Genome Instability and Molecular Cancer Therapeutics Lab



This lab investigates DNA damage response and repair network signaling in carcinogenesis, drug resistance and molecular cancer therapeutics. DNA damage response and repair signaling genes are tumor suppressors that constantly protect chromosomal DNA from environmental and metabolically generated genotoxins and from oncogenic replication stress. Mutations in these genes manifest into genome instability syndromes such as Fanconi anemia (FA) and Breast and Ovarian Cancer early onset (BRCA). In contrast, tumor cells also acquire resistance to chemo and radiation therapy by altered regulation of cell cycle checkpoints and DNA repair networks. These mechanisms and their regulation are highly complex, and often they are differentially regulated in tumor cells, particularly in the context of oncogenic or growth factor signals they adopt.

The basic science projects in this lab focus on the regulation of Fanconi anemia (FA) and Breast cancer (BRCA) mutated (FA-BRCA) tumor suppressor networks by post-translational modifications.

The translational research projects focus on identifying the role of tumor signaling (ex. Hedgehog, mTOR, oncogenic and metabolic stress, epigenetics and hypoxia) on cell cycle checkpoints and DNA repair networks in cancer cells and developing rationally designed therapeutic combinations to effectively kill tumor cells by chemo and radiation therapy. 


Palle-Lab picture resized.jpgFaculty and Staff

Kaushlendra Tripathi, Ph.D.
Research Associate

David W. Clark, Ph.D.
Postdoctoral Fellow

Chinnadurai Mani, Ph.D.
Postdoctoral Fellow

Ranganatha Somasagara, Ph.D.
Postdoctoral Fellow

Sebastian M. Spencer
Graduate Student


Palle model 1.jpgProjects

  • Rad18/Ra6- mediated ubiquitin signaling in regulation of FA-BRCA tumor suppressor pathway and its influence on chemo and radiation resistance
  • Hedgehog/Gli1 signaling mediated regulation of DDR and repair genes during carcinogenesis and chemoresistance: Development of rationally designed therapeutic combinations
  • Rad6-mediated ubiquitin signaling in ovarian cancer stem-cell signaling and chemoresistance: Development of novel small molecule inhibitors of Rad6 for ovarian cancer therapy
  • Novel functions and regulation of FANCJ/BRIP1 in regulation of DNA damage responses and chromatin remodeling
  • Novel nuclear functions of Trans-Golgi network protein PACS-1 in regulation of cell cycle and tumor signaling
  • Oxidative stress and altered estrogen metabolism mediated carcinogenesis in hormone responsive tissues



Core Labs

Palle Hedgehog signaling checkpoint resized.jpgCellular and Biomolecular Imaging Facility

Flow Cytometry and Imaging Core Laboratories

Mass Spectrometry and Proteomics Core Laboratory

Tumor Biobank



NIH/NIGMS  R01 R01 GM98956  (Palle)

Goal: To elucidate Rad18 mediated ubiquitin signaling mechanisms in regulation of DNA repair networks in response to replication stress and replication coupled DNA double strand breaks induced by chemotherapeutic agents such as Topo inhibitors and crosslinking agents. 


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