Klebsiella pneumoniae isolated from the urinary tract. Infect. Immun. 1997;65:2950-2958.
Not in our library10.1128/iai.65.7.2950-2958.1997
227.
Garcia-Gonzalez A.P., Ritter A.D., Shrestha S., Andersen E.C., Yilmaz L.S., Walhout A.J.M. Bacterial Metabolism Affects the C. elegans Response to Cancer Chemotherapeutics. Cell. 2017;169:431-441.
Not in our library10.1016/j.cell.2017.03.046
228.
Host-Microbe Co-metabolism Dictates Cancer Drug Efficacy in C. elegans · 2017
No notice
229.
Geller L.T., Barzily-Rokni M., Danino T., Jonas O.H., Shental N., Nejman D., Gavert N., Zwang Y., Cooper Z.A., Shee K., et al. Potential role of intratumor bacteria in mediating tumor resistance to the chemotherapeutic drug gemcitabine. Science. 2017;357:1156-1160.
Not in our library10.1126/science.aah5043
230.
Vande Voorde J., Sabuncuoglu S., Noppen S., Hofer A., Ranjbarian F., Fieuws S., Balzarini J., Liekens S. Nucleoside-catabolizing enzymes in mycoplasma-infected tumor cell cultures compromise the cytostatic activity of the anticancer drug gemcitabine. J. Biol Chem. 2014;289:13054-13065.
Not in our library10.1074/jbc.m114.558924
231.
Local bacteria affect the efficacy of chemotherapeutic drugs · 2015
No notice
232.
Geller L.T., Straussman R. Intratumoral bacteria may elicit chemoresistance by metabolizing anticancer agents. Mol. Cell Oncol. 2018;5:e1405139.
Not in our library10.1080/23723556.2017.1405139
233.
Sandrini M.P., Shannon O., Clausen A.R., Bjorck L., Piskur J. Deoxyribonucleoside kinases activate nucleoside antibiotics in severely pathogenic bacteria. Antimicrob. Agents Chemother. 2007;51:2726-2732.
Not in our library10.1128/aac.00081-07
234.
Sandrini M.P., Clausen A.R., On S.L., Aarestrup F.M., Munch-Petersen B., Piskur J. Nucleoside analogues are activated by bacterial deoxyribonucleoside kinases in a species-specific manner. J. Antimicrob. Chemother. 2007;60:510-520.
Not in our library10.1093/jac/dkm240
235.
Yuan L., Zhang S., Li H., Yang F., Mushtaq N., Ullah S., Shi Y., An C., Xu J. The influence of gut microbiota dysbiosis to the efficacy of 5-Fluorouracil treatment on colorectal cancer. Biomed. Pharmacother. 2018;108:184-193.
Not in our library10.1016/j.biopha.2018.08.165
236.
Vanlancker E., Vanhoecke B., Smet R., Props R., Van de Wiele T. 5-Fluorouracil sensitivity varies among oral micro-organisms. J. Med. Microbiol. 2016;65:775-783.
Not in our library10.1099/jmm.0.000292
237.
Singh V., Brecik M., Mukherjee R., Evans J.C., Svetlíková Z., Blaško J., Surade S., Blackburn J., Warner D.F., Mikušová K., et al. The complex mechanism of antimycobacterial action of 5-fluorouracil. Chem. Biol. 2015;22:63-75.
Not in our library10.1016/j.chembiol.2014.11.006
238.
Hamouda N., Sano T., Oikawa Y., Ozaki T., Shimakawa M., Matsumoto K., Amagase K., Higuchi K., Kato S. Apoptosis, Dysbiosis and Expression of Inflammatory Cytokines are Sequential Events in the Development of 5-Fluorouracil-Induced Intestinal Mucositis in Mice. Basic Clin. Pharmacol. Toxicol. 2017;121:159-168.
Not in our library10.1111/bcpt.12793
239.
Alteration of Gut Microbiota and Inflammatory Cytokine/Chemokine Profiles in 5-Fluorouracil Induced Intestinal Mucositis · 2017
No notice
240.
Amelioration of Chemotherapy-Induced Intestinal Mucositis by Orally Administered Probiotics in a Mouse Model · 2015
Corrected
241.
Kucuk C., Ozkan M., Akgun H., Muhtaroglu S., Sozuer E. The effect of granulocyte macrophage-colony stimulating factor on bacterial translocation after administration of 5-fluorouracil in rats. J. Surg. Res. 2005;128:15-20.
Not in our library10.1016/j.jss.2005.04.037
242.
Vida A., Kardos G., Kovacs T., Bodrogi B.L., Bai P. Deletion of poly(ADPribose) polymerase-1 changes the composition of the microbiome in the gut. Mol. Med. Rep. 2018;18:4335-4341.
Not in our library10.3892/mmr.2018.9474
243.
Larmonier C.B., Shehab K.W., Laubitz D., Jamwal D.R., Ghishan F.K., Kiela P.R. Transcriptional Reprogramming and Resistance to Colonic Mucosal Injury in Poly(ADP-ribose) Polymerase 1 (PARP1)-deficient Mice. J. Biol Chem. 2016;291:8918-8930.
