Ritu Pandey

Interests

Research

Cancer Bioinformatics, Multi-Omics data analysis and interpretation, Integrative Omics, Translational BioinformaticsMolecular profiling of different tumor types to identify unique biomarkers and genetic characteristics of certain type. Our main interest is to analyze the information generated from to identify drug targets and therapies that work better.

Courses

Scholarly Contributions

Journals/Publications

• Chakravarti, J., Pandey, R., Churko, J., Eschbacher, J., Mallick, S., Chen, Y., Hermes, B., Mallick, P., Stansfield, B., Pond, K. W., Thorne, C., Yuen, K., Little, A. S., & Zavros, Y. (2022). Development Of Human Pituitary Adenoma-Derived Organoids To Facilitate Effective Targeted Treatments Of Cushing's Disease.. Cells, 11(12).
• Wusterbarth, E., Chen, Y., Jecius, H., Krall, E., Runyan, R. B., Pandey, R., & Nfonsam, V. (2022). Cartilage Oligomeric Matrix Protein, COMP may be a Better Prognostic Marker Than CEACAM5 and Correlates With Colon Cancer Molecular Subtypes, Tumor Aggressiveness and Overall Survival. The Journal of surgical research, 270, 169-177.
• Pandey, R., Zhou, M., Chen, Y., Darmoul, D., Kisiel, C. C., Nfonsam, V. N., & Ignatenko, N. A. (2021). Molecular Pathways Associated with Kallikrein 6 Overexpression in Colorectal Cancer. Genes, 12(5).
• Rico, K., Duan, S., Pandey, R. L., Chen, Y., Chakrabarti, J. T., Starr, J., Zavros, Y., Else, T., Katona, B. W., Metz, D. C., & Merchant, J. L. (2021). Genome analysis identifies differences in the transcriptional targets of duodenal versus pancreatic neuroendocrine tumours. BMJ open gastroenterology, 8(1).
• Singh, N., Ramnarine, V. R., Song, J. H., Pandey, R., Padi, S. K., Nouri, M., Olive, V., Kobelev, M., Okumura, K., McCarthy, D., Hanna, M. M., Mukherjee, P., Sun, B., Lee, B. R., Parker, J. B., Chakravarti, D., Warfel, N. A., Zhou, M., Bearss, J. J., , Gibb, E. A., et al. (2021). The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer. Nature communications, 12(1), 7349.
• Larson, K. R., Kannaiyan, R., Pandey, R., Babiker, H., & Dark, M. (2020). A Comparative Analysis of Tumor and Plasma Circulating Tumor DNA in 145 Advanced Cancer Patients annotated by 3 Core Cellular Processes. Cancers.
• Pandey, R., Zhou, M., Islam, S., Chen, B., Barker, N. K., Langlais, P., Srivastava, A., Luo, M., Cooke, L. S., Weterings, E., & Mahadevan, D. (2019). Carcinoembryonic antigen cell adhesion molecule 6 (CEACAM6) in Pancreatic Ductal Adenocarcinoma (PDA): An integrative analysis of a novel therapeutic target. Scientific reports, 9(1), 18347.
• Padi, S. K., Luevano, L., An, N., Pandey, R., Singh, N., Song, J., Aster, J., Yu, X., Mehrotra, S., & Kraft, A. S. (2017). Targeting the PIM Protein Kinases for the Treatment of a T-cell Acute Lymphoblastic Leukemia Subset. Oncotarget.
• Sells, E., Pandey, R., Chen, H., Skovan, B. A., Cui, H., & Ignatenko, N. A. (2017). Specific microRNA-mRNA regulatory network of colon cancer invasion regulated by tissue kallikrein-related peptidase 6. Neoplasia.
• Greenwood, E., Maisel, S., Ebertz, D., Russ, A., Pandey, R., & Schroeder, J. (2016). Llgl1 prevents metaplastic survival driven by epidermal growth factor dependent migration. Oncotarget, 7(38), 60776-60792.
  More info

  We have previously demonstrated that Llgl1 loss results in a gain of mesenchymal phenotypes and a loss of apicobasal and planar polarity. We now demonstrate that these changes represent a fundamental shift in cellular phenotype. Llgl1 regulates the expression of multiple cell identity markers, including CD44, CD49f, and CD24, and the nuclear translocation of TAZ and Slug. Cells lacking Llgl1 form mammospheres, where survival and transplantability is dependent upon the Epidermal Growth Factor Receptor (EGFR). Additionally, Llgl1 loss allows cells to grow in soft-agar and maintain prolonged survival as orthotopic transplants in NOD-SCIDmice. Lineage tracing and wound healing experiments demonstrate that mammosphere survival is due to enhanced EGF-dependent migration. The loss of Llgl1 drives EGFR mislocalization and an EGFR mislocalization point mutation (P667A) drives these same phenotypes, including activation of AKT and TAZ nuclear translocation. Together, these data indicate that the loss of Llgl1 results in EGFR mislocalization, promoting pre-neoplastic changes.
• Baker, A. F., Malm, S. W., Pandey, R., Laughren, C., Cui, H., Roe, D., & Chambers, S. K. (2015). Evaluation of a hypoxia regulated gene panel in ovarian cancer. Cancer microenvironment : official journal of the International Cancer Microenvironment Society, 8(1), 45-56.
  More info

  A panel of nine hypoxia regulated genes, selected from a previously published fifty gene panel, was investigated for its ability to predict hypoxic ovarian cancer phenotypes. All nine genes including vascular endothelial growth factor A, glucose transporter 1, phosphoglycerate mutase 1, lactate dehydrogenase A, prolyl 4-hydroxylase, alpha-polypeptide 1, adrenomedullin, N-myc downstream regulated 1, aldolase A, and carbonic anhydrase 9 were upregulated in the HEY and OVCAR-3 human ovarian cell lines cultured in vitro under hypoxic compared to normoxic conditions as measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The gene panel was also elevated in HEY xenograft tumor tissue compared to HEY cells cultured in normoxia. The HEY xenograft tissue demonstrated heterogeneous positive immunohistochemical staining for the exogenous hypoxia biomarker pimonidazole, and the hypoxia regulated protein carbonic anhydrase IX. A quantitative nuclease protection assay (qNPA) was developed which included the nine hypoxia regulated genes. The qNPA assay provided similar results to those obtained using qRT-PCR for cultured cell lines. The qNPA assay was also evaluated using paraffin embedded fixed tissues including a set of five patient matched primary and metastatic serous cancers and four normal ovaries. In this small sample set the average gene expression was higher in primary and metastatic cancer tissue compared to normal ovaries for the majority of genes investigated. This study supports further evaluation by qNPA of this gene panel as an alternative or complimentary method to existing protein biomarkers to identify ovarian cancers with a hypoxic phenotype.