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Journal articles on the topic 'Breast – Cancer – Etiology'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

DenizAtasoy, DenizAtasoy, FatihAydogan FatihAydogan, SevgiErgin SevgiErgin, KenanMidilli KenanMidilli, SennurIlvan SennurIlvan, CihanUras CihanUras, and AliCengiz AliCengiz. "Male Breast Cancer: No Evidence of Human Papillomavirus Etiology." International Journal of Surgery and Medicine 4, no. 3 (2019): 1. http://dx.doi.org/10.5455/ijsm.male-breast-cancer.

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2

Pathak, Dorothy R., Janet R. Osuch, and Jianping He. "Breast carcinoma etiology." Cancer 88, S5 (March 1, 2000): 1230–38. http://dx.doi.org/10.1002/(sici)1097-0142(20000301)88:5+<1230::aid-cncr9>3.0.co;2-f.

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3

Tao, ZiQi, Aimin Shi, Cuntao Lu, Tao Song, Zhengguo Zhang, and Jing Zhao. "Breast Cancer: Epidemiology and Etiology." Cell Biochemistry and Biophysics 72, no. 2 (December 28, 2014): 333–38. http://dx.doi.org/10.1007/s12013-014-0459-6.

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4

Hans-Olov, Adami, Adams Gerald, Boyle Peter, Ewertz Marianne, C. Lee Nancy, Lund Eiliv, B. Miller Anthony, Olsson Håkan, Steel Michael, and Trichopoulos Dimitrios. "Chapter II. Breast-Cancer Etiology." International Journal of Cancer 46, S5 (1990): 22–39. http://dx.doi.org/10.1002/ijc.2910460704.

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5

Sharpe, Colin, and Jean-François Boivin. "The Etiology of Female Breast Cancer." Medical Principles and Practice 9, no. 1 (2000): 1–24. http://dx.doi.org/10.1159/000026115.

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6

Shull, James D., Kirsten L. Dennison, Aaron C. Chack, and Amy Trentham-Dietz. "Rat models of 17β-estradiol-induced mammary cancer reveal novel insights into breast cancer etiology and prevention." Physiological Genomics 50, no. 3 (March 1, 2018): 215–34. http://dx.doi.org/10.1152/physiolgenomics.00105.2017.

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Numerous laboratory and epidemiologic studies strongly implicate endogenous and exogenous estrogens in the etiology of breast cancer. Data summarized herein suggest that the ACI rat model of 17β-estradiol (E2)-induced mammary cancer is unique among rodent models in the extent to which it faithfully reflects the etiology and biology of luminal types of breast cancer, which together constitute ~70% of all breast cancers. E2 drives cancer development in this model through mechanisms that are largely dependent upon estrogen receptors and require progesterone and its receptors. Moreover, mammary cancer development appears to be associated with generation of oxidative stress and can be modified by multiple dietary factors, several of which may attenuate the actions of reactive oxygen species. Studies of susceptible ACI rats and resistant COP or BN rats provide novel insights into the genetic bases of susceptibility and the biological processes regulated by genetic determinants of susceptibility. This review summarizes research progress resulting from use of these physiologically relevant rat models to advance understanding of breast cancer etiology and prevention.

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7

ROHAN, T. E., and C. J. BAIN. "DIET IN THE ETIOLOGY OF BREAST CANCER." Epidemiologic Reviews 9, no. 1 (1987): 120–45. http://dx.doi.org/10.1093/oxfordjournals.epirev.a036299.

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8

Holland, J. F., and G. T. Pogo. "Possible etiology of human breast cancer: comment." Biomedicine & Pharmacotherapy 53, no. 7 (August 1999): 334. http://dx.doi.org/10.1016/s0753-3322(00)88507-8.

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9

Labat, ML. "Possible retroviral etiology of human breast cancer." Biomedicine & Pharmacotherapy 52, no. 1 (January 1998): 6–12. http://dx.doi.org/10.1016/s0753-3322(97)86236-1.

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10

Dumitrescu, Ramona G., and Peter G. Shields. "The etiology of alcohol-induced breast cancer." Alcohol 35, no. 3 (April 2005): 213–25. http://dx.doi.org/10.1016/j.alcohol.2005.04.005.

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11

Newman, Lisa A. "Parsing the Etiology of Breast Cancer Disparities." Journal of Clinical Oncology 34, no. 9 (March 20, 2016): 1013–14. http://dx.doi.org/10.1200/jco.2015.65.1877.

