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1,191 results on '"Stearns, Vered"'

3. Entinostat, nivolumab and ipilimumab for women with advanced HER2-negative breast cancer: a phase Ib trial

Author

Roussos Torres, Evanthia.T., Ho, Won J., Danilova, Ludmila, Tandurella, Joseph A., Leatherman, James, Rafie, Christine, Wang, Chenguang, Brufsky, Adam, LoRusso, Patricia, Chung, Vincent, Yuan, Yuan, Downs, Melinda, O’Connor, Ashley, Shin, Sarah M., Hernandez, Alexei, Engle, Elizabeth L., Piekarz, Richard, Streicher, Howard, Talebi, Zahra, Rudek, Michelle A., Zhu, Qingfeng, Anders, Robert A., Cimino-Mathews, Ashley, Fertig, Elana J., Jaffee, Elizabeth M., Stearns, Vered, and Connolly, Roisin M.

Published
2024
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5. TBCRC 039: a phase II study of preoperative ruxolitinib with or without paclitaxel for triple-negative inflammatory breast cancer

Author

Lynce, Filipa, Stevens, Laura E., Li, Zheqi, Brock, Jane E., Gulvady, Anushree, Huang, Ying, Nakhlis, Faina, Patel, Ashka, Force, Jeremy M., Haddad, Tufia C., Ueno, Naoto, Stearns, Vered, Wolff, Antonio C., Clark, Amy S., Bellon, Jennifer R., Richardson, Edward T., Balko, Justin M., Krop, Ian E., Winer, Eric P., Lange, Paulina, Hwang, E. Shelley, King, Tari A., Tolaney, Sara M., Thompson, Alastair, Gupta, Gaorav P., Mittendorf, Elizabeth A., Regan, Meredith M., Overmoyer, Beth, and Polyak, Kornelia

Published
2024
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7. Identifying homologous recombination deficiency in breast cancer: genomic instability score distributions differ among breast cancer subtypes

Author

Lenz, Lauren, Neff, Chris, Solimeno, Cara, Cogan, Elizabeth S., Abramson, Vandana G., Boughey, Judy C., Falkson, Carla, Goetz, Matthew P., Ford, James M., Gradishar, William J., Jankowitz, Rachel C., Kaklamani, Virginia G., Marcom, P. Kelly, Richardson, Andrea L., Storniolo, Anna Maria, Tung, Nadine M., Vinayak, Shaveta, Hodgson, Darren R., Lai, Zhongwu, Dearden, Simon, Hennessy, Bryan T., Mayer, Erica L., Mills, Gordon B., Slavin, Thomas P., Gutin, Alexander, Connolly, Roisin M., Telli, Melinda L., Stearns, Vered, Lanchbury, Jerry S., and Timms, Kirsten M.

Published
2023
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8. Updated Results of TBCRC026: Phase II Trial Correlating Standardized Uptake Value With Pathological Complete Response to Pertuzumab and Trastuzumab in Breast Cancer.

Author

Connolly, Roisin, Leal, Jeffrey, Solnes, Lilja, Huang, Chiung-Yu, Carpenter, Ashley, Gaffney, Katy, Abramson, Vandana, Carey, Lisa, Liu, Minetta, Rimawi, Mothaffar, Specht, Jennifer, Storniolo, Anna, Valero, Vicente, Vaklavas, Christos, Krop, Ian, Winer, Eric, Camp, Melissa, Miller, Robert, Wolff, Antonio, Cimino-Mathews, Ashley, Park, Ben, Wahl, Richard, and Stearns, Vered

Subjects
Adult, Aged, Aged, 80 and over, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Immunological, Antineoplastic Combined Chemotherapy Protocols, Breast Neoplasms, Chemotherapy, Adjuvant, Female, Fluorodeoxyglucose F18, Humans, Middle Aged, Neoadjuvant Therapy, Positron Emission Tomography Computed Tomography, Predictive Value of Tests, Radiopharmaceuticals, Receptor, ErbB-2, Time Factors, Trastuzumab, Treatment Outcome, United States
Abstract

