adamDr. Sowalsky is currently the Head of the Prostate Cancer Genetics Section at the NIH National Cancer Institute. His new focus of research is in detecting circulation tumor DNA or cell free DNA from a primary tumor and examining a correlation with prostate cancer progression.

Dr. Sowalsky's long-term research interests are to use a combination of laboratory research and emerging technologies to understand the molecular basis for progression of disease with respect to the genetic alterations that occur in cancers. Of particular interest to him is the contribution of the tumor microenvironment and its role in supporting or preventing the acquisition of malignant properties by the tumor. His research focuses on the progression of primary prostate cancer.

Men are diagnosed based with prostate cancer based on their biopsy's Gleason score, a sum of the two most common Gleason patterns (from 1 to 5) that describe tissue appearance and is used as a prognostic indicator for aggressiveness. The most common Gleason score is 6 [Gleason pattern 3 + Gleason pattern 3 (G3)], which lends itself to the most favorable prognosis. Upon diagnosis of G3 cancer, the patient may undergo a radical prostatectomy (surgical removal of the prostate) or delay surgery and enter active surveillance, where periodic biopsies monitor lower-risk, possibly indolent, cancer. In a small percentage of men who choose surveillance, repeat biopsy may show Gleason score 7, which indicates development of Gleason pattern 4 (G4), which has a much less favorable prognosis. Due to uncertainties of biopsy sampling, it is impossible to determine whether this G4 represents progression of G3 cancer biopsied previously. However, using laser-microdissected samples of adjacent G3 and G4 cancers from prostatectomies (see diagram), it has been found that some G3 cancers can indeed progress to G4, and we hypothesize that when G3 progresses to G4 it is biologically distinct from G3 that does not progress. By comprehensive molecular analysis of clonal G3 and G4 cancers he is examining mechanisms of progression. It is the hope that the results of these studies will have implications in the treatment of men recently diagnosed with G3 prostate cancer, improving early detection of higher-risk disease. Determining mechanisms of progression from G3 to G4 will also identify potential novel therapeutic targets for prevention or treatment.

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Education:

Postdoctoral Training: Harvard Medical School: 2010-2014

Ph.D.: Biochemistry, Tufts University Sackler School of Graduate Biomedical Sciences: 2004-2009

B.S.: Cell and Molecular Biology, The University of Texas at Austin: 2000-2003

Grant Support:

NIH 5T32CA811569, Training Grant in Cancer Biology: 2011-2013

DOD Prostate Cancer Research Program Postdoctoral Training Award, “Molecular Features of Gleason 3 Prostate Cancer Predictive of Progression to Gleason 4”: 2013-2015

NIH P50CA090381 Dana-Farber/Harvard Cancer Center SPORE in Prostate Cancer Career Development Award: 2014-2015

Publications (click underlined to go to publication):

  1. Gao S, Ye H, Gerrin S, Wang H, Sharma A, Chen S, Patnaik A, Sowalsky AG, Voznesensky O, Han W, Yu Z, Mostaghel EA, Nelson PS, Taplin ME, Balk SP, Cai C. ErbB2 Signaling Increases Androgen Receptor Expression in Abiraterone-Resistant Prostate Cancer. Clin Cancer Res. 2016 Mar 2. [Epub ahead of print] PMID: 26936914

  2. Sowalsky AG , Sager R, Schaefer RJ, Bratslavsky G, Pandolfi PP, Balk SP, Kotula L. Loss of Wave1 gene defines a subtype of lethal prostate cancer (2015). Oncotarget. 6(14):12383-91.

  3. Chen E, Sowalsky AG, Gao S, Cai C, Voznesensky O, Schaefer R, Loda M, True LD, Ye H, Troncoso P, Lis RT, Kantoff P, Montgomery B, Nelson PS, Bubley GJ, Balk SP, Taplin ME. Abiraterone Treatment in Castration-Resistant Prostate Cancer Selects for Progesterone Responsive Mutant Androgen Receptors (2015). Clin Cancer Res. 21(6):1273-80.

  4. Sowalsky AG , Xia Z, Wang L, Zhao H, Chen S, Bubley GJ, Balk SP, Li W. Whole Transcriptome Sequencing Reveals Extensive Unspliced mRNA in Metastatic Castration-Resistant Prostate Cancer (2014). Mol Cancer Res. 13(1):98-106.

  5. Yu Z, Chen S, Sowalsky AG, Voznesensky OS, Mostaghel EA, Nelson PS, Cai C, Balk SP. Rapid Induction of Androgen Receptor Splice Variants by Androgen Deprivation in Prostate Cancer (2014). Clin Cancer Res. 20(6):1590-1600.

  6. Cai, C., Wang, H., He, H., Chen, S., He, L., Ma, F., Mucci, L., Wang, Q., Fiore, C., Sowalsky, A., Loda, M., Liu, X., Brown, M., Balk, S., and Yuan, S.: ERG reprograms Androgen Receptor to regulate SOX9 in prostate cancer, The Journal of Clinical Investigation, 2013; 123: 1109-1122.

  7. Sowalsky, A. , Ye, H., Bubley, G., and Balk, S.: Clonal progression of prostate cancers from Gleason grade 3 to grade 4, Cancer Research, 2013; 73: 1050-1055.

  8. Alt-Holland, A., Sowalsky, A., Szwec-Levin Y., Shamis Y., Hatch, H., Feig L., and Garlick J.: Suppression of E-cadherin function drives the early stages of Ras-induced squamous cell carcinoma through upregulation of FAK and Src, The Journal of Investigative Dermatology, 2011; 131: 2306-2315.

  9. Sowalsky, A. , Alt-Holland, A., Shamis, Y., Garlick, J., Feig, L.: RalA function in dermal fibroblasts is required for the progression of squamous cell carcinoma of the skin, Cancer Research, 2011; 71: 758-67.

  10. Sowalsky, A. , Alt-Holland, A., Shamis, Y., Garlick, J., Feig, L.: RalA suppresses early stages of Ras-induced squamous cell carcinoma, Oncogene, 2010; 29: 45–55.