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12

Adami, Hans-Olov, Lisa B. Signorello, and Dimitrios Trichopoulos. "Towards an understanding of breast cancer etiology." Seminars in Cancer Biology 8, no. 4 (January 1998): 255–62. http://dx.doi.org/10.1006/scbi.1998.0077.

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13

Cavalieri, Ercole L., and Eleanor G. Rogan. "The etiology and prevention of breast cancer." Drug Discovery Today: Disease Mechanisms 9, no. 1-2 (June 2012): e55-e69. http://dx.doi.org/10.1016/j.ddmec.2013.02.001.

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14

Henson, Donald Earl, and Robert E. Tarone. "Involution and the etiology of breast cancer." Cancer 74, S1 (January 1994): 424–29. http://dx.doi.org/10.1002/cncr.2820741330.

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15

Ingle, James N. "Multicultural aspects of breast cancer etiology workshop." Cancer 88, S5 (March 1, 2000): 1265–66. http://dx.doi.org/10.1002/(sici)1097-0142(20000301)88:5+<1265::aid-cncr14>3.0.co;2-2.

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16

Calaf, G. M. "CARCINOGENICITY OF MALATHION AND ESTROGEN IN AN EXPERIMENTAL RAT MAMMARY GLAND MODEL." Siberian journal of oncology 17, no. 4 (September 4, 2018): 5–13. http://dx.doi.org/10.21294/1814-4861-2018-17-4-5-13.

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Breast cancer is considered a major and common health problem in both developing and developed countries. The etiology of breast cancer, the most frequent malignancy diagnosed in women in the western world, has remained unidentified. Chemicals as the organophosphorous pesticide malathion have been used to control a wide range of sucking and chewing pests of field crops, and are involved in the etiology of breast cancers. The association between breast cancer initiation and prolonged exposure to estrogen suggests that this hormone may also have an etiologic role in such a process. However, the key factors behind the initiation of breast cancer remain to be elucidated. The effect of environmental substances, such as malathion and estrogen was analyzed in an experimental rat mammary gland model. Different cytoplasmic proteins are key in the transformation of a normal cell to a malignant tumor cell and among these are the Ras super family and Ras homologous A (Rho-A). Both types of proteins were greater in animals treated with malathion than those with estrogens. E-Cadherins constitute a large family of cell surface proteins.Resultsshowed greater expression of E-Cadherin and vimentin than c-Ha-ras and Rho-A in rats treated by estrogens. In breast cancer, analysis using immunohistochemical markers is an essential component of routine pathological examinations, and plays an important role in the management of the disease by providing diagnostic and prognostic strategies.The aimof the present study was to identify markers that can be used as a prognostic tool for breast cancer patients.

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17

Guseynov, Arif, T. Guseynov, M. Bobkov, V. Blincov, and V. Odincov. "BREAST CANCER: general questions, clinic, diagnosis." Clinical Medicine and Pharmacology 8, no. 1 (May 24, 2022): 5–13. http://dx.doi.org/10.12737/2409-3750-2022-8-1-5-13.

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The lecture provides up-to-date information for doctors of various specialties: oncologists, surgeons, mammologists, general practitioners on breast cancer problems. The issues of etiology and pathogenesis, classification, clinic of breast tumors are highlighted, methods of modern diagnosis and differential diagnosis of breast cancer are described in detail.

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18

Fernandes, P. "Prolactin Physiology in the Etiology of Breast Cancer." Seminars in Reproductive Medicine 10, no. 03 (August 1992): 258–65. http://dx.doi.org/10.1055/s-2007-1018881.

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19

DeBruin, Lillian S., and P. David Josephy. "Perspectives on the chemical etiology of breast cancer." Environmental Health Perspectives 110, suppl 1 (February 2002): 119–28. http://dx.doi.org/10.1289/ehp.02110s1119.

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20

Tworoger, Shelley S., and Susan E. Hankinson. "Prolactin and Breast Cancer Etiology: An Epidemiologic Perspective." Journal of Mammary Gland Biology and Neoplasia 13, no. 1 (February 2, 2008): 41–53. http://dx.doi.org/10.1007/s10911-008-9063-y.

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21

Almendro, Vanessa, and Gemma Fuster. "Heterogeneity of breast cancer: etiology and clinical relevance." Clinical and Translational Oncology 13, no. 11 (November 2011): 767–73. http://dx.doi.org/10.1007/s12094-011-0731-9.

