Department of Molecular & Cellular Physiology,
Department of Molecular and Cellular Physiology
John Lamar is an Assistant Professor in the Department of Molecular and Cellular Physiology at Albany Medical College. He received his undergraduate degree from The State University of New York at Geneseo and a Ph.D. from Albany Medical College. He did his a postdoctoral work at the Koch Institute of Integrative Cancer Research at Massachusetts Institute of Technology where he focused on understanding molecular mechanisms that govern breast cancer and melanoma metastasis.
Dr. Lamar established his lab at Albany Medical College in October of 2015 and his work remains focused on identifying regulators of breast cancer and melanoma metastasis. His lab has developed a number of in vivo approaches to identify and study genes that influence metastasis formation and metastatic growth, and his team is using these approaches to investigate the roles of the transcriptional co-activators YAP and TAZ in metastasis. This work builds off of Dr. Lamar’s postdoctoral work, which demonstrated that inappropriately high YAP transcriptional activity promotes breast cancer and melanoma metastasis. Current projects are focused on identifying pathways in cancer cells that are essential for YAP/TAZ-mediated tumor progression and metastasis. The lab also studies a rare vascular sarcoma called epithelioid hemangioendothelioma (EHE). This rare tumor is driven by a chromosomal translocation that fuses part of the TAZ protein with the CAMTA1 protein. Dr. Lamar and his group aim to identify pathways that can be exploited to repress the activity of this fusion protein and potentially treat EHE.
Integrin alpha3beta1 potentiates TGFbeta-mediated induction of MMP-9 in immortalized keratinocytes.
The Journal of investigative dermatology Mar, 2008 | Pubmed ID: 17762853
An immortalization-dependent switch in integrin function up-regulates MMP-9 to enhance tumor cell invasion.
Cancer research Sep, 2008 | Pubmed ID: 18794124
Nephronectin is Correlated with Poor Prognosis in Breast Cancer and Promotes Metastasis via its Integrin-Binding Motifs.
Neoplasia (New York, N.Y.) 04, 2018 | Pubmed ID: 29539586
RUNX1 and RUNX3 protect against YAP-mediated EMT, stem-ness and shorter survival outcomes in breast cancer.
Oncotarget Mar, 2018 | Pubmed ID: 29581836
YAP/TAZ Activation as a Target for Treating Metastatic Cancer.
Cancers Apr, 2018 | Pubmed ID: 29642615
Epithelioid Hemangioendothelioma as a Model of YAP/TAZ-Driven Cancer: Insights from a Rare Fusion Sarcoma.
Cancers Jul, 2018 | Pubmed ID: 29996478
SRC tyrosine kinase activates the YAP/TAZ axis and thereby drives tumor growth and metastasis.
The Journal of biological chemistry 02, 2019 | Pubmed ID: 30559289
TAZ teases T cells with PD-L1.
Gland surgery Aug, 2019 | Pubmed ID: 31538054
The scaffold protein IQGAP1 is crucial for extravasation and metastasis.
Scientific reports Feb, 2020 | Pubmed ID: 32051509
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