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Anjali A. Shukla, Ph.D.

Laboratory of Cancer Biology and Genetics
Staff Scientist
Center for Cancer Research
National Cancer Institute
Building 37, Room 5046
Bethesda, MD 20892-4254


Anjali Shukla earned a B.Sc. (Honors) in chemistry and an M.Sc. in biochemistry from the Banaras Hindu University, Varanasi, India. Dr. Shukla graduated from the Jawaharlal Nehru University, New Delhi, India. Her graduate work focused on the role of calcium and reactive oxygen species in radiation therapy of cancer. She then moved to the Laboratory of Cancer Genetics and Biology, NCI with Dr. Stuart Yuspa as a visiting postdoctoral fellow and later as a research fellow. In 2013, Dr. Shukla joined Dr. Kent Hunter's laboratory as a staff scientist.

Dr. Shukla has been recognized both locally and nationally for her work. She is the recipient of several awards including the NIH FARE Award, Aspen Cancer Conference Fellowship, Society of Investigative Dermatology Travel Award, Anita Roberts Young Scientist Scholarship and the NCI Director's Innovation Award. Her work was recognized as one of the top scientific advances in the NCI Center for Cancer Research in 2009.


Dr. Shukla's postdoctoral research focused on elucidating signaling pathways involved in skin carcinogenesis. The TGF-β signaling pathway has been one of her major interests. Dr. Shukla illuminated a novel nuclear function for the p53-regulated protein CLIC4, which via protein-protein interactions prevents dephosphorylation of phospho-Smads in the nucleus, thus enhancing and prolonging TGF-β signaling. As a follow-up to this discovery, Dr. Shukla showed that the absence of nuclear CLIC4, detected in multiple human and murine cancers and tumor cells, is associated with resistance to TGF-β growth inhibition. Using a skin tumor model, she showed that reconstitution of nuclear CLIC4 in tumor cells restores TGF-β responsiveness and inhibits tumor growth in vivo. Using gene ablation and expression array strategies, Dr. Shukla has shown that high CLIC4 expression in cancer stroma is TGF-β mediated and responsible for conversion of fibroblasts to myofibroblasts and that it is absolutely required for the expression of factors that are fundamental to the tumor-enhancing effects of cancer stroma and this is through a mechanism involving p38 MAPK activation.

Her current research focuses on delineating changes in the regulatory genome during metastatic progression in breast cancer by employing DNase hypersensitivity (DHS) analysis followed by sequencing in mammary tumor cell line models that recapitulate breast cancer progression. She also uses DNase-seq on primary mouse mammary tumors to uncover polymorphisms that might confer differential metastasis susceptibility to different mouse genotypes. In another project, she investigates the role of the bromodomain family of proteins BRD2, BRD3 and BRD4 in breast cancer metastasis.

This page was last updated on 5/29/2014.