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22

Grossman, Eugene M. "RE: “DIET IN THE ETIOLOGY OF BREAST CANCER”." American Journal of Epidemiology 128, no. 3 (September 1988): 678. http://dx.doi.org/10.1093/oxfordjournals.aje.a115016.

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23

Polednak, A. P. "Pre-eclampsia, autoimmune diseases and breast cancer etiology." Medical Hypotheses 44, no. 5 (May 1995): 414–18. http://dx.doi.org/10.1016/0306-9877(95)90271-6.

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24

Küpeli Akkol, Esra, Hilal Bardakci, Timur Hakan Barak, Michael Aschner, Gökçe Şeker Karatoprak, Haroon Khan, and Yaseen Hussain. "Herbal Ingredients in the Prevention of Breast Cancer: Comprehensive Review of Potential Molecular Targets and Role of Natural Products." Oxidative Medicine and Cellular Longevity 2022 (August 16, 2022): 1–23. http://dx.doi.org/10.1155/2022/6044640.

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Among various cancers, breast cancer is the most prevalent type in women throughout the world. Breast cancer treatment is challenging due to complex nature of the etiology of disease. Cell division cycle alterations are often encountered in a variety of cancer types including breast cancer. Common treatments include chemotherapy, surgery, radiotherapy, and hormonal therapy; however, adverse effects and multidrug resistance lead to complications and noncompliance. Accordingly, there is an increasing demand for natural products from medicinal plants and foods. This review summarizes molecular mechanisms of signaling pathways in breast cancer and identifies mechanisms by which natural compounds may exert their efficacy in the treatment of breast cancer.

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25

Mert, Gülten. "National action plan on Breast Cancer Workshop on Multicultural Aspects of Breast Cancer Etiology." Cancer 94, no. 7 (March 28, 2002): 2113. http://dx.doi.org/10.1002/cncr.10412.

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26

Allott, Emma H., Yue Shan, Mengjie Chen, Xuezheng Sun, Susana Garcia-Recio, Erin L. Kirk, Andrew F. Olshan, et al. "Bimodal age distribution at diagnosis in breast cancer persists across molecular and genomic classifications." Breast Cancer Research and Treatment 179, no. 1 (September 18, 2019): 185–95. http://dx.doi.org/10.1007/s10549-019-05442-2.

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Abstract Purpose Female breast cancer demonstrates bimodal age frequency distribution patterns at diagnosis, interpretable as two main etiologic subtypes or groupings of tumors with shared risk factors. While RNA-based methods including PAM50 have identified well-established clinical subtypes, age distribution patterns at diagnosis as a proxy for etiologic subtype are not established for molecular and genomic tumor classifications. Methods We evaluated smoothed age frequency distributions at diagnosis for Carolina Breast Cancer Study cases within immunohistochemistry-based and RNA-based expression categories. Akaike information criterion (AIC) values compared the fit of single density versus two-component mixture models. Two-component mixture models estimated the proportion of early-onset and late-onset categories by immunohistochemistry-based ER (n = 2860), and by RNA-based ESR1 and PAM50 subtype (n = 1965). PAM50 findings were validated using pooled publicly available data (n = 8103). Results Breast cancers were best characterized by bimodal age distribution at diagnosis with incidence peaks near 45 and 65 years, regardless of molecular characteristics. However, proportional composition of early-onset and late-onset age distributions varied by molecular and genomic characteristics. Higher ER-protein and ESR1-RNA categories showed a greater proportion of late age-at-onset. Similarly, PAM50 subtypes showed a shifting age-at-onset distribution, with most pronounced early-onset and late-onset peaks found in Basal-like and Luminal A, respectively. Conclusions Bimodal age distribution at diagnosis was detected in the Carolina Breast Cancer Study, similar to national cancer registry data. Our data support two fundamental age-defined etiologic breast cancer subtypes that persist across molecular and genomic characteristics. Better criteria to distinguish etiologic subtypes could improve understanding of breast cancer etiology and contribute to prevention efforts.

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27

Wei, Esther K., Kathleen Y. Wolin, and Graham A. Colditz. "Time Course of Risk Factors in Cancer Etiology and Progression." Journal of Clinical Oncology 28, no. 26 (September 10, 2010): 4052–57. http://dx.doi.org/10.1200/jco.2009.26.9324.

