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Cover page of the Journal of Health Sciences

 Table of Contents  
Year : 2018  |  Volume : 11  |  Issue : 1  |  Page : 1-2

The role of microbiome in cancer

1 KLES Kidney Foundation, KLES Dr. Prabhakar Kore Hospital and Medical Research Centre; Department of Urology, KLE Academy of Higher Education and Research, JNMC Campus, Belagavi 590 - 010, Karnataka, India
2 Department of Urology, KLES Kidney Foundation, KLES Dr. Prabhakar Kore Hospital and Medical Research Centre, Belagavi 590 - 010, Karnataka, India

Date of Web Publication17-Jan-2018

Correspondence Address:
Dr. R B Nerli
KLES Dr. Prabhakar Kore Hospital and Medical Research Centre, KLES Kidney Foundation, Belgaum - 590 010, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/kleuhsj.kleuhsj_323_17

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How to cite this article:
Nerli R B, Ghagane SC. The role of microbiome in cancer. Indian J Health Sci Biomed Res 2018;11:1-2

How to cite this URL:
Nerli R B, Ghagane SC. The role of microbiome in cancer. Indian J Health Sci Biomed Res [serial online] 2018 [cited 2019 Aug 24];11:1-2. Available from: http://www.ijournalhs.org/text.asp?2018/11/1/1/223432

Cancer has become a leading cause of morbidity and mortality worldwide. In addition to the tremendous suffering it inflicts, cancer is a reason for significant economic burden both to the sufferer and to the nation.[1] Recently, a high-impact report suggested that cancer is primarily stochastic or “bad luck” because of the accumulation of spontaneous mutations during DNA replication in tissues where stem cells undergo a relatively large number of cell divisions;[2] however, it is widely believed that the environment too significantly influences the risk of cancer.[3],[4] Numerous epidemiologic and occupational health studies support the importance of lifestyle factors and exposure to known or suspected carcinogens in the development of cancer. In fact, it is estimated that 15%–20% of cancers are driven by infectious agents; 20%–30% are largely caused by tobacco use; and 30%–35% are associated with diet, physical activity, and/or energy balance (e.g., obesity). Ultraviolet radiation from sunlight, alcohol, and many other substances (e.g., asbestos, benzene, and radon) also play a role, both alone and in combination (i.e., mixed exposures), although relative risk depends on the dose and duration of each exposure and the genetic background of each individual.[5],[6]

The microbiota that inhabits our gastrointestinal tract and other anatomic sites can be considered environmental factors to which we are continuously exposed at high doses throughout life. Most of these microbes are commensal bacteria and until recently have been difficult to culture, which has limited our understanding. However, during the past decade, the advent of metagenomic sequencing approaches that combine next-generation DNA sequencing technologies with the computational analysis of targeted (16S ribosomal RNA hypervariable regions) or whole-genome shotgun sequence reads has documented the diversity and abundance of microbes at different body sites in a culture-independent manner.[7],[8]

It is well known that prostatitis and prostatitis symptoms are associated with an increased risk of prostate cancer.[9],[10] It is probably that bacteria induce a chronic inflammatory state in the prostate that could result in enhanced production of pro-inflammatory cytokines. Both neutrophils and macrophages release pro-inflammatory molecules such as nitric oxide that have the propensity to cause genetic damage which could pave the way for enhanced cell proliferation and cancer. This is particularly interesting in the light of the reports that low-grade inflammation does exist in cancer. Yu et al.[11] investigated the type of microbiota in the expressed prostatic secretions (EPSs) of patients with prostate cancer and benign prostatic hyperplasia (BPH) by the polymerase chain reaction-denaturing gradient gel electrophoresis method using universal bacterial primers and reported that the prostate cancer group had a significantly increased number of Bacteroidetes bacteria, Alphaproteobacteria, Firmicutes bacteria, Lachnospiraceae, Propionicimonas, Sphingomonas, and Ochrobactrum and a decrease in Eubacterium and Defluviicoccus compared to the BPH group. Based on these results, they suggested that there were significant changes in the microbial population in EPS, urine, and seminal fluid of individuals with prostate cancer and BPH, indicating a possible role for these bacteria in these two conditions.

