Tumors are made up of cancer cells and also of normal cell types and extracellular molecules that surround, support and feed the cancer cells. There is abundant communication between the cancer cells and the normal elements; and a tumor can change its environment, and the environment can affect how a tumor grows and spreads.

About one third of all people with cancer die of cachexia (severe muscle wasting). Cachexia affects people at the later stages of disease and causes debilitating muscle weakness. It is associated with reduced response to therapy and poor prognosis.

Learn more about cachexia

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The ElShamy group

Dr. ElShamy’s interests encompass basic, clinical and translational cancer research and research programs in his laboratory focus on identifying and improving treatments for breast and ovarian cancers, especially metastatic diseases. The ElShamy research group is focused on tackling breast cancer as an interactive entity composed of tumor cells and their microenvironment. The tumor microenvironment contains a variety of activated entities, such as mesenchymal stem cells and macrophages, which are intimately involved in increasing tumor progression and cancer spreading to other organs. The ElShamy approach aims to therapeutically target both the microenvironment and the tumor cells to achieve a higher level of remission.

The ongoing research conducted by the ElShamy group is based on the hypothesis that tumor cell dissemination and metastasis is an early event and not an end point of the disease. If that hypothesis is correct, current treatment options that are effective in killing primary tumor cells will fail to target and remove the true patient killers, the already disseminated metastatic precursors. Dr. ElShamy studies metastasis as part of the earliest breast cancer lesions. The hope is that, if successful, this information will allow us to develop novel therapeutic regimens to block tumor progression, and therapeutic resistance.

The DerMardirossian group
A major challenge in cancer is to identify ways to limit cancer invasion. One approach to prevent invasion is to find ways to prevent cancer cell spread in response to environmental signals. Cell leading edge protrusion, via structures such as lamellipodia and filopodia, is the decisive step in initiating and directing cell migration. Dr. DerMardirossian’s research program is to dissect the underlying biological factors and pathways that regulate lamellipodia and filopodia. This information is critical to our understanding in the mechanisms underlying normal physiological function and the consequences of dysregulation under pathological conditions as cancer. A critical key in dissemination process is the ability of cells to coordinate signaling pathways with cytoskeleton dynamics. As critical coordinators of the cytoskeleton machinery, RhoGTPases and their regulators GEFs and GAPs are key players for cell movement. Many tumors show increased expression and/or activation of RhoGTPases and their regulators. Ongoing projects in the lab are the analysis of the role of RhoGTPases, GEFs and GAPs, and their new binding partners identified in the lab in regulating lamellipodia and filopodia and subsequently, cell migration and invasion to design new strategies to control the aberrant activation of RhoGTPases in cancer.

Experimental approaches used in Dr. DerMardirossian’s lab includes techniques of biochemistry, state-of-the-art confocal microscopy, high throughput screening, computational methods to drug design, and mouse xenograft models.

Select Publications

Blanchard Z, Paul BT, Craft B, ElShamy WM. BRCA1-IRIS inactivation overcomes paclitaxel resistance in triple negative breast cancers. Breast Cancer Res. 2015 Jan 13;17:5.


Sinha A, Paul BT, Sullivan LM, Sims H, El Bastawisy A, Yousef HF, Zekri AN, Bahnassy AA, ElShamy WM. BRCA1-IRIS overexpression promotes and maintains the tumor initiating phenotype: implications for triple negative breast cancer early lesions. Oncotarget. 2017 Feb 7;8(6):10114-10135.


Gardner L, Malik R, Shimizu Y, Mullins N, ElShamy WM. Geminin overexpression prevents the completion of topoisomerase IIα chromosome decatenation, leading to aneuploidy in human mammary epithelial cells. Breast Cancer Res. 2011 May 19;13(3):R53.


Blanchard Z, Mullins N, Ellipeddi P, Lage JM, McKinney S, El-Etriby R, Zhang X, Isokpehi R, Hernandez B, Elshamy WM. Geminin overexpression promotes imatinib sensitive breast cancer: a novel treatment approach for aggressive breast cancers, including a subset of triple negative. PLoS One. 2014 Apr 30;9(4):e95663.


Ananthula S, Sinha A, El Gassim M, Batth S, Marshall GD Jr, Gardner LH, Shimizu Y, ElShamy WM. Geminin overexpression-dependent recruitment and crosstalk with mesenchymal stem cells enhance aggressiveness in triple negative breast cancers. Oncotarget. 2016 Apr 12;7(15):20869-89.


Ryan D, Sinha A, Bogan D, Davies J, Koziol J, ElShamy W. A niche that triggers aggressiveness within BRCA1-IRIS overexpressing triple negative tumors is supported by reciprocal interactions with the microenvironment. Oncotarget. 2017 8:103182-103206.


Dagliyan O, Karginov AV, Yagishita S, Gale ME, Wang H, DerMardirossian C, Wells CM, Dokholyan NV, Kasai H, Hahn KM. Engineering Pak1 Allosteric Switches. ACS Synth Biol. 2017 Jul 21;6(7):1257-1262. doi: 10.1021/acssynbio.6b00359. Epub 2017 Apr 6. PMID: 28365983; PMCID: PMC5562282.


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Our research programs are funded primarily by grants from the National Institutes of Health (NIH). Private donations help to accelerate the progress of research through the purchase of laboratory supplies and equipment or the recruitment of additional laboratory personnel. Thank you!

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