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Interpreting the Role of INS and GLUT4 in Type 2 Diabetes Mellitus and Breast Cancer Patients

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dc.contributor.author Bhutta, Saria Shafiq
dc.date.accessioned 2024-02-15T10:32:05Z
dc.date.available 2024-02-15T10:32:05Z
dc.date.issued 2021
dc.identifier.other 277420
dc.identifier.uri http://10.250.8.41:8080/xmlui/handle/123456789/42194
dc.description Supervisor : Dr. Attya Bhatti en_US
dc.description.abstract Type 2 Diabetes Mellitus and breast cancer are two most quickly prevailing morbidities that often exist parallel to each other. Along with environmental factors genetic factor is the huge one in such conditions. INS and GLUT4 are the genes that are dysregulated in both diseases. INS codes for insulin secretion through pancreatic beta cells that helps the body to utilize the glucose while GLUT4 is insulin dependent glucose transporter. According to literature INS is overexpressed in cancer and early stage of T2DM. While GLUT4 is down-regulated in T2DM and up-regulated in Breast Cancer. The aim of this study was to analyze the expression of two genes in such disorders and linking the disease occurrence. The purpose is providing common biomarkers for prognosis, diagnosis, and therapeutics. String and Enrichr web analysis were done to confirm the role of the two genes in T2DM and breast cancer pathways. Reverse Transcriptase PCR was done for amplification of gene-primers. Real Time PCR was done for expression comparison in four study groups i.e. breast cancer, T2DM, breast cancer + diabetes Mellitus group and the control group. 5 samples of BC, 4 samples of DM, 2 samples of BC+DM and 7 control samples were processed. Our results evaluated that the GLUT4 and INS expression was same as mentioned in literature and the expression difference in disease vs control was statistically significant. en_US
dc.language.iso en en_US
dc.publisher Atta Ur Rahman School of Applied Biosciences (ASAB), NUST en_US
dc.title Interpreting the Role of INS and GLUT4 in Type 2 Diabetes Mellitus and Breast Cancer Patients en_US
dc.type Thesis en_US


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