Not in our library10.1074/jbc.m116.714386
244.
Zhu X.X., Yang X.J., Chao Y.L., Zheng H.M., Sheng H.F., Liu H.Y., He Y., Zhou H.W. The Potential Effect of Oral Microbiota in the Prediction of Mucositis During Radiotherapy for Nasopharyngeal Carcinoma. EBioMedicine. 2017;18:23-31.
Not in our library10.1016/j.ebiom.2017.02.002
245.
Sonis S.T. The Chicken or the Egg? Changes in Oral Microbiota as Cause or Consequence of Mucositis During Radiation Therapy. EBioMedicine. 2017;18:7-8.
Not in our library10.1016/j.ebiom.2017.03.017
246.
Faecal microbiota transplantation protects against radiation‐induced toxicity · 2017
No notice
247.
Banerjee J., Mishra N., Dhas Y. Metagenomics: A new horizon in cancer research. Meta Gene. 2015;5:84-89.
Not in our library10.1016/j.mgene.2015.05.005
248.
Martinez-Outschoorn U.E., Prisco M., Ertel A., Tsirigos A., Lin Z., Pavlides S., Wang C., Flomenberg N., Knudsen E.S., Howell A., et al. Ketones and lactate increase cancer cell “stemness,” driving recurrence, metastasis and poor clinical outcome in breast cancer: Achieving personalized medicine via Metabolo-Genomics. Cell Cycle. 2011;10:1271-1286.
Not in our library10.4161/cc.10.8.15330
249.
Cancer stem cell metabolism · 2016
No notice
250.
Guppy M., Leedman P., Zu X., Russell V. Contribution by different fuels and metabolic pathways to the total ATP turnover of proliferating MCF-7 breast cancer cells. Biochem. J. 2002;364:309-315.
Not in our library10.1042/bj3640309
251.
Viale A., Corti D., Draetta G.F. Tumors and mitochondrial respiration: A neglected connection. Cancer Res. 2015;75:3685-3686.
Not in our library10.1158/0008-5472.can-15-0491
252.
Alam M.M., Lal S., FitzGerald K.E., Zhang L. A holistic view of cancer bioenergetics: Mitochondrial function and respiration play fundamental roles in the development and progression of diverse tumors. Clin. Transl. Med. 2016;5:3.
Not in our library10.1186/s40169-016-0082-9
253.
Shapira N. The potential contribution of dietary factors to breast cancer prevention. Eur. J. Cancer Prev. 2017;26:385-395.
Not in our library10.1097/cej.0000000000000406
254.
Antimetabolic Effects of Polyphenols in Breast Cancer Cells: Focus on Glucose Uptake and Metabolism · 2018
Not checked
255.
Backhed F., Ding H., Wang T., Hooper L.V., Koh G.Y., Nagy A., Semenkovich C.F., Gordon J.I. The gut microbiota as an environmental factor that regulates fat storage. Proc. Natl. Acad. Sci. USA. 2004;101:15718-15723.
Not in our library10.1073/pnas.0407076101
256.
Sundaram S., Yan L. High-fat Diet Enhances Mammary Tumorigenesis and Pulmonary Metastasis and Alters Inflammatory and Angiogenic Profiles in MMTV-PyMT Mice. Anticancer Res. 2016;36:6279-6287.
Not in our library10.21873/anticanres.11223
257.
Maffei V.J., Kim S., Blanchard E.t., Luo M., Jazwinski S.M., Taylor C.M., Welsh D.A. Biological Aging and the Human Gut Microbiota. J. Gerontol. A Biol. Sci. Med. Sci. 2017;72:1474-1482.
Not in our library10.1093/gerona/glx042
258.
Wang W., Wang J., Li J., Yan P., Jin Y., Zhang R., Yue W., Guo Q., Geng J. Cholecystectomy Damages Aging-Associated Intestinal Microbiota Construction. Front. Microbiol. 2018;9:1402.
Not in our library10.3389/fmicb.2018.01402
259.
Kim S., Jazwinski S.M. The Gut Microbiota and Healthy Aging: A Mini-Review. Gerontology. 2018;64:513-520.
Not in our library10.1159/000490615
260.
Mahmoudian Dehkordi S., Arnold M., Nho K., Ahmad S., Jia W., Xie G., Louie G., Kueider-Paisley A., Moseley M.A., Thompson J.W., et al. Altered bile acid profile associates with cognitive impairment in Alzheimer’s disease-An emerging role for gut microbiome. Alzheimers Dement. 2019;15:76-92.
Not in our library10.1016/j.jalz.2018.07.217
261.
Grasset E., Puel A., Charpentier J., Collet X., Christensen J.E., Terce F., Burcelin R. A Specific Gut Microbiota Dysbiosis of Type 2 Diabetic Mice Induces GLP-1 Resistance through an Enteric NO-Dependent and Gut-Brain Axis Mechanism. Cell Metab. 2017;25:1075-1090.e5.
