scholarly journals Chemotherapeutic Resistance Genes of Breast Cancer Patients – An Overview

2021 ◽  
Author(s):  
Anagha Kollamparambil Ajith ◽  
Sasikala Subramani ◽  
Agaath Hedina Manickam ◽  
Sivasamy Ramasamy
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Patients ◽  
Hippo Pathway ◽  
Chemotherapy Resistance ◽  
Gene Families ◽  
Breast Cancer Patients ◽  
Drug Induced ◽  
Human Genes ◽  
Cell Cycle Alteration

Purpose: Cancer is the leading challenge to human health since the dawn of early Egyptian manuscripts, where they found tumour from fossils in the modernized twentieth century. Increasing rate of incidence and death from cancer in the past few years is thought provoking. Among all type of cancers, breast cancer is very common among women and diverse in character. Drug resistance is the challenging aspect for traditional chemotherapy. Methods: Data was collected from online platform without any time restriction. After screening and evaluation, 66 articles were considered for this study. This review is a summarized collection of information from published studies on human genes associated with drug resistance in breast cancer treatment. Results: Analysis of these findings highlights the importance of MAP kinase and ABC gene families in creating resistance barriers. Genes involved in cell cycle alteration, apoptosis, and hippo pathway were also linked with drug resistance particularly in breast cancer. Conclusion: The exact mechanism of chemotherapy resistance is still unresolved and unexplained the drug resistance seen in breast cancer patients were multifactorial. Drug induced up regulation or down regulation of genes contributes unusual protein expression and ultimately leads to resistance. The ultimate focus of this review is to identify the genes having pivotal role in chemotherapy resistance in breast cancer.

scholarly journals ELOVL2: a novel tumor suppressor attenuating tamoxifen resistance in breast cancer

2020 ◽  
Author(s):  
Dawoon Jeong ◽  
Juyeon Ham ◽  
Hyeon Woo Kim ◽  
Heejoo Kim ◽  
Hwee Won Ji ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Patients ◽  
Tumor Tissue ◽  
Tamoxifen Resistance ◽  
Colony Formation Assay ◽  
Breast Cancer Patients ◽  
Methylation Analysis ◽  
Genome Wide ◽  
Mcf 7

Abstract Background To comprehensively understand the molecular mechanism of tamoxifen resistance (TamR) acquisition by epigenetically regulated genes, it is essential to identify pivotal genes by genome-wide methylation analysis and verify their function in xenograft animal model and cancer patients. Methods The MCF-7/TamR breast cancer cell line was developed and a genome-wide methylation array was performed. The methylation and expression of ELOVL2 was validated in cultured cells, xenografted tumor tissue, and breast cancer patients by methylation-specific PCR, qRT-PCR, Western blot analysis, and immunohistochemistry. Deregulation of ELOVL2 and THEM4 was achieved using siRNA or generating stable transfectants. Tam sensitivity, cell growth, and apoptosis were monitored by colorimetric and colony formation assay and flow cytometric analysis. Pathway analysis was performed to generate networks for the differentially methylated genes in the MCF-7/TamR cells and for the differentially expressed genes in the ELOVL2-overexpressing cells. Results Genome-wide methylation analysis in the MCF-7/TamR cells identified elongation of very-long chain fatty acid protein 2 (ELOVL2) to be significantly hypermethylated and downregulated, which was further verified in the tumor tissues from TamR breast cancer patients (n = 28) compared with those from Tam-sensitive (TamS) patients (n = 33) (P < 0.001). Immunohistochemical analysis of tissues from cancer patients showed lower expression of ELOVL2 in the TamR than TamS tissues. Growth of the MCF-7/TamR cells overexpressing ELOVL2 was retarded in cell culture and also in xenograft tumor tissue. Strikingly, ELOVL2 attenuated resistance to Tam up to 70% judged by the colorimetric and colony formation assay and xenograft mouse model. ELOVL2 contributed to the recovery of Tam sensitivity by regulating a group of genes in the AKT and ERα signaling pathways, e.g., THEM4, which plays crucial roles in drug resistance. Conclusions ELOVL2 was hypermethylated and downregulated in TamR breast cancer patients compared with TamS patients. ELOVL2 is responsible for the recovery of Tam sensitivity. AKT- and ERα-hubbed networks are pivotal in ELOVL2 signaling, where THEM4 contributes to the relaying ELOVL2 signaling. This study implies that deregulation of a gene in fatty acid metabolism can lead to drug resistance, giving insight into the development of a new therapeutic strategy for drug-resistant breast cancer.

