Environmental Determinants of Breast Cancer

Hiatt, Robert A.; Brody, Julia Green

doi:10.1146/annurev-publhealth-040617-014101

Cited by 84 publications

(70 citation statements)

References 152 publications

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“…The vast majority of breast cancers are diagnosed over the age of 50 and aging has been is associated with the accumulation of genetic, epigenetic, and hormonal alterations [25 , 26] . Several other factors have been associated with an increased occurrence of breast cancers including mammographic density [27] , reproductive factors (early age of menarche, late menopause, low parity, late age at first birth [28 , 29] ), anthropometric features (height [30] and body mass index for postmenopausal women [31] , hormone replacement therapy [32] , oral contraceptive pills [33] , exposure to diethylstilbestrol [34] , previous exposure to radiation therapy [35] , lifestyle factors (physical activity [36] , alcohol consumption [37] , night shift [38] ), and exposure to various chemicals [39] .…”

Section: Breast Cancer Risk Factorsmentioning

confidence: 99%

Breast cancers, mammary stem cells, and cancer stem cells, characteristics, and hypotheses

Taurin

Alkhalifa

2020

Neoplasia

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Highlights Breast cancer is a complex disease arising from the association and cumulation of multiple genetic alterations and environmental factors likely to alter cellular functions. The implication of stem cells in breast cancer’s origin and development has been debated for many years. Analogies between stem cells and cancer cells can be drawn on many levels. Importantly not all cancer cells are stem cells or exhibit properties similar to stem cells. There is no universal cell surface marker of the breast cancer stem cells, imputable to the diversity of the cell of origin, the heterogeneity and fluidity of the microenvironments, and a plethora of possible mutational events. Breast cancer stem cell targeting should hold a great promise for preventing metastasis, reducing the risk of drug resistance, and decreasing recurrence. However, only a few clinical trials assess the effectiveness of treatments on this specific cancer cell population. Additional considerations for the targeting of breast cancer stem cells need to be given to the tumor microenvironment. It is known to promote self-renewal, plasticity, and resistance to treatments. The fate of breast cancer stem cells is indissociable from its environment.

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Section: Breast Cancer Risk Factorsmentioning

confidence: 99%

Breast cancers, mammary stem cells, and cancer stem cells, characteristics, and hypotheses

Taurin

Alkhalifa

2020

Neoplasia

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“…Breast cancer (BC) is the leading cause of cancer-associated death (15%: 626,679 cases) and the most commonly diagnosed cancer (24%: 2,088,849 cases) among women worldwide 1 . BC is characterized by a complex interaction between environmental factors and biological aspects, such as gene deregulation, hormone disruption or ethnicity 2–4 . Despite subtype-specific treatment efforts, advanced BC with distant organ metastases is considered incurable 2 .…”

Section: Introductionmentioning

confidence: 99%

In silico analyses reveal new putative Breast Cancer RNA-binding proteins

Guerrero

López‐Cortés

García-Cárdenas

et al. 2020

Preprint

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Breast cancer (BC) is the leading cause of cancer-associated death among women worldwide. Despite treatment efforts, advanced BC with distant organ metastases is considered incurable. A better understanding of BC molecular processes is therefore of great interest to identify new therapeutic targets. Although large-scale efforts, such as The Cancer Genome Atlas (TCGA), have completely redefined cancer drug development, diagnosis, and treatment, additional key aspects of tumor biology remain to be discovered. In that respect, post-transcriptional regulation of tumorigenesis represents an understudied aspect of cancer research. As key regulators of this process, RNA-binding proteins (RBPs) are emerging as critical modulators of tumorigenesis but only few have defined roles in BC. To unravel new putative BC RBPs, we have performed in silico analyses of all human RBPs in three major cancer databases (TCGA-Breast Invasive Carcinoma, the Human Protein Atlas, and the Cancer Dependency Map project) along with complementary bioinformatics resources (STRING protein-protein interactions and the Network of Cancer Genes 6.0). Thus, we have identified six putative BC progressors (MRPL13, SCAMP3, CDC5L, DARS2, PUF60, and PLEC), and five BC suppressors RBPs (SUPT6H, MEX3C, UPF1, CNOT1, and TNKS1BP1). These proteins have never been studied in BC but show similar cancer-associated features than well-known BC proteins. Further research should focus on the mechanisms by which these proteins promote or suppress breast tumorigenesis, holding the promise of new therapeutic pathways along with novel drug development strategies.

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“…Several studies have attempted to assess the association between the exposure to environmental chemicals and breast cancer or some relevant outcome of breast cancer (eg, obesity) . Accumulating evidence from experimental, clinical, and ecological research has suggested that environmental factors play an important role in one or more possible pathways in the etiology of breast cancer; therefore, it is necessary to pay attention to the environmental causes of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Long‐term exposure to extremely low‐dose of nicotine and 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) induce non‐malignant breast epithelial cell transformation through activation of the a9‐nicotinic acetylcholine receptor‐mediated signaling pathway

Fararjeh

Chen

et al. 2018

Environmental Toxicology

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Breast cancer (BC) is the most common cancer affecting women worldwide and has been associated with active tobacco smoking. Low levels of nicotine (Nic) and 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK), have been detected in cases of second‐hand smoke (SHS). However, the correlation between SHS and BC risk remains controversial. In this study, we investigated whether the physiological SHS achievable dose of Nic and tobacco specific nitrosamine, NNK act together to induce breast carcinogenesis using an in vitro breast cell carcinogenesis model. Immortalized non‐tumorigenic breast epithelial cell line, HBL‐100 used for a time‐course assay, was exposed to very low levels of either Nic or NNK, or both. The time‐course assay consisted of 23 cycles of nitrosamines treatment. In each cycle, HBL‐100 cells were exposed to 1pM of Nic and/or 100 femtM of NNK for 48 hours. Cells were passaged every 3 days and harvested after 10, 15, and 23 cycles. Our results demonstrated that the tumorigenicity of HBL‐100, defined by soft agar colony forming, proliferation, migration and invasion abilities, was enhanced by co‐exposure to physiologically SHS achievable doses of Nic and NNK. In addition, α9‐nAChR signaling activation, which plays an important role in cellular proliferation and cell survival, was also observed. Importantly, an increase in stemness properties including the prevalence of CD44+/CD24− cells, increase Nanog expression and mammosphere‐forming ability were also observed. Our results indicate that chronic and long term exposure to environmental tobacco smoke, may induce breast cell carcinogenesis even at extremely low doses.

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Environmental Determinants of Breast Cancer

Cited by 84 publications

References 152 publications

Breast cancers, mammary stem cells, and cancer stem cells, characteristics, and hypotheses

Breast cancers, mammary stem cells, and cancer stem cells, characteristics, and hypotheses

In silico analyses reveal new putative Breast Cancer RNA-binding proteins

Long‐term exposure to extremely low‐dose of nicotine and 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) induce non‐malignant breast epithelial cell transformation through activation of the a9‐nicotinic acetylcholine receptor‐mediated signaling pathway

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