Christoforos Thomas, PhD, received his bachelor’s degree from Aristotle University of Thessaloniki in Greece and pursued his doctoral training at the University of Ioannina Medical School in Greece (1998-2004) to study the redox regulation of cancer cell cycle progression. Dr. Thomas conducted postdoctoral research at Karolinska Institute in Sweden (2005-2009) to investigate the biology of estrogen receptors in cancer. He then joined the University of Houston’s Center of Nuclear Receptors and Cell Signaling as Research Assistant Professor (2010-2017) and after continuing as Adjunct Assistant Professor at the University of Pennsylvania Perelman School of Medicine and the Abramson Cancer Center he was recruited to Houston Methodist Research Institute in February 2022.

Dr. Thomas’s laboratory has focused on the following research:

• Investigating the mechanisms by which estrogen receptors (ERs) influence cancer initiation, progression and response to therapy. The lab has focused on interactions of ERs with p53, stress response and growth factor receptor signaling in breast and lung cancer.
• Delineating pathways that regulate ER expression in cells. Chromatin modifiers impacting transcription together with signaling kinases and ubiquitin proteasome pathway that control protein stability have been investigated as potential drivers of altered ER expression in malignant breast with the aim to identify novel factors with prognostic and therapeutic value.
• Exploring estrogen receptor beta (ERβ) as novel biomarker and therapeutic target in inflammatory breast cancer (IBC) that represents the most aggressive form of breast cancer. Associating ERβ with clinical phenotypes and evaluating ERβ agonists as anti-metastatic regimen in preclinical IBC models has been the focus of our studies.
• Studying the involvement of abnormal estrogen signaling in breast tumorigenesis in the context of defective p53 pathway using mouse models that mimic the pathology of Li-Fraumeni Syndrome (LFS) and breast cancer tissues from affected individuals.
• Determining how ER signaling influences breast cancer progression by altering the tumor microenvironment using novel mouse models of breast cancer with altered ER signaling.