PURPOSE: Predictive biomarkers to identify patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer who may benefit from targeted therapy alone are required. We hypothesized that early measurements of tumor maximum standardized uptake value corrected for lean body mass (SULmax) on 18F-labeled fluorodeoxyglucose positron emission tomography-computed tomography (PET-CT) would predict pathologic complete response (pCR) to pertuzumab and trastuzumab (PT). PATIENTS AND METHODS: Patients with stage II or III, estrogen receptor-negative, HER2-positive breast cancer received four cycles of neoadjuvant PT. 18F-labeled fluorodeoxyglucose positron emission tomography-computed tomography was performed at baseline and 15 days after PT initiation (C1D15). Eighty evaluable patients were required to test the null hypothesis that the area under the curve of percent change in SULmax by C1D15 predicting pCR is ≤ 0.65, with a one-sided type I error rate of 10%. RESULTS: Eighty-eight women were enrolled (83 evaluable), and 85% (75 of 88) completed all four cycles of PT. pCR after PT alone was 22%. Receiver operator characteristic analysis of percent change in SULmax by C1D15 yielded an area under the curve of 0.72 (80% CI, 0.64 to 0.80; one-sided P = .12), which did not reject the null hypothesis. However, between patients who obtained pCR and who did not, a significant difference in median percent reduction in SULmax by C1D15 was observed (63.8% v 41.8%; P = .004) and SULmax reduction ≥ 40% was more prevalent (83% v 52%; P = .03; positive predictive value, 31%). Participants not obtaining a 40% reduction in SULmax by C1D15 were unlikely to obtain pCR (negative predictive value, 91%). CONCLUSION: Although the primary objective was not met, early changes in SULmax predict response to PT in estrogen receptor-negative and HER2-positive breast cancer. Once optimized, this quantitative imaging strategy may facilitate tailoring of therapy in this setting.

Published
2021

11. RNA-Seq based gene expression profiling of baseline and on-treatment breast tumors to predict response to HER2-directed therapy, without chemotherapy (TBCRC026).

Author

Hennessy, Maeve, primary, Fernández, Aranzazu, additional, Huang, Chiung Yu, additional, Cimino-Mathews, Ashley, additional, Denbow, Rita, additional, Abramson, Vandana G, additional, Rimawi, Mothaffar F., additional, Specht, Jennifer M., additional, Storniolo, Anna Maria, additional, Valero, Vicente, additional, Vaklavas, Chris, additional, Winer, Eric P., additional, Krop, Ian E., additional, Wolff, Antonio C., additional, Wahl, Richard L., additional, Thompson, E Aubrey, additional, Stearns, Vered, additional, Perou, Charles, additional, Carey, Lisa A., additional, and Connolly, Roisin M., additional

Published
2024
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12. Interim FDG-PET/CT for predicting response of HER2-positive breast cancer to neoadjuvant therapy: ECOG-ACRIN EA1211/DIRECT trial.

Author

Hennessy, Maeve, primary, Gatsonis, Constantine, additional, Jacene, Heather, additional, Connolly, Roisin M., additional, Burnette, Brian Leslie, additional, Stringer-Reasor, Erica Michelle, additional, Romanoff, Justin, additional, Taurone, Alexander, additional, O'Sullivan, Ciara Catherine, additional, Le-Petross, Huong T., additional, Lawhn Heath, Courtney, additional, Stearns, Vered, additional, Fowler, Amy M., additional, Tang, Shou-Ching, additional, Sepulveda, Karla, additional, DeMichele, Angela, additional, Mankoff, David A., additional, and Wolff, Antonio C., additional

Published
2024
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17. Association of treatment-emergent symptoms identified by patient-reported outcomes with adjuvant endocrine therapy discontinuation

Author

Smith, Karen Lisa, Verma, Neha, Blackford, Amanda L., Lehman, Jennifer, Westbrook, Kelly, Lim, David, Fetting, John, Wolff, Antonio C., Jelovac, Daniela, Miller, Robert S., Connolly, Roisin, Armstrong, Deborah K., Nunes, Raquel, Visvanathan, Kala, Riley, Carol, Papathakis, Katie, Zafman, Nelli, Sheng, Jennifer Y., Snyder, Claire, and Stearns, Vered

Published
2022
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21. Personalized Medicine in the Oncology Clinic: Implementation and Outcomes of the Johns Hopkins Molecular Tumor Board

Author

Dalton, W Brian, Forde, Patrick M, Kang, Hyunseok, Connolly, Roisin M, Stearns, Vered, Gocke, Christopher D, Eshleman, James R, Axilbund, Jennifer, Petry, Dana, Geoghegan, Cindy, Wolff, Antonio C, Loeb, David M, Pratilas, Christine A, Meyer, Christian F, Christenson, Eric S, Slater, Shannon A, Ensminger, Jennifer, Parsons, Heather A, Park, Ben H, and Lauring, Josh

