Genomic profiling of breast cancer

Pandey, Abha; Singh, Alok Kumar; Maurya, Sanjeev Kumar; Rai, Rajani; Tewari, Mallika; Kumar, Mohan; Shukla, H. S.

doi:10.1002/jso.21249

Cited by 4 publications

(3 citation statements)

References 74 publications

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“…Epigenetic changes play a major role in various genes that are potentially involved in human malignancies including breast cancer (BC) (Jones and Baylin, 2002;Widschwendter and Jones, 2002;Georgiou et al, 2007;Pandey et al, 2009). These changes involve the interplay between DNA methylation, histone modifications, and expression of noncoding RNAs in the regulation of gene transcription.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic silencing of BRCA1 gene associated with demographic and pathologic factors in sporadic breast cancer

Singh

Pandey

Tewari

et al. 2011

European Journal of Cancer Prevention

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Breast cancer (BC) is a leading cause of cancer-related deaths among women worldwide, and this study further demonstrates that the women of Varanasi (north India) are not untouched by this fatal disease. During BC development, epigenetic activity plays a key role in silencing gene expression. Its widespread occurrence in the cancer genome could inactivate many cellular pathways including DNA repair, cell cycle control, apoptosis, cell adherence, and detoxification. In this study, our aim was to determine the penetrance of BRCA1 promoter methylation and its correlation with pathological and demographic factors in sporadic BC in an Indian population. Our analysis included 127 patients who were diagnosed with sporadic BC. Methylation-specific PCR for the BRCA1 promoter was used during the study and correlated with pathological and demographic factors. Methylation of the BRCA1 promoter was detected in 8.7% (11/127) of the tumors. Correlation of promoter methylation with demographic factors and clinicopathological markers revealed the following data: (i) BRCA1 methylation was more frequently observed in tumor samples taken from premenopausal or perimenopausal women (P=0.026), (ii) methylation of the BRCA1 promoter negatively correlated with estrogen receptor (P=0.040), progesterone receptor (P=0.013), and epidermal growth factor receptor-2 (P=0.002), (iii) the overall promoter methylation was higher in more advanced stages (P=0.036) of the disease. This study has immense implications for understanding epigenetic mechanisms in BC development. The result suggests that the epigenetic silencing of BRCA1 is uncommon and is associated with the triple-negative phenotype.

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Section: Introductionmentioning

confidence: 99%

Epigenetic silencing of BRCA1 gene associated with demographic and pathologic factors in sporadic breast cancer

Singh

Pandey

Tewari

et al. 2011

European Journal of Cancer Prevention

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“…oncogenes (i.e., erbB-2, MYC) and tumor suppressor genes (i.e., BRCA1, BRCA2, p53) involved in malignant transformation of the cell in the specific case of breast carcinoma. 16,17,36,37 Correlation of Ki-67 and p27…”

Section: Discussionmentioning

confidence: 99%

Expression of Ki‐67 and p27^Kip1 in fine‐needle aspirates from breast carcinoma and benign breast diseases

Ramljak

Sučić

Vrdoljak³

et al. 2011

Diagnostic Cytopathology

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Cell atypia in breast fine needle aspiration (FNA) can introduce some diagnostic difficulties. Molecules reflecting proliferative cell potential, such as Ki-67 and p27(Kip1) , can help in recognizing the true biological nature of a cell. Thus, the objective of the study was to analyze the difference in Ki-67 and p27(Kip1) cell immunoexpression in breast FNA specimens between fibroadenomas, fibrocystic changes (FCC) with atypia, and breast carcinoma. Microscopic analyses of cell cytomorphology and Ki-67 and p27(Kip1) breast cell immunoexpression were done after standard Pappenheim and immunocytochemical staining (labeled streptavidin-biotin, LSAB) method in autostainer DakoCytomation TechMate™. The study included 50 patients with breast carcinoma, 20 patients with fibroadenoma, and 20 patients with FCC with atypia. High Ki-67 and low or absent p27(Kip1) were found in most patients with breast carcinoma, while majority of FCC with atypia were characterized by low Ki-67 and moderate to high p27(Kip1) cell immunoexpression. Majority of fibroadenomas were associated with low Ki-67 and low to moderate p27(Kip1) cell immunoexpression indicating progressive decrease in cell cycle inhibition, but still not so high proliferative activity as in carcinoma. However, although statistically significant difference for Ki-67 and p27(Kip1) was found between breast lesions in our study, the large ranges observed for each marker make them essentially useless for better cytological diagnosis in a single case. Regarding their opposite role in cell cycle, inverse correlation of Ki-67 and p27(Kip1) was noticed. Poorly differentiated carcinoma cells had mostly high Ki-67 and low p27(Kip1) cell immunoexpression.