Not in our library10.1016/j.cmet.2017.04.013
262.
Dysbiosis of Gut Microbiota Associated with Clinical Parameters in Polycystic Ovary Syndrome · 2017
No notice
263.
Chu H., Duan Y., Yang L., Schnabl B. Small metabolites, possible big changes: A microbiota-centered view of non-alcoholic fatty liver disease. Gut. 2019;68:359-370.
Not in our library10.1136/gutjnl-2018-316307
264.
Maruvada P., Leone V., Kaplan L.M., Chang E.B. The Human Microbiome and Obesity: Moving beyond Associations. Cell Host Microbe. 2017;22:589-599.
Not in our library10.1016/j.chom.2017.10.005
265.
Loomba R., Seguritan V., Li W., Long T., Klitgord N., Bhatt A., Dulai P.S., Caussy C., Bettencourt R., Highlander S.K., et al. Gut Microbiome-Based Metagenomic Signature for Non-invasive Detection of Advanced Fibrosis in Human Nonalcoholic Fatty Liver Disease. Cell Metab. 2017;25:1054-1062.
Not in our library10.1016/j.cmet.2017.04.001
266.
Mardinoglu A., Wu H., Bjornson E., Zhang C., Hakkarainen A., Räsänen S.M., Lee S., Mancina R.M., Bergentall M., Pietiläinen K.H., et al. An Integrated Understanding of the Rapid Metabolic Benefits of a Carbohydrate-Restricted Diet on Hepatic Steatosis in Humans. Cell Metab. 2018;27:559-571.e5.
Not in our library10.1016/j.cmet.2018.01.005
267.
Lofterod T., Mortensen E.S., Nalwoga H., Wilsgaard T., Frydenberg H., Risberg T., Eggen A.E., McTiernan A., Aziz S., Wist E.A., et al. Impact of pre-diagnostic triglycerides and HDL-cholesterol on breast cancer recurrence and survival by breast cancer subtypes. BMC Cancer. 2018;18:654.
Not in our library10.1186/s12885-018-4568-2
268.
Miler J.J., Novotny P., Walker P.D., Harris J.R., MacLennan I.P. Neisseria gonorrhoeae and ABO isohemagglutinins. Infect. Immun. 1977;15:713-719.
Not in our library10.1128/iai.15.3.713-719.1977
269.
Potter E.V. Blood group antibodies induced by pneumococcal vaccine. J. Pediatr. 1982;100:836-837.
Not in our library10.1016/s0022-3476(82)80610-0
270.
Yadav S.K., Boppana S., Ito N., Mindur J.E., Mathay M.T., Patel A., Dhib-Jalbut S., Ito K. Gut dysbiosis breaks immunological tolerance toward the central nervous system during young adulthood. Proc. Natl. Acad. Sci. USA. 2017;114:E9318-E9327.
Not in our library10.1073/pnas.1615715114
271.
Age-Associated Microbial Dysbiosis Promotes Intestinal Permeability, Systemic Inflammation, and Macrophage Dysfunction · 2017
Corrected
272.
Viaud S., Daillere R., Boneca I.G., Lepage P., Pittet M.J., Ghiringhelli F., Trinchieri G., Goldszmid R., Zitvogel L. Harnessing the intestinal microbiome for optimal therapeutic immunomodulation. Cancer Res. 2014;74:4217-4221.
Not in our library10.1158/0008-5472.can-14-0987
273.
Zitvogel L., Ayyoub M., Routy B., Kroemer G. Microbiome and Anticancer Immunosurveillance. Cell. 2016;165:276-287.
Not in our library10.1016/j.cell.2016.03.001
274.
Li W., Han L., Yu P., Ma C., Wu X., Moore J.E., Xu J. Molecular characterization of skin microbiota between cancer cachexia patients and healthy volunteers. Microb. Ecol. 2014;67:679-689.
Not in our library10.1007/s00248-013-0345-6
275.
Bindels L.B., Neyrinck A.M., Salazar N., Taminiau B., Druart C., Muccioli G.G., François E., Blecker C., Richel A., Daube G., et al. Non Digestible Oligosaccharides Modulate the Gut Microbiota to Control the Development of Leukemia and Associated Cachexia in Mice. PLoS ONE. 2015;10:e0131009.
Not in our library10.1371/journal.pone.0131009
276.
Bindels L.B., Neyrinck A.M., Claus S.P., Le Roy C.I., Grangette C., Pot B., Martinez I., Walter J., Cani P.D., Delzenne N.M. Synbiotic approach restores intestinal homeostasis and prolongs survival in leukaemic mice with cachexia. ISME J. 2016;10:1456-1470.
Not in our library10.1038/ismej.2015.209
277.
Bischoff S.C. Microbiota and aging. Curr. Opin. Clin. Nutr. Metab. Care. 2016;19:26-30.
Not in our library10.1097/mco.0000000000000242

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