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Patient Safety, Clinical Research, Cancer, Brain Cancer, Brain Disorders, Genetics, Clinical Trials and Supportive Activities, Rare Diseases, Good Health and Well Being, Oncology and carcinogenesis
Abstract

Tumor genomic profiling for personalized oncology therapy is being widely applied in clinical practice even as it is being evaluated more formally in clinical trials. Given the complexities of genomic data and its application to clinical use, molecular tumor boards with diverse expertise can provide guidance to oncologists and patients seeking to implement personalized genetically targeted therapy in practice. A multidisciplinary molecular tumor board reviewed tumor molecular profiling reports from consecutive referrals at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins over a 3-year period. The tumor board weighed evidence for actionability of genomic alterations identified by molecular profiling and provided recommendations including US Food and Drug Administration-approved drug therapy, clinical trials of matched targeted therapy, off-label use of such therapy, and additional tumor or germline genetic testing. One hundred fifty-five patients were reviewed. Actionable genomic alterations were identified in 132 patients (85%). Off-label therapies were recommended in 37 patients (24%). Eleven patients were treated off-label, and 13 patients were enrolled onto clinical trials of matched targeted therapies. Median progression-free survival of patients treated with matched therapies was 5 months (95% CI, 2.9 months to not reached), and the progression-free survival probability at 6 months was 43%(95% CI, 26% to 71%). Lack of locally available clinical trials was the major limitation on clinical actionability of tumor profiling reports. The molecular tumor board recommended off-label targeted therapies for a quarter of all patients reviewed. Outcomes were heterogeneous, although 43% of patients receiving genomically matched therapy derived clinical benefit lasting at least 6 months. Until more data become available from precision oncology trials, molecular tumor boards can help guide appropriate use of tumor molecular testing to direct therapy.

Published
2017

23. Adjunctive Statistical Standardization of Adjuvant Estrogen Receptor and Progesterone Receptor in Canadian Cancer Trials Group MA.27 Postmenopausal Breast Cancer Trial of Exemestane Versus Anastrozole.

Author

Chapman, Judith-Anne W., Bayani, Jane, SenGupta, Sandip, Bartlett, John M.S., Piper, Tammy, Quintayo, Mary Anne, Virk, Shakeel, Goss, Paul E., Ingle, James N., Ellis, Matthew J., Sledge, George W., Budd, G. Thomas, Rabaglio, Manuela, Ansari, Rafat H., Tozer, Richard, D'Souza, David P., Chalchal, Haji, Spadafora, Silvana, Stearns, Vered, and Perez, Edith A.

Published
2024
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33. TBCRC009: A Multicenter Phase II Clinical Trial of Platinum Monotherapy With Biomarker Assessment in Metastatic Triple-Negative Breast Cancer

Author

Isakoff, Steven J, Mayer, Erica L, He, Lei, Traina, Tiffany A, Carey, Lisa A, Krag, Karen J, Rugo, Hope S, Liu, Minetta C, Stearns, Vered, Come, Steven E, Timms, Kirsten M, Hartman, Anne-Renee, Borger, Darrel R, Finkelstein, Dianne M, Garber, Judy E, Ryan, Paula D, Winer, Eric P, Goss, Paul E, and Ellisen, Leif W

