Pathology and Molecular Pathology of Breast Cancer

Marchiò, Caterina; Geyer, Felipe C.; Reis‐Filho, Jorge S.

doi:10.1007/978-3-319-35153-7_12

Cited by 2 publications

(3 citation statements)

References 340 publications

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“…Development of the human breast initiates from the milk lines of the fetus’s ventral surface, at the fifth week of gestation [ 1 , 2 ]. Until the 15th week of gestation, the breast bud will undergo the necessary cellular changes, towards mesenchymal condensation, on the chest wall at the site of mammary-gland development [ 1 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…After birth, the re-initiation of normal breast development takes place at puberty, coinciding with the onset of the cyclical secretion of the major sex hormones, estrogen and progesterone, which are the driving force of mammary-gland development and function in the adult life. Estrogen acts on the estrogen receptor (ER) of mammary-epithelial cells, inducing proliferation and causing duct elongation and epithelium thickening [ 2 ]. At the same time, estrogen affects, in a positive way, the periductal stromal elements, which supports expanding ducts and lobules [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

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Cellular Senescence in Normal Mammary Gland and Breast Cancer. Implications for Cancer Therapy

Sirinian

Peroukidis²,

Kriegsmann

et al. 2022

Genes

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Cellular senescence (CS) is a major homeostatic biological process, which plays a key role in normal tissue development and provides protection from stressful cell insults. The role of CS in mammary-gland development and breast cancer is not well understood. While there is a lack of experimental data on the role of CS in the development of the pre-pubertal mammary gland, there is evidence for a biphasic senescence response in adult normal-mammary-epithelial cells, where the bypass of the first senescence barrier (M0) seems to be a key step in the development of premalignant lesions, with genetic abnormalities that resemble in situ breast carcinoma. Further, there is accumulating evidence for the role of cellular senescence in breast-cancer response, regarding treatment and patient outcome. Here, we review the current literature on cellular senescence, in epithelial-mammary cells, breast-cancer cells, and breast-tumor-microenvironment-resident cells. Furthermore, we discuss its putative role in breast-cancer response, regarding treatment and disease progression. In addition, we provide preliminary evidence of CS in breast-cancer-microenvironment cells, such as tumor-associated fibroblasts and tumor-infiltrating lymphocytes, by employing the novel GL13 lipofuscin stain, as a marker of cellular senescence.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cellular Senescence in Normal Mammary Gland and Breast Cancer. Implications for Cancer Therapy

Sirinian

Peroukidis²,

Kriegsmann

et al. 2022

Genes

View full text Add to dashboard Cite

show abstract

“…Concerning the biology of breast cancer, there are two distinct biological entities in relevance to the expression of hormone receptors. More specifically estrogen receptor (ER) expression divides malignant breast tumors in ER-positive and ER-negative disease groups and these two entities present with fundamentally different biology, clinical course, and response to therapy [2]. Regarding therapeutic choices and outcomes, ER-negative breast cancer presents limited options other than chemo-and/or radiation therapy while patient outcomes upon treatment are poor compared to treatment of ER-positive disease [3].…”

Section: Introductionmentioning

confidence: 99%

RANK-C Expression Sensitizes ER-Negative, EGFR-Positive Breast Cancer Cells to EGFR-Tyrosine Kinase Inhibitors (TKIs)

Sirinian

Papanastasiou

Degn

et al. 2021

Genes

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Background: We have previously shown that overexpression of RANK-c in ER-negative breast cancer cell lines attenuates aggressive properties of cancer cells, partially through a RANK-c /EGFR interaction. EGFR inhibition through TKIs in breast cancer has been tested in triple-negative disease settings with limited clinical benefit for patients. Here we test if expression of RANK-c in ER-negative breast cancer cells in conjunction with treatment with TK inhibitors (erlotinib or gefitinib) can affect survival and colony-forming capacity of cancer cells. Methods: Stably expressing MDA-MB-231-RANK-c and SKBR3-RANK-c cells were employed to test proliferation and colony formation in the presence of TKIs. In addition, Western blot analysis was performed to dissect EGFR related signaling cascades upon TK inhibition in the presence of RANK-c. Results: Interestingly the two RANK-c expressing, ER-negative cells lines presented with a distinct phenotype concerning TKI sensitivity upon treatment. MDA-MB-231-RANK-c cells had a higher sensitivity upon gefitinib treatment, while erlotinib decreased the proliferation rate of SKBR3-RANK-c cells. Further, colony formation assays for MDA-MB-231-RANK-c cells showed a decrease in the number and size of colonies developed in the presence of erlotinib. In addition, RANK-c seems to alter signaling through EGFR after TKI treatment in a cell type-specific manner. Conclusions: Our results indicate that ER-negative breast cancer cells that express RANK-c alter their sensitivity profile against tyrosine kinase inhibitors (erlotinib and gefitinib) in a cell type-specific and culture substrate-dependent manner.

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Pathology and Molecular Pathology of Breast Cancer

Cited by 2 publications

References 340 publications

Cellular Senescence in Normal Mammary Gland and Breast Cancer. Implications for Cancer Therapy

Cellular Senescence in Normal Mammary Gland and Breast Cancer. Implications for Cancer Therapy

RANK-C Expression Sensitizes ER-Negative, EGFR-Positive Breast Cancer Cells to EGFR-Tyrosine Kinase Inhibitors (TKIs)

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