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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
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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