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Your search keyword '"Majumdar, Sumana"' showing total 9 results
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9 results on '"Majumdar, Sumana"'

1. Evolution of core archetypal phenotypes in progressive high grade serous ovarian cancer

Author

Nath, Aritro, Cosgrove, Patrick A., Mirsafian, Hoda, Christie, Elizabeth L., Pflieger, Lance, Copeland, Benjamin, Majumdar, Sumana, Cristea, Mihaela C., Han, Ernest S., Lee, Stephen J., Wang, Edward W., Fereday, Sian, Traficante, Nadia, Salgia, Ravi, Werner, Theresa, Cohen, Adam L., Moos, Philip, Chang, Jeffrey T., Bowtell, David D. L., and Bild, Andrea H.

Published
2021
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2. A one-two punch therapy strategy to target chemoresistance in ER+ breast cancer

Author

Chi, Feng, Liu, Jiayi, Brady, Samuel W, Cosgrove, Patrick A, Nath, Aritro, McQuerry, Jasmine A, Majumdar, Sumana, Moos, Philip J, Chang, Jeffrey T, Kahn, Michael, and Bild, Andrea H

Abstract

Cancer cell phenotypes evolve during a tumor treatment. In some cases, tumor cells acquire cancer stem cell-like (CSL) traits such as resistance to chemotherapy and diminished differentiation; therefore, targeting these cells may be therapeutically beneficial. In this study, we show that in progressive estrogen receptor positive (ER+) metastatic breast cancer patients, resistant tumor subclones that emerge following chemotherapy have increased CSL abundance. Further, in vitro organoid growth of ER+ patient cancer cells also shows that chemotherapy treatment leads to increased abundance of ALDH+/CD44+ CSL cells. Chemotherapy induced CSL abundance is blocked by treatment with an HDAC inhibitor, belinostat. Further, belinostat treatment diminished both mammosphere formation and size following chemotherapy, also indicating a decrease in progenitor CSL traits. Single-cell RNA sequencing analysis with patient samples showed that HDAC targets and MYC signaling were promoted by chemotherapy and inhibited upon belinostat treatment. These findings indicate that HDAC inhibition can block chemotherapy-induced drug resistant phenotypes with one-two punch strategy in refractory breast cancer cells.

Published
2020
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4. Increased expression of deleted in malignant brain tumors (DMBT1) gene in precancerous gastric lesions: Findings from human and animal studies

Author

Garay, Jone, primary, Piazuelo, M. Blanca, additional, Lopez-Carrillo, Lizbeth, additional, Leal, Yelda A., additional, Majumdar, Sumana, additional, Li, Li, additional, Cruz-Rodriguez, Nataly, additional, Serrano-Gomez, Silvia J., additional, Busso, Carlos S., additional, Schneider, Barbara G., additional, Delgado, Alberto G., additional, Bravo, Luis E., additional, Crist, Angela M., additional, Meadows, Stryder M., additional, Camargo, M. Constanza, additional, Wilson, Keith T., additional, Correa, Pelayo, additional, and Zabaleta, Jovanny, additional

Published
2017
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5. IL1B-CGTC haplotype is associated with colorectal cancer in admixed individuals with increased African ancestry

Author

Sanabria-Salas, María Carolina, primary, Hernández-Suárez, Gustavo, additional, Umaña-Pérez, Adriana, additional, Rawlik, Konrad, additional, Tenesa, Albert, additional, Serrano-López, Martha Lucía, additional, Sánchez de Gómez, Myriam, additional, Rojas, Martha Patricia, additional, Bravo, Luis Eduardo, additional, Albis, Rosario, additional, Plata, José Luis, additional, Green, Heather, additional, Borgovan, Theodor, additional, Li, Li, additional, Majumdar, Sumana, additional, Garai, Jone, additional, Lee, Edward, additional, Ashktorab, Hassan, additional, Brim, Hassan, additional, Margolin, David, additional, Fejerman, Laura, additional, and Zabaleta, Jovanny, additional

Published
2017
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9. Identification of speckle-type POZ protein somatic mutations in African American prostate cancer.

Author

Buckles, Eric, Chiping Qian, Tadros, Andrew, Majumdar, Sumana, Cvitanovic, Jennifer, Zabaleta, Jovanny, Estrada, John, Wilson, John, and Wanguo Liu

Abstract

The speckle-type POZ protein (SPOP) is a tumor suppressor in prostate cancer (PCa). SPOP somatic mutations have been reported in up to 15% of PCa of those of European descent. However, the genetic roles of SPOP in African American (AA)-PCa are currently unknown. We sequenced the SPOP gene to identify somatic mutations in 49 AA prostate tumors and identified three missense mutations (p.Y87C, p.F102S, and p.G111E) in five AA prostate tumors (10%) and one synonymous variant (p.I106I) in one tumor. Intriguingly, all of mutations and variants clustered in exon six, and all of the mutations altered conserved amino acids. Moreover, two mutations (p.F102S and p.G111E) have only been identified in AA-PCa to date. Quantitative real-time polymerase chain reaction analysis showed a lower level of SPOP expression in tumors carrying SPOP mutations than their matched normal prostate tissues. In addition, SPOP mutations and novel variants were detected in 5 of 27 aggressive PCa and one of 22 less aggressive PCa ( P < 0.05). Further studies with increased sample size are needed to validate the clinicopathological significance of these SPOP mutations in AA-PCa. [ABSTRACT FROM AUTHOR]

Published
2014
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