Subjects
Genetics, Cancer, Clinical Research, Clinical Trials and Supportive Activities, Breast Cancer, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Good Health and Well Being, Adult, Aged, Antineoplastic Agents, BRCA1 Protein, BRCA2 Protein, Biomarkers, Tumor, Carboplatin, Cisplatin, Class I Phosphatidylinositol 3-Kinases, Drug Administration Schedule, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genomic Instability, Heterozygote, Humans, Loss of Heterozygosity, Middle Aged, Mutation, Neoplasm Staging, Phosphatidylinositol 3-Kinases, Treatment Outcome, Triple Negative Breast Neoplasms, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeThe identification of patients with metastatic triple-negative breast cancer (mTNBC) who are expected to benefit from platinum-based chemotherapy is of interest. We conducted a single-arm phase II clinical trial of single-agent platinum for mTNBC with biomarker correlates.Patients and methodsPatients with mTNBC received first- or second-line cisplatin (75 mg/m(2)) or carboplatin (area under the concentration-time curve 6) by physician's choice once every 3 weeks. Coprimary end points were objective response rate (RR) and response prediction by p63/p73 gene expression. Secondary and exploratory end points included toxicity assessment, RR in cisplatin versus carboplatin, and RR in molecularly defined subgroups, including BRCA1/2 mutation carriers.ResultsPatients (N = 86; 69 as first-line therapy) received cisplatin (n = 43) or carboplatin (n = 43). RR was 25.6% (95% CI, 16.8% to 36%) and was numerically higher with cisplatin (32.6%) than with carboplatin (18.7%). RR was 54.5% in patients with germline BRCA1/2 mutations (n = 11). In patients without BRCA1/2 mutations (n = 66), exploratory analyses showed that a BRCA-like genomic instability signature (n = 32) discriminated responding and nonresponding tumors (mean homologous recombination deficiency-loss of heterozygosity/homologous recombination deficiency-large-scale state transitions [HRD-LOH/HRD-LST] scores were 12.68 and 5.11, respectively), whereas predefined analysis by p63/p73 expression status (n = 61), p53 and PIK3CA mutation status (n = 53), or PAM50 gene expression subtype (n = 55) did not. Five of the six long-term responders alive at a median of 4.5 years lacked germline BRCA1/2 mutations, and two of them had increased tumor HRD-LOH/HRD-LST scores.ConclusionPlatinum agents are active in mTNBC, especially in patients with germline BRCA1/2 mutations. A measure of tumor DNA repair function may identify patients without mutations who could benefit from platinum therapy agents. Prospective controlled confirmatory trials are warranted.

Published
2015

35. NCCN Working Group report: designing clinical trials in the era of multiple biomarkers and targeted therapies.

Author

Venook, Alan P, Arcila, Maria E, Benson, Al B, Berry, Donald A, Camidge, David Ross, Carlson, Robert W, Choueiri, Toni K, Guild, Valerie, Kalemkerian, Gregory P, Kurzrock, Razelle, Lovly, Christine M, McKee, Amy E, Morgan, Robert J, Olszanski, Anthony J, Redman, Mary W, Stearns, Vered, McClure, Joan, and Birkeland, Marian L

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Clinical Research, Genetics, Clinical Trials and Supportive Activities, 8.4 Research design and methodologies (health services), Health and social care services research, Good Health and Well Being, Biomarkers, Clinical Trials as Topic, Humans, Neoplasms, Precision Medicine, Research Design, Oncology & Carcinogenesis, Oncology and carcinogenesis, Health services and systems
Abstract

Defining treatment-susceptible or -resistant populations of patients with cancer through the use of genetically defined biomarkers has revolutionized cancer care in recent years for some disease/patient groups. Research continues to show that histologically defined diseases are diverse in their expression of unique mutations or other genetic alterations, however, which presents opportunities for the development of personalized cancer treatments, but increased difficulty in testing these therapies, because potential patient populations are divided into ever smaller numbers. To address some of the growing challenges in biomarker development and clinical trial design, NCCN assembled a group of experts across specialties and solid tumor disease types to begin to define the problems and to consider alternate ways of designing clinical trials in the era of multiple biomarkers and targeted therapies. Results from that discussion are presented, focusing on issues of clinical trial design from the perspective of statisticians, clinical researchers, regulators, pathologists, and information developers.

Published
2014

38. Feasibility of Symptom Monitoring During the First Year of Endocrine Therapy for Early Breast Cancer Using Patient-Reported Outcomes Collected via Smartphone App

Author

Smith, Karen Lisa, primary, Tsai, Hua-Ling, additional, Lim, David, additional, Wang, Chenguang, additional, Nunes, Raquel, additional, Wilkinson, Mary J., additional, Sheng, Jennifer Y., additional, Couzi, Rima, additional, Fetting, John, additional, Riley, Carol, additional, Wolff, Antonio C., additional, Santa-Maria, Cesar A., additional, Papathakis, Katie, additional, Collins-Chase, Lauren, additional, Hilton, Christie, additional, Thorner, Elissa, additional, Montanari, Amanda, additional, Ikejiani, Dara, additional, Snyder, Claire, additional, and Stearns, Vered, additional

Published
2023
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43. Timed Sequential Treatment With Cyclophosphamide, Doxorubicin, and an Allogeneic Granulocyte-Macrophage Colony-Stimulating Factor–Secreting Breast Tumor Vaccine: A Chemotherapy Dose-Ranging Factorial Study of Safety and Immune Activation