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“…Over activation of this EGFR induces multiple downstream cell signaling pathways including RAS/RAF/MEK/ERK1/2 pathway and contributes to cancer development, metastasis, and resistance to chemotherapy (Okamoto, ). Similarly, arachidonic acid metabolism has been suggested to play an important role in oral carcinogenesis (Pandey et al, ).…”

Section: Introductionmentioning

confidence: 99%

Helioxanthin suppresses the cross talk of COX-2/PGE2 and EGFR/ERK pathway to inhibit Arecoline-induced Oral Cancer Cell (T28) proliferation and blocks tumor growth in xenografted nude mice

et al. 2015

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Helioxanthin, an active compound from Taiwania cryptomerioides Hayata, has been shown to have various biological activities. However, their anticancer effect in oral squamous cell carcinoma has not been well established yet. Helioxanthin inhibited the proliferation of oral squamous cell carcinoma cells in a dose-dependent manner by inducing G2/M phase arrest. Similarly, helioxanthin inhibited cyclooxygenase-2, (COX-2), phosphorylated EGFR, and extracellular-signal-regulated kinases (ERK) protein level and further reduced the nuclear accumulation of phosphorylated epidermal growth factor receptor (pEGFR) and activator protein-1(AP-1) family protein, c-fos. Moreover, helioxanthin at the dose of 20 and 30 mg kg for 15 days reduced the tumor growth in animal model. This study demonstrated that Helioxanthin exerts its anticancer activity against oral cancer cells by downregulating EGFR/ERK/c-fos signaling pathway to inhibit COX-2 level and by activating cyclin-dependent kinase inhibitor (p27) to further induce G2/M cell cycle arrest. This helioxanthin may serve as a novel candidate for oral cancer prevention. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 2045-2056, 2016.

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Genomic profiling of breast cancer

Cited by 4 publications

References 74 publications

Epigenetic silencing of BRCA1 gene associated with demographic and pathologic factors in sporadic breast cancer

Epigenetic silencing of BRCA1 gene associated with demographic and pathologic factors in sporadic breast cancer

Expression of Ki‐67 and p27^Kip1 in fine‐needle aspirates from breast carcinoma and benign breast diseases

Helioxanthin suppresses the cross talk of COX-2/PGE2 and EGFR/ERK pathway to inhibit Arecoline-induced Oral Cancer Cell (T28) proliferation and blocks tumor growth in xenografted nude mice

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Genomic profiling of breast cancer

Cited by 4 publications

References 74 publications

Epigenetic silencing of BRCA1 gene associated with demographic and pathologic factors in sporadic breast cancer

Epigenetic silencing of BRCA1 gene associated with demographic and pathologic factors in sporadic breast cancer

Expression of Ki‐67 and p27Kip1 in fine‐needle aspirates from breast carcinoma and benign breast diseases

Helioxanthin suppresses the cross talk of COX-2/PGE2 and EGFR/ERK pathway to inhibit Arecoline-induced Oral Cancer Cell (T28) proliferation and blocks tumor growth in xenografted nude mice

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Expression of Ki‐67 and p27^Kip1 in fine‐needle aspirates from breast carcinoma and benign breast diseases