Apostolia M. Tsimberidou

ORCID: 0000-0003-2713-233X
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About
Contact & Profiles
Research Areas
  • Cancer Genomics and Diagnostics
  • Lung Cancer Treatments and Mutations
  • CAR-T cell therapy research
  • Colorectal Cancer Treatments and Studies
  • PI3K/AKT/mTOR signaling in cancer
  • Chronic Lymphocytic Leukemia Research
  • Advanced Breast Cancer Therapies
  • Cancer Research and Treatments
  • Cancer Immunotherapy and Biomarkers
  • Lymphoma Diagnosis and Treatment
  • Cancer Treatment and Pharmacology
  • Acute Myeloid Leukemia Research
  • Pancreatic and Hepatic Oncology Research
  • Economic and Financial Impacts of Cancer
  • Biomedical Ethics and Regulation
  • Health Systems, Economic Evaluations, Quality of Life
  • Genetic factors in colorectal cancer
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Multiple Myeloma Research and Treatments
  • HER2/EGFR in Cancer Research
  • Histone Deacetylase Inhibitors Research
  • Cancer-related Molecular Pathways
  • Protein Degradation and Inhibitors
  • Immunotherapy and Immune Responses
  • Melanoma and MAPK Pathways

The University of Texas MD Anderson Cancer Center
2016-2025

Bayer (Germany)
2019

Roche (Switzerland)
2019

Covance (United States)
2019

Parker Institute for Cancer Immunotherapy
2019

Array BioPharma (United States)
2018

Novartis (Switzerland)
2018

Merck (Japan)
2018

Prometheus (United States)
2018

Bristol-Myers Squibb (Germany)
2018

Abstract Purpose: We initiated a personalized medicine program in the context of early clinical trials, using targeted agents matched with tumor molecular aberrations. Herein, we report our observations. Patient and Methods: Patients advanced cancer were treated Clinical Center for Targeted Therapy. Molecular analysis was conducted MD Anderson Laboratory Improvement Amendments (CLIA)–certified laboratory. whose tumors had an aberration therapy, when available. Treatment assignment not...

10.1158/1078-0432.ccr-12-1627 article EN Clinical Cancer Research 2012-09-11

Mutations of the PIK3CA gene may predict response to phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target rapamycin (mTOR) inhibitors. Concomitant mutations in mitogen-activated protein kinase (MAPK) pathway mediate resistance.Tumors from patients with breast, cervical, endometrial, and ovarian cancer referred Clinical Center for Targeted Therapy (Phase I Program) were analyzed PIK3CA, KRAS, NRAS, BRAF mutations. Patients treated, whenever feasible, agents targeting PI3K/AKT/mTOR...

10.1200/jco.2011.36.1196 article EN Journal of Clinical Oncology 2012-01-24

Preclinical data suggest that PIK3CA mutations predict response to PI3K/AKT/mTOR inhibitors. Concomitant KRAS or BRAF may mediate resistance. Therefore, tumors from patients referred the phase I program for targeted therapy starting in October 2008 were analyzed using PCR-based DNA sequencing of exons 9 and 20. Consecutive with diverse tumor types mutation treated whenever possible agents targeting pathway. Overall, detected 25 217 (11.5%; exon 9, n = 11; 20, 14). In more than 10 tested,...

10.1158/1535-7163.mct-10-0994 article EN Molecular Cancer Therapeutics 2011-01-08

Abstract Purpose: Little prospective data are available on clinical outcomes and immune correlates from combination radiation immunotherapy. We conducted a phase I trial (NCT02239900) testing stereotactic ablative radiotherapy (SABR) with ipilimumab. Experimental Design: SABR was given either concurrently (1 day after the first dose) or sequentially week second ipilimumab (3 mg/kg every 3 weeks for 4 doses) to five treatment groups: concurrent 50 Gy (in fractions) liver; sequential lung; 60...

10.1158/1078-0432.ccr-16-1432 article EN Clinical Cancer Research 2016-09-20

PIK3CA mutations may predict response to PI3K/AKT/mTOR inhibitors in patients with advanced cancers, but the relevance of mutation subtype has not been investigated. Patients diverse cancers referred Clinical Center for Targeted Therapy were analyzed and, if possible, KRAS mutations. treated, whenever agents targeting pathway. Overall, 105 (10%) 1,012 tested harbored Sixty-six (median 3 prior therapies) PIK3CA-mutant patients, including 16 individuals (of 55 tested) simultaneous mutations,...