Polymorphic Sites (1236 and 3435) in Multi Drug Resistance Gene 1 Influencing Drug Response in Breast Cancer Patients

2007 ◽  
Vol 3 (6) ◽  
pp. 453-460 ◽  
Author(s):  
Shaswati Khan . ◽  
Kaiser Jamil . ◽  
G. Prabhavathy Das . ◽  
Ch. Mohana Vamsy . ◽  
Sudha Murthy .
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Patients ◽  
Resistance Gene ◽  
Drug Response ◽  
Multi Drug Resistance ◽  
Breast Cancer Patients ◽  
Drug Resistance Gene

Utility of microsieve device for enumeration and miRNA expression profiling of CTCs for personalized cancer management.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e22107-e22107
Author(s):  
Steven Tucker ◽  
Karen Mei Ling Tan ◽  
Sai Mun Leong ◽  
Chua Hui Wen ◽  
Delly Fareda Jumaat ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Patients ◽  
Expression Profiling ◽  
Microrna Expression ◽  
Size Exclusion ◽  
Breast Cancer Patients ◽  
Peripheral Cell ◽  
Mesenchymal Transition ◽  
Cancer Management

e22107 Background: Although a rare peripheral cell population, circulating tumor cells (CTCs) represent a potential alternative to serial invasive biopsies as a source of tissue in monitoring clinical states of non-hematological malignancies. CTCs harvested from a single patient are a heterogeneous mixture of cells differing in their transcriptome expressional profiles, metastatic potential and drug resistance properties. Mere identification and enumeration of CTCs are unable to provide qualitative information about individual CTC biology. The presence of a few highly malignant, metastasis-capable CTCs and cancer stem cells among the other less aggressive CTCs in the circulating population will not be apparent from CTC counts alone. Methods: We developed a high-throughput size-exclusion microsieve device (CellSievo, Singapore) to isolate CTCs (defined as DAPI-positive, CD45-negative cells), regardless of the cell surface receptors expressed, from 74 breast cancer patients. Using CTCs eluted from the microsieve post-capture, we performed microRNA expression profiling to further characterize breast cancer CTCs. Results: Using CellSievo’s microsieve device, we obtained an average mean CTC count of 21.2 (+/- 31.8; range=0-112.5) per 7.5ml peripheral blood, for breast cancer patients, as opposed to 1.3 (+/-1.6, range 0-5.0) for healthy subjects. Viable CTCs from breast cancer patients were successfully harvested for downstream microRNA profiling. CTCs from breast cancer patients were routinely found to express microRNA profiles mediating epithelial-to-mesenchymal transition, tumor invasion, and regulation of chemotherapeutic drug resistance to tamoxifen, anthracyclines, taxanes, and trastuzumab. Serial monitoring of microRNA expression pattern of CTCs could identify emergence of novel tumor populations with distinct microRNA expression patterns during or after anticancer therapy (detailed microRNA expression data to be presented). Conclusions: Our results suggest that microRNA biomarkers derived from peripheral CTCs can yield highly useful information and offer prognostic and predictive applications for therapeutics and companion diagnostic development.

scholarly journals Exploiting the apoptotic actions of oestrogen to reverse antihormonal drug resistance in oestrogen receptor positive breast cancer patients

The Breast ◽  
2007 ◽  
Vol 16 ◽  
pp. 105-113 ◽  
Author(s):  
V. Craig Jordan ◽  
Joan Lewis-Wambi ◽  
Helen Kim ◽  
Heather Cunliffe ◽  
Eric Ariazi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Patients ◽  
Oestrogen Receptor ◽  
Breast Cancer Patients ◽  
Positive Breast Cancer
Sign in / Sign up

Export Citation Format

Share Document