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Patients with cancer increasingly ask what they can do to change their lifestyles and improve outcomes. Risk factors for onset of cancer may differ substantially from those that modify survival with implications for counseling. This review focuses on recent data derived from population-based studies of causes of cancer and of patients with cancer to contrast risk factors for etiology with those that impact survival. For different cancer sites, the level of information to inform the timing of lifestyle exposures and risk of disease onset or progression after diagnosis is often limited. For breast cancer, timing of some exposures, such as radiation, is particularly important. For other exposures, such as physical activity, higher levels may prevent onset and also improve survival. For colon cancer, study of precursor polyps has provided additional insight to timing. Extensive data indicate that physical activity reduces risk of colon cancer, and more limited data suggest that exposure after diagnosis improves survival. Dietary factors including folate and calcium may also reduce risk of onset. More limited data on prostate cancer point to obesity increasing risk of aggressive or advanced disease. Timing of change in lifestyle for change in risk of onset and for survival is important but understudied among patients with cancer. Counseling patients with cancer to increase physical activity and avoid weight gain may improve outcomes. Advice to family members on lifestyle may become increasingly important for breast and other cancers where family history is a strong risk factor.

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28

Bose, Muthiah, Jan Benada, Jayashree Vijay Thatte, Savvas Kinalis, Bent Ejlertsen, Finn Cilius Nielsen, Claus Storgaard Sørensen, and Maria Rossing. "A catalog of curated breast cancer genes." Breast Cancer Research and Treatment 191, no. 2 (November 10, 2021): 431–41. http://dx.doi.org/10.1007/s10549-021-06441-y.

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Abstract Purpose Decades of research have identified multiple genetic variants associated with breast cancer etiology. However, there is no database that archives breast cancer genes and variants responsible for predisposition. We set out to build a dynamic repository of curated breast cancer genes. Methods A comprehensive literature search was performed in PubMed and Google Scholar, followed by data extraction and harmonization for downstream analysis. Results Using a subset of 345 studies, we cataloged 652 breast cancer-associated loci across the genome. A majority of these were present in the non-coding region (i.e., intergenic (101) and intronic (345)), whereas only 158 were located within an exon. Using the odds ratio, we identified 429 loci to increase the disease risk and 198 to confer protection against breast cancer, whereas 25 were identified to both increase disease risk and confer protection against breast cancer. Chromosomal ideogram analysis indicated that chromosomes 17 and 19 have the highest density of breast cancer loci. We manually annotated and collated breast cancer genes in which a previous association between rare-monogenic variant and breast cancer has been documented. Finally, network and functional enrichment analysis revealed that steroid metabolism and DNA repair pathways were predominant among breast cancer genes and variants. Conclusions We have built an online interactive catalog of curated breast cancer genes (https://cbcg.dk). This will expedite clinical diagnostics and support the ongoing efforts in managing breast cancer etiology. Moreover, the database will serve as an essential repository when designing new breast cancer multigene panels.

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29

Pedroza, Diego A., Ramadevi Subramani, and Rajkumar Lakshmanaswamy. "Classical and Non-Classical Progesterone Signaling in Breast Cancers." Cancers 12, no. 9 (August 27, 2020): 2440. http://dx.doi.org/10.3390/cancers12092440.

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Much emphasis is placed on estrogen (E2) and estrogen receptor (ER) signaling as most research is focused on understanding E2 and ER’s ability to enhance proliferative signals in breast cancers. Progesterone (P4) is important for normal mammary gland development, function and menstrual control. However, P4 and its receptors (PRs) in breast cancer etiology continue to be understudied and its role in breast cancer remains controversial. The Women’s Health Initiative (WHI) clinical trial clearly demonstrated the importance of progestogens in breast cancer development. P4 has historically been associated with classical-signaling through nuclear receptors, however non-classical P4 signaling via membrane receptors has been described. Progestogens have the ability to bind to nuclear and membrane receptors and studies have demonstrated that both can promote breast cancer cell proliferation and breast tumor growth. In this review, we attempt to understand the classical and non-classical signaling role of P4 in breast cancers because both nuclear and membrane receptors could become viable therapeutic options for breast cancer patients.

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30

Brinton, Louise A., Tim J. Key, Laurence N. Kolonel, Karin B. Michels, Howard D. Sesso, Giske Ursin, Stephen K. Van Den Eeden, et al. "Prediagnostic Sex Steroid Hormones in Relation to Male Breast Cancer Risk." Journal of Clinical Oncology 33, no. 18 (June 20, 2015): 2041–50. http://dx.doi.org/10.1200/jco.2014.59.1602.