Author

Emens, Leisha A, Asquith, Justin M, Leatherman, James M, Kobrin, Barry J, Petrik, Silvia, Laiko, Marina, Levi, Joy, Daphtary, Maithili M, Biedrzycki, Barbara, Wolff, Antonio C, Stearns, Vered, Disis, Mary L, Ye, Xiaobu, Piantadosi, Steven, Fetting, John H, Davidson, Nancy E, and Jaffee, Elizabeth M

Subjects
Cancer, Clinical Research, Biotechnology, Breast Cancer, Vaccine Related, Prevention, Clinical Trials and Supportive Activities, Immunization, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Good Health and Well Being, Adult, Aged, Antineoplastic Combined Chemotherapy Protocols, Breast Neoplasms, CD4-Positive T-Lymphocytes, Cancer Vaccines, Cell Line, Combined Modality Therapy, Cyclophosphamide, Dose-Response Relationship, Drug, Doxorubicin, Drug Administration Schedule, Female, Granulocyte-Macrophage Colony-Stimulating Factor, Humans, Immunization Schedule, Immunotherapy, Adoptive, Middle Aged, Receptor, ErbB-2, Time Factors, Transfection, Treatment Outcome, Receptor, erbB-2, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeGranulocyte-macrophage colony-stimulating factor (GM-CSF) -secreting tumor vaccines have demonstrated bioactivity but may be limited by disease burdens and immune tolerance. We tested the hypothesis that cyclophosphamide (CY) and doxorubicin (DOX) can enhance vaccine-induced immunity in patients with breast cancer.Patients and methodsWe conducted a 3 x 3 factorial (response surface) dose-ranging study of CY, DOX, and an HER2-positive, allogeneic, GM-CSF-secreting tumor vaccine in 28 patients with metastatic breast cancer. Patients received three monthly immunizations, with a boost 6 to 8 months from study entry. Primary objectives included safety and determination of the chemotherapy doses that maximize HER2-specific immunity.ResultsTwenty-eight patients received at least one immunization, and 16 patients received four immunizations. No dose-limiting toxicities were observed. HER2-specific delayed-type hypersensitivity developed in most patients who received vaccine alone or with 200 mg/m(2) CY. HER2-specific antibody responses were enhanced by 200 mg/m(2) CY and 35 mg/m(2) DOX, but higher CY doses suppressed immunity. Analyses revealed that CY at 200 mg/m(2) and DOX at 35 mg/m(2) is the combination that produced the highest antibody responses.ConclusionFirst, immunotherapy with an allogeneic, HER2-positive, GM-CSF-secreting breast tumor vaccine alone or with CY and DOX is safe and induces HER2-specific immunity in patients with metastatic breast cancer. Second, the immunomodulatory activity of low-dose CY has a narrow therapeutic window, with an optimal dose not exceeding 200 mg/m(2). Third, factorial designs provide an opportunity to identify the most active combination of interacting drugs in patients. Further investigation of the impact of chemotherapy on vaccine-induced immunity is warranted.

Published
2009

44. Correlation of SUV on Early Interim PET with Recurrence-Free Survival and Overall Survival in Primary Operable HER2-Positive Breast Cancer (the TBCRC026 Trial)

Author

Hennessy, Maeve A., primary, Leal, Jeffrey P., additional, Huang, Chiung-Yu, additional, Solnes, Lilja B., additional, Denbow, Rita, additional, Abramson, Vandana G., additional, Carey, Lisa A., additional, Liu, Minetta C., additional, Rimawi, Mothaffar, additional, Specht, Jennifer, additional, Storniolo, Anna Maria, additional, Valero, Vicente, additional, Vaklavas, Christos, additional, Winer, Eric P., additional, Krop, Ian E., additional, Wolff, Antonio C., additional, Cimino-Mathews, Ashley, additional, Wahl, Richard L., additional, Stearns, Vered, additional, and Connolly, Roisin M., additional

Published
2023
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46. Supplementary Data from Entinostat Decreases Immune Suppression to Promote Antitumor Responses in a HER2+ Breast Tumor Microenvironment

