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31 results on '"Gomez, Eduardo Cortes"'

3. CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone mRNA processing

Author

Alahmari, Abdulrahman A., primary, Chaubey, Aditi H., additional, Jonnakuti, Venkata S., additional, Tisdale, Arwen A., additional, Schwarz, Carla D., additional, Cornwell, Abigail C., additional, Maraszek, Kathryn E., additional, Paterson, Emily J., additional, Kim, Minsuh, additional, Venkat, Swati, additional, Gomez, Eduardo Cortes, additional, Wang, Jianmin, additional, Gurova, Katerina V., additional, Yalamanchili, Hari Krishna, additional, and Feigin, Michael E., additional

Published
2024
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8. PTEN Loss Expands the Histopathologic Diversity and Lineage Plasticity of Lung Cancers Initiated by Rb1/Trp53 Deletion

Author

Zhang, Letian, primary, Liu, Congrong, additional, Zhang, Bo, additional, Zheng, Jie, additional, Singh, Prashant K., additional, Bshara, Wiam, additional, Wang, Jianmin, additional, Gomez, Eduardo Cortes, additional, Zhang, Xiaojing, additional, Wang, Yanqing, additional, Zhu, Xiang, additional, and Goodrich, David W., additional

Published
2022
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9. Abstract B042: Inhibition of CPSF3 attenuates pancreatic cancer cell proliferation through disruption of histone processing

Author

Alahmari, Abdulrahman A., primary, Chaubey, Aditi, additional, Tisdale, Arwen, additional, Schwarz, Carla, additional, Cornwell, Abigail, additional, Maraszek, Kathryn, additional, Paterson, Emily, additional, Kim, Minsuh, additional, Venkat, Swati, additional, Gomez, Eduardo Cortes, additional, Wang, Jianmin, additional, Gurova, Katerina, additional, and Feigin, Michael E., additional

Published
2022
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10. Abstract 786: STAG2 acts as a transcriptional repressor and promotes invasion of muscle invasive bladder cancer cells

Author

Athans, Sarah R., primary, Krishnan, Nithya, additional, Ramakrishnan, Swathi, additional, Gomez, Eduardo Cortes, additional, Lage-Vickers, Sofia, additional, Rak, Monika, additional, Kazmierczak, Zara, additional, Stablewski, Aimee, additional, Attwood, Kristopher, additional, Wang, Jianmin, additional, and Woloszynska, Anna, additional

Published
2022
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12. CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone processing

Author

Alahmari, Abdulrahman. A., primary, Chaubey, Aditi H., additional, Tisdale, Arwen A., additional, Schwarz, Carla D., additional, Cornwell, Abigail C., additional, Maraszek, Kathryn E., additional, Paterson, Emily J., additional, Kim, Minsuh, additional, Venkat, Swati, additional, Gomez, Eduardo Cortes, additional, Wang, Jianmin, additional, Gurova, Katerina V., additional, and Feigin, Michael E., additional

Published
2022
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14. Fungal mycobiome drives IL-33 secretion and type 2 immunity in pancreatic cancer

Author

Alam, Aftab, primary, Levanduski, Eric, additional, Denz, Parker, additional, Villavicencio, Helena Solleiro, additional, Bhatta, Maulasri, additional, Alhorebi, Lamees, additional, Zhang, Yali, additional, Gomez, Eduardo Cortes, additional, Morreale, Brian, additional, Senchanthisai, Sharon, additional, Li, Jun, additional, Turowski, Steven G., additional, Sexton, Sandra, additional, Sait, Sheila Jani, additional, Singh, Prashant K., additional, Wang, Jianmin, additional, Maitra, Anirban, additional, Kalinski, Pawel, additional, DePinho, Ronald A., additional, Wang, Huamin, additional, Liao, Wenting, additional, Abrams, Scott I., additional, Segal, Brahm H., additional, and Dey, Prasenjit, additional

Published
2022
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15. Hypoxic Tumor Microenvironment Induces Metabolic Enzyme PFKFB4 Acquiring Invasive Cancer Phenotype to Drive Metastasis