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Purpose Although previous studies have implicated a variety of hormone-related risk factors in the etiology of male breast cancers, no previous studies have examined the effects of endogenous hormones. Patients and Methods Within the Male Breast Cancer Pooling Project, an international consortium comprising 21 case-control and cohort investigations, a subset of seven prospective cohort studies were able to contribute prediagnostic serum or plasma samples for hormone quantitation. Using a nested case-control design, multivariable unconditional logistic regression analyses estimated odds ratios and 95% CIs for associations between male breast cancer risk and 11 individual estrogens and androgens, as well as selected ratios of these analytes. Results Data from 101 cases and 217 matched controls were analyzed. After adjustment for age and date of blood draw, race, and body mass index, androgens were found to be largely unrelated to risk, but circulating estradiol levels showed a significant association. Men in the highest quartile had an odds ratio of 2.47 (95% CI, 1.10 to 5.58) compared with those in the lowest quartile (trend P = .06). Assessment of estradiol as a ratio to various individual androgens or sum of androgens showed no further enhancement of risk. These relations were not significantly modified by either age or body mass index, although estradiol was slightly more strongly related to breast cancers occurring among younger (age < 67 years) than older men. Conclusion Our results support the notion of an important role for estradiol in the etiology of male breast cancers, similar to female breast cancers.

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31

Caygill, Christine P. J., and Michael J. Hill. "Trends in European Breast Cancer Incidence and Possible Etiology." Tumori Journal 77, no. 2 (April 1991): 126–29. http://dx.doi.org/10.1177/030089169107700207.

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32

Friedenreich, Christine M. "The Role of Physical Activity in Breast Cancer Etiology." Seminars in Oncology 37, no. 3 (June 2010): 297–302. http://dx.doi.org/10.1053/j.seminoncol.2010.05.008.

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33

Pogo, Beatriz G. T., and James F. Holland. "Possibilities of a viral etiology for human breast cancer." Biological Trace Element Research 56, no. 1 (January 1997): 131–42. http://dx.doi.org/10.1007/bf02778989.

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34

Michels, Karin B., and Fei Xue. "Role of birthweight in the etiology of breast cancer." International Journal of Cancer 119, no. 9 (July 5, 2006): 2007–25. http://dx.doi.org/10.1002/ijc.22004.

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35

Preeti Tanaji Mane, Sangram Prakash Patil, Balaji Sopanrao Wakure, and Pravin Shridhar Wakte. "Breast cancer: understanding etiology, addressing molecular signaling pathways, identifying therapeutic targets and strategizing the treatment." International Journal of Research in Pharmaceutical Sciences 12, no. 3 (July 1, 2021): 1757–69. http://dx.doi.org/10.26452/ijrps.v12i3.4779.

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Breast cancer has messed the life of a greater number of women being the most common cancer affecting them worldwide. A number of risk factors contribute the breast malignancy, however, genetic drift is accountable the most. Depending on the cell origin, invasiveness and receptors involved, breast cancer is classified into various subtypes. The accurate diagnosis of breast cancer is important as it defines the prognosis and directs the type of treatment required. A number of major signaling pathways involved in breast tumorigenesis and its development include estrogen receptors (ERs), HER2, Wnt/β-catenin, Notch, Hedgehog (Hh), PI3K and mTOR pathway. Furthermore, certain enzymes like Cyclin dependent kinases and breast tumor kinases also play a vital role in cell cycle regulation and therefore, in the development of breast neoplasms. Recent studies have also enlightened the role of non-coding RNAs in breast cancer development. This review discusses various aspects of breast cancer such as its etiology, subtypes, various signaling pathways involved, targets projected by these pathways and the current treatment options based on a few of these targets. Also, the role of different genes, enzymes and non-coding RNAs related to breast tumorigenesis and development is discussed.

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36

Dennison, Kirsten L., Nyssa Becker Samanas, Quincy Eckert Harenda, Maureen Peters Hickman, Nicole L. Seiler, Lina Ding, and James D. Shull. "Development and characterization of a novel rat model of estrogen-induced mammary cancer." Endocrine-Related Cancer 22, no. 2 (April 2015): 239–48. http://dx.doi.org/10.1530/erc-14-0539.