Cavarretta et al.[12] recently reported on the microbiome profile of tumor, peritumor, and nontumor tissues in 16 radical prostatectomy specimens. They observed significant differences in specific microbial populations among tumor/peritumor and nontumor prostate specimens at certain taxonomic levels. Among genera, Propionibacterium spp. were the most abundant. Staphylococcus spp. were more represented in the tumor/peritumor tissues (P< 0.05). The authors concluded that the prostate contained a plethora of bacteria, which set themselves within the gland with a distribution dependent on the nature of the tissue, thus suggesting a possible pathophysiological correlation between the composition of the local microbial niche and the presence of the tumor itself.

Similarly, Shrestha et al.[13] profiled the urinary microbiome in men with positive versus negative biopsies for prostate cancer. They identified a cluster of pro-inflammatory bacteria previously implicated in urogenital infections in a subset of samples. Many species, including known uropathogens, were significantly and differentially abundant among cancer and benign samples, in low versus higher grade cancers and in relation to prostate inflammation type and degree. The authors concluded that there was a prevalence of pro-inflammatory bacteria and uropathogens in the urinary tract of men with prostate cancer.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Mariotto AB, Yabroff KR, Shao Y, Feuer EJ, Brown ML. Projections of the cost of cancer care in the United States: 2010-2020. J Natl Cancer Inst 2011;103:117-28.  Back to cited text no. 1
Tomasetti C, Vogelstein B. Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 2015;347:78-81.  Back to cited text no. 2
Ashford NA, Bauman P, Brown HS, Clapp RW, Finkel AM, Gee D, et al. Cancer risk: Role of environment. Science 2015;347:727.  Back to cited text no. 3
Harris CC. Editorial. Carcinogenesis 2016;37:1.  Back to cited text no. 4
Bhatt AP, Redinbo MR, Bultman SJ. The role of the microbiome in cancer development and therapy. CA Cancer J Clin 2017;67:326-44.  Back to cited text no. 5
Ghagane SC, Nerli RB, Hiremath MB, Wagh AT, Magdum PV. Incidence of prostate cancer at a single tertiary care center in North Karnataka. Indian J Cancer 2016;53:429-31.  Back to cited text no. 6
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Goodrich JK, Di Rienzi SC, Poole AC, Koren O, Walters WA, Caporaso JG, et al. Conducting a microbiome study. Cell 2014;158:250-62.  Back to cited text no. 7
Weinstock GM. Genomic approaches to studying the human microbiota. Nature 2012;489:250-6.  Back to cited text no. 8
Cheng I, Witte JS, Jacobsen SJ, Haque R, Quinn VP, Quesenberry CP, et al. Prostatitis, sexually transmitted diseases, and prostate cancer: The California men's health study. PLoS One 2010;5:e8736.  Back to cited text no. 9
Nerli RB, Patil R, Sharma V, Ghagane SC, Hiremath MB. Cystic prostatic carcinoma. Clin Oncol 2016;1:1154.  Back to cited text no. 10
Yu H, Meng H, Zhou F, Ni X, Shen S, Das UN, et al. Urinary microbiota in patients with prostate cancer and benign prostatic hyperplasia. Arch Med Sci 2015;11:385-94.  Back to cited text no. 11
Cavarretta I, Ferrarese R, Cazzaniga W, Saita D, Lucianò R, Ceresola ER, et al. The microbiome of the prostate tumor microenvironment. Eur Urol 2017;72:625-31.  Back to cited text no. 12
Shrestha E, White JR, Yu SH, Kulac I, Ertunc O, De Marzo AM, et al. Profiling the urinary microbiome in men with positive versus negative biopsies for prostate cancer. J Urol. 2018;199:161-71.  Back to cited text no. 13


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