Author

Dai, Tao, primary, Rosario, Spencer R., additional, Katsuta, Eriko, additional, Paterson, Emily J., additional, Novickis, Aaron T., additional, Dessai, Abhisha Sawant, additional, Gomez, Eduardo Cortes, additional, Zhu, Bokai, additional, Liu, Song, additional, Wang, Hai, additional, Abrams, Scott I., additional, Sheshadri, Mukund, additional, Bshara, Wiam, additional, and Dasgupta, Subhamoy, additional

Published
2022
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16. PTENLoss Expands the Histopathologic Diversity and Lineage Plasticity of Lung Cancers Initiated by Rb1/Trp53Deletion

Author

Zhang, Letian, Liu, Congrong, Zhang, Bo, Zheng, Jie, Singh, Prashant K., Bshara, Wiam, Wang, Jianmin, Gomez, Eduardo Cortes, Zhang, Xiaojing, Wang, Yanqing, Zhu, Xiang, and Goodrich, David W.

Abstract

High-grade neuroendocrine tumors of the lung such as SCLC are recalcitrant cancers for which more effective systemic therapies are needed. Despite their histopathologic and molecular heterogeneity, they are generally treated as a single disease entity with similar chemotherapy regimens. Whereas marked clinical responses can be observed, they are short-lived. Inter- and intratumoral heterogeneity is considered a confounding factor in these unsatisfactory clinical outcomes, yet the origin of this heterogeneity and its impact on therapeutic responses is not well understood.

Published
2023
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17. Genes Relevant to Tissue Response to Cancer Therapy Display Diurnal Variation in mRNA Expression in Human Oral Mucosa

Author

Gu, Fangyi, primary, Gomez, Eduardo Cortes, additional, Chen, Jianhong, additional, Buas, Matthew F., additional, Schlecht, Nicolas F., additional, Hulme, Karen, additional, Kulkarni, Shweta Vishwas, additional, Singh, Prashant K., additional, O’Connor, Richard, additional, Ambrosone, Christine B., additional, Singh, Anurag K., additional, and Wang, Jianmin, additional

Published
2021
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19. Bacterial colonization and TH17 immunity are shaped by intestinal sialylation in neonatal mice.

Author

Irons, Eric E, Gomez, Eduardo Cortes, Andersen, Valerie L, and Lau, Joseph T Y

Subjects
*BACTERIAL colonies, *INTESTINES, *COLONIZATION (Ecology), *IMMUNITY, *MICE, *GUT microbiome
Abstract

Interactions between the neonate host and its gut microbiome are central to the development of a healthy immune system. However, the mechanisms by which animals alter early colonization of microbiota for their benefit remain unclear. Here, we investigated the role of early-life expression of the α2,6-sialyltransferase ST6GAL1 in microbiome phylogeny and mucosal immunity. Fecal, upper respiratory, and oral microbiomes of pups expressing or lacking St6gal1 were analyzed by 16S rRNA sequencing. At weaning, the fecal microbiome of St6gal1 -KO mice had reduced Clostridiodes, Coprobacillus, and Adlercreutzia , but increased Helicobacter and Bilophila. Pooled fecal microbiomes from syngeneic donors were transferred to antibiotic-treated wild-type mice, before analysis of recipient mucosal immune responses by flow cytometry, RT-qPCR, microscopy, and ELISA. Transfer of St6gal1- KO microbiome induced a mucosal Th17 response, with expression of T-bet and IL-17, and IL-22-dependent gut lengthening. Early life intestinal sialylation was characterized by RT-qPCR, immunoblot, microscopy, and sialyltransferase enzyme assays in genetic mouse models at rest or with glucocorticoid receptor modulators. St6gal1 expression was greatest in the duodenum, where it was mediated by the P1 promoter and efficiently inhibited by dexamethasone. Our data show that the inability to produce α2,6-sialyl ligands contributes to microbiome-dependent Th17 inflammation, highlighting a pathway by which the intestinal glycosylation regulates mucosal immunity. [ABSTRACT FROM AUTHOR]

Published
2022
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20. Efficacy and Safety of Pembrolizumab in Combination With Bevacizumab and Oral Metronomic Cyclophosphamide in the Treatment of Recurrent Ovarian Cancer

Author

Zsiros, Emese, primary, Lynam, Sarah, additional, Attwood, Kristopher M., additional, Wang, Chong, additional, Chilakapati, Shanmuga, additional, Gomez, Eduardo Cortes, additional, Liu, Song, additional, Akers, Stacey, additional, Lele, Shashikant, additional, Frederick, Peter J., additional, and Odunsi, Kunle, additional

Published
2021
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25. Genes Relevant to Tissue Response to Cancer Therapy Display Diurnal Variation in mRNA Expression in Human Oral Mucosa.