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The ACI rat model of 17β-estradiol (E2)-induced mammary cancer is highly relevant for use in establishing the endocrine, genetic, and environmental bases of breast cancer etiology and identifying novel agents and strategies for preventing breast cancer. E2 treatment rapidly induces mammary cancer in female ACI rats and simultaneously induces pituitary lactotroph hyperplasia and adenoma. The pituitary tumors can result in undesired morbidity, which compromises long-term studies focused on mammary cancer etiology and prevention. We have defined the genetic bases of susceptibility to E2-induced mammary cancers and pituitary tumors and have utilized the knowledge gained in these studies to develop a novel inbred rat strain, designated ACWi, that retains the high degree of susceptibility to E2-induced mammary cancer exhibited by ACI rats, but lacks the treatment-related morbidity associated with pituitary lactotroph hyperplasia/adenoma. When treated with E2, female ACWi rats developed palpable mammary cancer at a median latency of 116 days, an incidence of 100% by 161 days and exhibited an average of 15.6 mammary tumors per rat following 196 days of treatment. These parameters did not differ from those observed for contemporaneously treated ACI rats. None of the E2-treated ACWi rats were killed before the intended experimental end point due to any treatment-related morbidity other than mammary cancer burden, whereas 20% of contemporaneously treated ACI rats exhibited treatment-related morbidity that necessitated premature killing. The ACWi rat strain is well suited for use by those in the research community, focusing on breast cancer etiology and prevention.

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Munshi, Anusheel, Kaustav Talapatra, and Debanarayan Dutta. "Breast cancer radiotherapy and cardiac risk." Oncology Reviews 4, no. 3 (December 5, 2011): 137. http://dx.doi.org/10.4081/oncol.2010.137.

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Breast cancer is the leading cause of morbidity and mortality in women in the developed world and its incidence in the developing world is on the rise. Management of breast cancer requires a multimodality approach and an integration of the services of surgery, radiation, and medical oncology. Radiotherapy after mastectomy or breast conservation leads to reduction in local recurrence by two-thirds. Recent trials and metaanalyses have also demonstrated overall survival benefit with radiotherapy. Of late, however, there has been concern regarding side effects of radiotherapy in breast cancer. Among these the cardiac risk has been particularly been of concern. This review discusses the etiology, manifestations, and evidence in relation to implication of breast cancer radiotherapy in cardiac adverse effects.

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Santivasi, Wil L., Meghan M. Routt, and Alicia M. Terando. "Idiopathic Thrombocytopenic Purpura after Mastectomy and Axillary Lymph Node Dissection." Case Reports in Surgery 2014 (2014): 1–2. http://dx.doi.org/10.1155/2014/316064.

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First described in 1916, idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease resulting in the destruction of platelets. Here, we present a case of an 85-year-old patient diagnosed with invasive ductal carcinoma of the breast whose surgical treatment was complicated postoperatively by acute-onset thrombocytopenia with a resultant hematoma at the operative site. Diagnostic Workup revealed no clear etiology for the thrombocytopenia; therefore, a presumptive diagnosis of idiopathic thrombocytopenic purpura was made. Previous literature has associated the development of idiopathic thrombocytopenic purpura with breast cancer. However, to the authors’ knowledge, there are no reported cases of ITP presenting immediately following surgical intervention for breast cancer in the absence of other etiologic factors.

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Weiss, Joli R., Kirsten B. Moysich, and Helen Swede. "Epidemiology of Male Breast Cancer." Cancer Epidemiology, Biomarkers & Prevention 14, no. 1 (January 1, 2005): 20–26. http://dx.doi.org/10.1158/1055-9965.20.14.1.

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Abstract Breast cancer in men is a rare disease, accounting for ∼1% of all breast cancer cases. Although the epidemiologic literature regarding female breast cancer is extensive, relatively little is known about the etiology of male breast cancer (MBC). This review is intended to summarize the existing body of evidence on genetic and epidemiologic risk factors for breast cancer in men. Overall, the epidemiology of MBC presents similarities with the epidemiology of female breast cancer. Major genetic factors associated with an increased risk of breast cancer for men include BRCA2 mutations, which are believed to account for the majority of inherited breast cancer in men, Klinefelter syndrome, and a positive family history. Suspected genetic factors include AR gene mutations, CYP17 polymorphism, Cowden syndrome, and CHEK2. Epidemiologic risk factors for MBC include disorders relating to hormonal imbalances, such as obesity, testicular disorders (e.g., cryptorchidism, mumps orchitis, and orchiectomy), and radiation exposure. Suspected epidemiologic risk factors include prostate cancer,prostate cancer treatment, gynecomastia, occupational exposures (e.g., electromagnetic fields, polycyclic aromatic hydrocarbons, and high temperatures), dietary factors (e.g., meat intake and fruit and vegetable consumption), and alcohol intake.

