During the past ten years, Dr. Parham Jabbarzadeh Kaboli, a dedicated researcher with an h-Index of 26, has charted an impressive academic journey in cancer pharmacology, pharmacogenomics, and drug discovery. Beginning with a strong foundation in herbal medicine, he earned his PhD in Pharmacology from the prestigious University Putra Malaysia. Under the guidance of mentors like Dr. King-Hwa Ling and Professor Johnson Stanslas, Parham transitioned to the multifaceted disciplines of Pharmacology and Toxicology, significantly impacting his academic trajectory. His contributions to breast cancer research include groundbreaking work on c-MET receptor tyrosine kinase and galectin-9 signaling pathways. Parham\u2019s current postdoctoral research at China Medical University in Taiwan, mentored by President Mien-Chie Hung, continues to drive advancements in cancer biology and treatment. His journey exemplifies international collaboration and dedication to scientific exploration.<\/p>\n
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Triple-negative breast cancer (TNBC) is challenging, making up 15\u201320% of all breast cancer cases. This study examined how certain drugs, like lapatinib (a dual tyrosine kinase inhibitor targeting EGFR and Her2) and berberine (a plant-based compound), affect TNBC cells. We found that lapatinib activates a protein called Akt in MDA-MB231 TNBC cells, which could contribute to the cancer\u2019s resistance to treatment. We also studied the genetic profiles of different TNBC cell lines and patients. Interestingly, lapatinib and berberine enhanced Akt activity in TNBC cells, making them more resistant to treatment. These findings suggest that these drugs may not be effective in treating TNBC and could even make the cancer more resistant to therapy.<\/p>\n
Our recent research analyzed the gene expression of specific cancer-promoting proteins in ten different triple-negative breast cancer (TNBC) cell lines and TNBC patients, utilizing GEO and TCGA databases. Our current findings have highlighted that the majority of the chosen cell lines, including MDA-MB231 and TNBC patients, exhibit decreased levels of AKT1, PIK3CA, PTEN, and EGFR genes while showing increased levels of KRAS and DNMTs. These observations suggest that these genes are associated with the invasive nature of TNBC.<\/p>\n\n\n\n\n\n
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c-MET, also known as hepatocyte growth factor receptor (HGFR), is a receptor tyrosine kinase that plays a crucial role in various solid tumors like lung, breast, and liver cancers. Recent single-cell analysis has revealed that c-MET significantly impacts the composition of immune cells within the tumor microenvironment. It promotes an immunosuppressive environment by transforming anti-cancer M1 macrophages into tumorigenic M2 macrophages and converting CD4+Th cells into Treg cells by upregulating PD-L1, TGF-\u03b2, and IL-10. Our current research explores the potential of targeting c-MET as an immunotherapeutic strategy.<\/p>\n
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Traditionally, c-MET was known to have a single ligand, HGF. However, our recent research has discovered new ligands for c-MET in breast cancer. These newly identified ligands can potentially disrupt anticancer immunotherapy efforts by altering the immune cell composition within the tumor microenvironment, ultimately hindering the body\u2019s ability to combat cancer effectively. This discovery highlights the need for a deeper understanding of c-MET\u2019s role in breast cancer and its implications for immunotherapeutic approaches.<\/p><\/div>\n
In our future team, we plan to jump much deeper into the c-MET mechanism and the functional roles of interactions of c-MET with its novel ligands. The results have yet to be published.<\/span><\/span>
<\/p>\n\n\n\n\n\nPicture Gallery
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