Author

FANGYI GU, GOMEZ, EDUARDO CORTES, JIANHONG CHEN, BUAS, MATTHEW F., SCHLECHT, NICOLAS F., HULME, KAREN, KULKARNI, SHWETA VISHWAS, SINGH, PRASHANT K., O'CONNOR, RICHARD, AMBROSONE, CHRISTINE B., SINGH, ANURAG K., and JIANMIN WANG

Subjects
*TUMOR treatment, *BIOMARKERS, *CIRCADIAN rhythms, *GENE expression, *CELL cycle, *MELATONIN, *MESSENGER RNA, *QUESTIONNAIRES, *ORAL mucosa
Abstract

Background: To address a critical gap for application of cancer chronotherapy of when would be the best time(s) for treating an individual cancer patient, we conducted a pilot study to characterize diurnal variations of gene expression in oral mucosal tissue, which is vulnerable to damage from cancer therapies. Methods: We conducted RNA-seq assay on individual oral mucosal samples collected from 11 healthy volunteers every 4 hours (6 time points). Using a cosine-based method, we estimated the individual and average values of peak-time and amplitude for each gene. Correlations between gene expression peak-times and age was examined, adjusting for individual's sleep timing. Results: Among candidate gene pathways that are relevant to treatment response, 7 of 16 genes (PER3, CIART, TEF, PER1, PER2, CRY2, ARNTL) involved in circadian regulation and 1 of 118 genes (WEE1) involved in cell cycle regulation achieved p-value ≤ 0.1 and relative amplitude>0.1. The average peak times were approximately 10:15 for PER3, CIART and TEF, 10:45 for PER1, 13:00 for WEE1, PER2 and CRY2, and 19:30 for ARNTL. Ranges in peak times across individuals differed by gene (e.g., 8 hours for PER1; 16.7 hours for WEE1). Older people had later peak times for PER1 (r = 0.77, p = 0.03) and PER3 (r = 0.69, p-value = 0.06). Conclusion: In oral mucosa, expression of some genes relevant to treatment response displayed diurnal variation. These genes may be candidates for development of biomarkers for optimizing individual timing of cancer therapy using non-invasively collected oral mucosa. [ABSTRACT FROM AUTHOR]

Published
2021
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26. Intratumoral and Intertumoral Genomic Heterogeneity of Multifocal Localized Prostate Cancer Impacts Molecular Classifications and Genomic Prognosticators

Author

Wei, Lei, primary, Wang, Jianmin, additional, Lampert, Erika, additional, Schlanger, Simon, additional, DePriest, Adam D., additional, Hu, Qiang, additional, Gomez, Eduardo Cortes, additional, Murakam, Mitsuko, additional, Glenn, Sean T., additional, Conroy, Jeffrey, additional, Morrison, Carl, additional, Azabdaftari, Gissou, additional, Mohler, James L., additional, Liu, Song, additional, and Heemers, Hannelore V., additional

Published
2017
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27. Genomic profiling is predictive of response to cisplatin treatment but not to PI3K inhibition in bladder cancer patient-derived xenografts

Author

Wei, Lei, primary, Chintala, Sreenivasulu, additional, Ciamporcero, Eric, additional, Ramakrishnan, Swathi, additional, Elbanna, May, additional, Wang, Jianmin, additional, Hu, Qiang, additional, Glenn, Sean T., additional, Murakami, Mitsuko, additional, Liu, Lu, additional, Gomez, Eduardo Cortes, additional, Sun, Yuchen, additional, Conroy, Jacob, additional, Miles, Kiersten Marie, additional, Malathi, Kullappan, additional, Ramaiah, Sudha, additional, Anbarasu, Anand, additional, Woloszynska-Read, Anna, additional, Johnson, Candace S., additional, Conroy, Jeffrey, additional, Liu, Song, additional, Morrison, Carl D., additional, and Pili, Roberto, additional