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40

John, Esther M., Lisa M. Hines, Amanda I. Phipps, Jocelyn Koo, Teri A. Longacre, Sue A. Ingles, Kathy B. Baumgartner, Martha L. Slattery, and Anna H. Wu. "Reproductive history, breast-feeding and risk of triple negative breast cancer: The Breast Cancer Etiology in Minorities (BEM) study." International Journal of Cancer 142, no. 11 (January 30, 2018): 2273–85. http://dx.doi.org/10.1002/ijc.31258.

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41

Lynge, Elsebeth, Linda Kaerlev, Jørn Olsen, Svend Sabroe, Noemia Afonso, Wolfgang Ahrens, Mikael Eriksson, et al. "Rare cancers of unknown etiology: lessons learned from a European multi-center case–control study." European Journal of Epidemiology 35, no. 10 (July 17, 2020): 937–48. http://dx.doi.org/10.1007/s10654-020-00663-y.

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Abstract Rare cancers together constitute one fourth of cancers. As some rare cancers are caused by occupational exposures, a systematic search for further associations might contribute to future prevention. We undertook a European, multi-center case–control study of occupational risks for cancers of small intestine, bone sarcoma, uveal melanoma, mycosis fungoides, thymus, male biliary tract and breast. Incident cases aged 35–69 years and sex-and age-matched population/colon cancer controls were interviewed, including a complete list of jobs. Associations between occupational exposure and cancer were assessed with unconditional logistic regression controlled for sex, age, country, and known confounders, and reported as odds ratios (OR) with 95% confidence intervals (CI). Interviewed were 1053 cases, 2062 population, and 1084 colon cancer controls. Male biliary tract cancer was associated with exposure to oils with polychlorinated biphenyls; OR 2.8 (95% CI 1.3–5.9); male breast cancer with exposure to trichloroethylene; OR 1.9 (95% CI 1.1–3.3); bone sarcoma with job as a carpenter/joiner; OR 4.3 (95% CI 1.7–10.5); and uveal melanoma with job as a welder/sheet metal worker; OR 1.95 (95% CI 1.08–3.52); and cook; OR 2.4 (95% CI 1.4–4.3). A confirmatory study of printers enhanced suspicion of 1,2-dichloropropane as a risk for biliary tract cancer. Results contributed to evidence for classification of welding and 1,2-dichloropronane as human carcinogens. However, despite efforts across nine countries, for some cancer sites only about 100 cases were interviewed. The Rare Cancer Study illustrated both the strengths and limitations of explorative studies for identification of etiological leads.

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Bono, Aldo, Marzia Baldi, Andrea Maurichi, and Stefano Tomatis. "Distribution of melanoma on breast surface suggests its etiology." International Journal of Cancer 105, no. 3 (April 14, 2003): 434. http://dx.doi.org/10.1002/ijc.11084.

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Li, Jiaomei, Zhaohong Zheng, Min Liu, Yiping Ren, Yue Ruan, and Duo Li. "Relationship between the n-3 index, serum metabolites and breast cancer risk." Food & Function 12, no. 17 (2021): 7741–48. http://dx.doi.org/10.1039/d1fo01245b.

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The present study suggests that low n-3 index might be a potential risk factor for breast cancer, and serum metabolites 16α-hydroxy DHEA 3-sulfate may play an important role linking n-3 PUFA deficiency and breast disease etiology.

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Sen, Selen, and Dilek Aygin. "Role Of Environmental Carcinogens in The Etiology Of Breast Cancer." Sakarya Medical Journal 4, no. 3 (2014): 109–14. http://dx.doi.org/10.5505/sakaryamj.2014.06078.

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Kumar, Nagi B., Angelina Fink, Silvina Levis, Ping Xu, Roy Tamura, and Jeffrey Krischer. "Thyroid function in the etiology of fatigue in breast cancer." Oncotarget 9, no. 39 (May 22, 2018): 25723–37. http://dx.doi.org/10.18632/oncotarget.25438.

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Bolf, Eric L., Brian L. Sprague, and Frances E. Carr. "A Linkage Between Thyroid and Breast Cancer: A Common Etiology?" Cancer Epidemiology Biomarkers & Prevention 28, no. 4 (December 12, 2018): 643–49. http://dx.doi.org/10.1158/1055-9965.epi-18-0877.