Author

Sidiropoulos, Dimitrios N., primary, Rafie, Christine I., primary, Jang, Julie K., primary, Castanon, Sofi, primary, Baugh, Aaron G., primary, Gonzalez, Edgar, primary, Christmas, Brian J., primary, Narumi, Valerie H., primary, Davis-Marcisak, Emily F., primary, Sharma, Gaurav, primary, Bigelow, Emma, primary, Vaghasia, Ajay, primary, Gupta, Anuj, primary, Skaist, Alyza, primary, Considine, Michael, primary, Wheelan, Sarah J., primary, Ganesan, Sathish Kumar, primary, Yu, Min, primary, Yegnasubramanian, Srinivasan, primary, Stearns, Vered, primary, Connolly, Roisin M., primary, Gaykalova, Daria A., primary, Kagohara, Luciane T., primary, Jaffee, Elizabeth M., primary, Fertig, Elana J., primary, and Roussos Torres, Evanthia T., primary

Published
2023
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47. Data from Entinostat Decreases Immune Suppression to Promote Antitumor Responses in a HER2+ Breast Tumor Microenvironment

Author

Sidiropoulos, Dimitrios N., primary, Rafie, Christine I., primary, Jang, Julie K., primary, Castanon, Sofi, primary, Baugh, Aaron G., primary, Gonzalez, Edgar, primary, Christmas, Brian J., primary, Narumi, Valerie H., primary, Davis-Marcisak, Emily F., primary, Sharma, Gaurav, primary, Bigelow, Emma, primary, Vaghasia, Ajay, primary, Gupta, Anuj, primary, Skaist, Alyza, primary, Considine, Michael, primary, Wheelan, Sarah J., primary, Ganesan, Sathish Kumar, primary, Yu, Min, primary, Yegnasubramanian, Srinivasan, primary, Stearns, Vered, primary, Connolly, Roisin M., primary, Gaykalova, Daria A., primary, Kagohara, Luciane T., primary, Jaffee, Elizabeth M., primary, Fertig, Elana J., primary, and Roussos Torres, Evanthia T., primary

Published
2023
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48. Data from Development of an Automated Liquid Biopsy Assay for Methylated Markers in Advanced Breast Cancer

Author

Fackler, Mary Jo, primary, Tulac, Suzana, primary, Venkatesan, Neesha, primary, Aslam, Adam J., primary, de Guzman, Timothy N., primary, Mercado-Rodriguez, Claudia, primary, Cope, Leslie M., primary, Downs, Bradley M., primary, Vali, Abdul Hussain, primary, Ding, Wanjun, primary, Lehman, Jennifer, primary, Denbow, Rita, primary, Reynolds, Jeffrey, primary, Buckley, Morgan E., primary, Visvanathan, Kala, primary, Umbricht, Christopher B., primary, Wolff, Antonio C., primary, Stearns, Vered, primary, Bates, Michael, primary, Lai, Edwin W., primary, and Sukumar, Saraswati, primary

Published
2023
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49. Supplementary Fig S3 from Development of an Automated Liquid Biopsy Assay for Methylated Markers in Advanced Breast Cancer

Author

Fackler, Mary Jo, primary, Tulac, Suzana, primary, Venkatesan, Neesha, primary, Aslam, Adam J., primary, de Guzman, Timothy N., primary, Mercado-Rodriguez, Claudia, primary, Cope, Leslie M., primary, Downs, Bradley M., primary, Vali, Abdul Hussain, primary, Ding, Wanjun, primary, Lehman, Jennifer, primary, Denbow, Rita, primary, Reynolds, Jeffrey, primary, Buckley, Morgan E., primary, Visvanathan, Kala, primary, Umbricht, Christopher B., primary, Wolff, Antonio C., primary, Stearns, Vered, primary, Bates, Michael, primary, Lai, Edwin W., primary, and Sukumar, Saraswati, primary

Published
2023
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50. Abstract 5167: Entinostat's modulation of myeloid derived suppressor cells through the STAT3-NFκB-AP-1 axis decreases suppressive signaling

Author

Baugh, Aaron G., primary, Gonzalez, Edgar, additional, Narumi, Valerie H., additional, Castanon, Sofi, additional, Kreger, Jesse, additional, Leatherman, James, additional, Ho, Won Jin, additional, Cimino-Mathews, Ashley, additional, Stearns, Vered, additional, Connolly, Roisin M., additional, Jaffee, Elizabeth M., additional, MacLean, Adam L., additional, and Torres, Evanthia T. Roussos, additional

Published
2023
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