Our laboratory is interested in understanding the genetic and epigenetic basis in male germ cell tumor (GCT) and cervical cancer. 


GCT, a common malignancy in young males, is a complex tumor system where germ cells undergo transformation and exhibit embryonal and extra-embryonal like differentiation patterns. We identified a critical region of heterozygous deletion and epigenetic silencing of genes in a large region at 12q22 implicating the role of both genetic and epigenetic alterations in suppressing a chromosomal domain. We are currently further exploring the genetic and epigenetic mechanisms of tumor suppression related to 12q22 deletions in GCT. 


Carcinoma of uterine cervix is a common malignancy among women worldwide. Most cervical cancers are preceded by distinct preneoplastic epithelial changes, which progress to invasive cancer, thus providing opportunities to study genetic alterations at an early stage of transformation. In a genome-wide search for genetic and epigenetic alterations, we identified several sites of deletions, gene amplifications, and specific gene pathways in invasive cancer. We are currently characterizing the target amplified and deleted genes, and identifying their origin in the development of precancerous lesions to develop a genetic prognostic model for progression.

 Selected Publications

1. Narayan G, Arias-Pulido H, Nandula SV, Basso K, Sugirtharaj DD, Vargas H, Mansukhani M, Villella J, Meyer L, Schneider A, Gissmann L, Dürst M,  Pothuri B, Murty VV: Promoter Hypermethylation of FANCF: Disruption of Fanconi Anemia-BRCA Pathway in Cervical Cancer. Cancer Res 64: 2994-2997, 2004.
   
2. Narayan G, Goparaju C, Arias-Pulido H, Kaufmann AM, Schneider A, Durst M, Mansukhani M, Pothuri B, Murty VV. Promoter hypermethylation-mediated inactivation of multiple Slit-Robo pathway genes in cervical cancer progression. Molecular Cancer  5:16, 2006.
   
3. Narayan G, Goparaju C, Arias-Pulido H, Kaufmann AM, Schneider A, Durst M, Mansukhani M, Pothuri B, Murty VV. Promoter hypermethylation-mediated inactivation of multiple Slit-Robo pathway genes in cervical cancer progression. Molecular Cancer 2006, 5:16.
   
4. Subramaniyam S, Nandula SV, Nichols G, Weiner M, Satwani P, Bachir Alobeid B, Bhagat G, Murty VV. Do RARA/PML Fusion Gene Deletions Confer Resistance to ATRA Based Therapy in Patients with Acute Promyelocytic Leukemia? Leukemia. 20:2193-2195, 2006.
   
5. Narayan G, Bourdon V, Chaganti S, Arias-Pulido H, Nandula SV, Rao PH, Gissmann L, Durst M, Schneider A, Pothuri B, Mansukhani M, Basso K, Chaganti RS, Murty VV. Gene dosage alterations revealed by cDNA microarray analysis in cervical cancer: Identification of candidate amplified and overexpressed genes. Genes Chromosomes Cancer 46: 373-384, 2007.
   
6. Zudaire E, Cuesta N, Murty V, Woodson K, Adams L, Gonzalez N, Martínez A, Narayan G, Kirsch I, Franklin W, Hirsch F, Birrer M, Cuttitta F. The aryl hydrocarbon receptor repressor is a putative tumor suppressor gene in multiple human cancers. J Clin Invest. 118: 640-650, 2008.
   
7. Scotto L, Narayan G, Nandula SV, Arias-Pulido H, Subramaniyam S, Schneider A, Kaufmann AM, Wright JD, Pothuri B, Mansukhani M, Murty VV. Identification of Copy Number Gain and Overexpressed Genes on Chromosome Arm 20q by an Integrative Genomic Approach in Cervical Cancer: Potential Role in Progression. Genes Chromosomes and Cancer  47: 755-765, 2008.
   
8. Scotto L, Narayan G, Nandula SV, Subramaniyam S, Kaufmann AM, Wright JD, Pothuri B, Mansukhani M, Schneider A, Arias-Pulido A, Murty VV. Integrative genomics analysis of chromosome 5p gain in cervical cancer reveals target over-expressed genes, including Drosha. Molecular Cancer 7: 58, 2008.