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Rozanov, I. D., E. A. Rozanova, E. I. Shirikov, A. S. Balkanov, L. E. Gaganov, and E. A. Stepanova. "PULMONARY EMBOLISM IN BREAST CANCER: ETIOLOGY, PATHOPHYSIOLOGY AND TREATMENT APPROACHES." Almanac of Clinical Medicine 44, no. 5 (January 1, 2016): 580–86. http://dx.doi.org/10.18786/2072-0505-2016-44-5-580-586.

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Amberger, Melissa, Nancy Presnick, and Gerard Baltazar. "Large Bowel Obstruction Subsequent to Resected Lobular Breast Carcinoma: An Unconventional Etiology of Malignant Obstruction." Case Reports in Surgery 2018 (June 13, 2018): 1–4. http://dx.doi.org/10.1155/2018/6085730.

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Introduction. Breast cancer metastasis to the gastrointestinal tract is rare and mostly limited to case reports which recommend consideration of metastasis when breast cancer patients particularly those with invasive lobular carcinoma present with new gastrointestinal complaints. Presentation of case. We report a 50-year-old female who presented with gastrointestinal symptoms of nausea and vomiting determined to be the result of large bowel obstruction secondary to rectosigmoid metastasis and carcinomatosis of breast invasive lobular carcinoma. She was treated with diverting loop sigmoid colostomy for her large bowel obstruction. Discussion. Our case reflects the importance of gastrointestinal surveillance of patients with a history of breast cancer. Current National Comprehensive Cancer Network (NCCN) guidelines for stage I-II breast cancer suggest posttreatment lab and imaging evaluation for metastasis only if new symptoms present. Conclusion. We observed an unusually rapid disease progression, requiring evaluation of new gastrointestinal symptoms. Assessment for GI tract metastatic involvement should be done as early as progression to symptomatic disease can result in need for further invasive surgery in advanced stages of cancer.

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Sher, Gulab, Nadia Aziz Salman, Michal Kulinski, Rayyan Abdulaziz Fadel, Vinod Kumar Gupta, Ambika Anand, Salahddin Gehani, et al. "Prevalence and Type Distribution of High-Risk Human Papillomavirus (HPV) in Breast Cancer: A Qatar Based Study." Cancers 12, no. 6 (June 10, 2020): 1528. http://dx.doi.org/10.3390/cancers12061528.

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Human papillomavirus (HPV) has been implicated in the etiology of a variety of human cancers. Studies investigating the presence of high-risk (HR) HPV in breast tissue have generated considerable controversy over its role as a potential risk factor for breast cancer (BC). This is the first investigation reporting the prevalence and type distribution of high-risk HPV infection in breast tissue in the population of Qatar. A prospective comparison blind research study herein reconnoitered the presence of twelve HR-HPV types’ DNA using multiplex PCR by screening a total of 150 fresh breast tissue specimens. Data obtained shows that HR-HPV types were found in 10% of subjects with breast cancer; of which the presence of HPV was confirmed in 4/33 (12.12%) of invasive carcinomas. These findings, the first reported from the population of Qatar, suggest that the selective presence of HPV in breast tissue is likely to be a related factor in the progression of certain cases of breast cancer.

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Chen, Wenwen, Zhongyu Li, Pengwei Deng, Zhengnan Li, Yuhai Xu, Hongjing Li, Wentao Su, and Jianhua Qin. "Advances of Exosomal miRNAs in Breast Cancer Progression and Diagnosis." Diagnostics 11, no. 11 (November 20, 2021): 2151. http://dx.doi.org/10.3390/diagnostics11112151.

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Breast cancer is one of the most commonly diagnosed malignancies and the leading cause of cancer death in women worldwide. Although many factors associated with breast cancer have been identified, the definite etiology of breast cancer is still unclear. In addition, early diagnosis of breast cancer remains challenging. Exosomes are membrane-bound nanovesicles secreted by most types of cells and contain a series of biologically important molecules, such as lipids, proteins, and miRNAs, etc. Emerging evidence shows that exosomes can affect the status of cells by transmitting substances and messages among cells and are involved in various physiological and pathological processes. In breast cancer, exosomes play a significant role in breast tumorigenesis and progression through transfer miRNAs which can be potential biomarkers for early diagnosis of breast cancer. This review discusses the potential utility of exosomal miRNAs in breast cancer progression such as tumorigenesis, metastasis, immune regulation and drug resistance, and further in breast cancer diagnosis.

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