10.1158/0008-5472.can-12-1726 article EN Cancer Research 2012-10-13

Innovative molecular diagnostics deployed in the clinic enable new ways to stratify patients into appropriate treatment regimens. These approaches may resolve a major challenge for early-phase clinical trials, which is recruit who, while having failed previous treatments, nevertheless respond molecularly targeted drugs. We report findings of prospective, single-center study conducted with diverse refractory cancers who underwent comprehensive genomic profiling (CGP; next-generation...

10.1158/0008-5472.can-15-3043 article EN Cancer Research 2016-05-19

Despite a wealth of preclinical studies, it is unclear whether PIK3CA or phosphatase and tensin homolog (PTEN) gene aberrations are actionable in the clinical setting. Of 1,656 patients with advanced, refractory cancers tested for PTEN abnormalities, mutations were found 9% (146/1,589), loss and/or mutation was 13% (149/1,157). In multicovariable analysis, treatment phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target rapamycin (mTOR) inhibitor only independent factor predicting...

10.1016/j.celrep.2013.12.035 article EN cc-by-nc-nd Cell Reports 2014-01-01

Abstract In vitro, EGFR inhibition, combined with the BRAF inhibitor vemurafenib, causes synergistic cytotoxicity for BRAFV600E metastatic colorectal cancer, further augmented by irinotecan. The safety and efficacy of irinotecan, cetuximab in BRAF-mutated malignancies are not defined. this 3+3 phase I study, patients BRAFV600E-advanced solid cancers received irinotecan escalating doses vemurafenib. Nineteen (18 cancer 1 appendiceal cancer) were enrolled. Three experienced dose-limiting...

10.1158/2159-8290.cd-16-0050 article EN Cancer Discovery 2016-10-12

Abstract Purpose: The purpose of this study was to confirm our previous results that targeted agents matched with tumor molecular alterations were associated improved outcomes compared nonmatched therapy in patients advanced cancer. Experimental Design: Outcomes who referred for treatment on phase I clinical trials at University Texas MD Anderson Cancer Center (Houston, TX) from March 2011 January 2012 between those had received and whom no available. Two-month landmark analyses overall...

10.1158/1078-0432.ccr-14-0603 article EN Clinical Cancer Research 2014-07-02

Abstract Microsatellite stable metastatic colorectal cancer (MSS mCRC; mismatch repair proficient) has previously responded poorly to immune checkpoint blockade. Botensilimab (BOT) is an Fc-enhanced multifunctional anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) antibody designed expand therapy cold/poorly immunogenic solid tumors, such as MSS mCRC. BOT with or without balstilimab (BAL; anti-PD-1 antibody) being evaluated in ongoing expanded phase 1 study. The primary endpoint...

10.1038/s41591-024-03083-7 article EN cc-by Nature Medicine 2024-06-13

The confluence of new technologies with artificial intelligence (AI) and machine learning (ML) analytical techniques is rapidly advancing the field precision oncology, promising to improve diagnostic approaches therapeutic strategies for patients cancer. By analyzing multi-dimensional, multiomic, spatial pathology, radiomic data, these enable a deeper understanding intricate molecular pathways, aiding in identification critical nodes within tumor's biology optimize treatment selection....

10.1038/s41746-025-01471-y article EN cc-by-nc-nd npj Digital Medicine 2025-01-31

The purpose of this study was to assess the incidence, presenting characteristics, and treatment outcomes Richter's syndrome (RS) factors predicting response survival.An electronic database search patients with chronic lymphocytic leukemia (CLL)/small lymphoma (SLL) who presented at University Texas M.D. Anderson Cancer Center (Houston, TX) between January 1975 June 2005 performed, patient medical records were reviewed.Of 3,986 CLL/SLL, 204 (5.1%) had possible RS, 148 (3.7%) biopsy- or...

10.1200/jco.2005.05.0187 article EN Journal of Clinical Oncology 2006-05-18
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