Published
2016
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28. Inhibition of LSD1 in MDS progenitors restores differentiation of CD141Hiconventional dendritic cells

Author

Srivastava, Pragya, Tzetzo, Stephanie L., Gomez, Eduardo Cortes, Eng, Kevin H., Jani Sait, Sheila N., Kuechle, Joseph B., Singh, Prashant K., De Jong, Kitty, Wiatrowski, Kyle R., Peresie, Jennifer, Dimitroff, Ava, Lynch, Miranda L., Wang, Jianmin, Abrams, Scott I., Griffiths, Elizabeth A., and Nemeth, Michael J.

Abstract

The use of immunotherapy to treat patients with myelodysplastic syndromes (MDS) shows promise but is limited by our incomplete understanding of the immunologic milieu. In solid tumors, CD141Hiconventional dendritic cells (CD141HicDCs) are necessary for antitumor immunosurveillance and the response to immunotherapy. Here, we found that CD141HicDCs are reduced in MDS bone marrow and based on the premise established in solid tumors, we hypothesized that reduced numbers of CD141HicDCs are associated with inferior overall survival in MDS patients. We found that MDS patients with reduced numbers of CD141HicDCs, but not other DC populations, showed reduced overall survival. To examine the basis for reduction in CD141HicDCs, we found fewer numbers of progenitors committed to DC differentiation in the MDS bone marrow and these progenitors expressed lower levels of interferon regulatory factor-8 (IRF8), a master regulator of CD141HicDC differentiation. To rescue impaired CD141HicDC differentiation, we used pharmacologic inhibition of lysine-specific demethylase 1A (LSD1) to promote CD141HicDC differentiation by MDS progenitors. These data reveal a previously unrecognized element of the MDS immunologic milieu. Epigenetic regulation of CD141HicDC differentiation offers an intriguing opportunity for intervention and a potential adjunct to immunotherapy for patients with MDS.

Published
2020
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31. The Granulocyte Progenitor Stage Is a Key Target of IRF8-Mediated Regulation of Myeloid-Derived Suppressor Cell Production.

Author

Netherby, Colleen S., Messmer, Michelle N., Burkard-Mande, Lauren, Colligan, Sean, Miller, Austin, Gomez, Eduardo Cortes, Jianmin Wang, Nemeth, Michael J., and Abrams, Scott I.

Subjects
*TUMOR classification, *SUPPRESSOR cells, *ANTINEOPLASTIC agents, *TRANSCRIPTION factors, *IMMUNOTHERAPY
Abstract

Alterations in myelopoiesis are common across various tumor types, resulting in immature populations termed myeloid-derived suppressor cells (MDSCs). MDSC burden correlates with poorer clinical outcomes, credited to their ability to suppress antitumor immunity. MDSCs consist of two major subsets, monocytic and polymorphonuclear (PMN). Intriguingly, the latter subset predominates in many patients and tumor models, although the mechanisms favoring PMN-MDSC responses remain poorly understood. Ordinarily, lineage-restricted transcription factors regulate myelopoiesis that collectively dictate cell fate. One integral player is IFN regulatory factor (IRF)-8, which promotes monocyte/dendritic cell differentiation while limiting granulocyte development. We recently showed that IRF8 inversely controls MDSC burden in tumor models, particularly the PMN-MDSC subset. However, where IRF8 acts in the pathway of myeloid differentiation to influence PMN-MDSC production has remained unknown. In this study, we showed that: 1) tumor growth was associated with a selective expansion of newly defined IRF8lo granulocyte progenitors (GPs); 2) tumor-derived GPs had an increased ability to form PMN-MDSCs; 3) tumor-derived GPs shared gene expression patterns with IRF8-/- GPs, suggesting that IRF8 loss underlies GP expansion; and 4) enforced IRF8 overexpression in vivo selectively constrained tumor-induced GP expansion. These findings support the hypothesis that PMN-MDSCs result from selective expansion of IRF8lo GPs, and that strategies targeting IRF8 expression may limit their load to improve immunotherapy efficacy. [ABSTRACT FROM AUTHOR]

Published
2017
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