A5087780746- Cancer-related Molecular Pathways
- Lung Cancer Research Studies
- Advanced Breast Cancer Therapies
- Calcium signaling and nucleotide metabolism
- Cancer Cells and Metastasis
- Adenosine and Purinergic Signaling
- PARP inhibition in cancer therapy
- RNA modifications and cancer
- Microtubule and mitosis dynamics
- CAR-T cell therapy research
- Cancer Immunotherapy and Biomarkers
- Synthesis and Biological Evaluation
- MicroRNA in disease regulation
- Wnt/β-catenin signaling in development and cancer
- Epigenetics and DNA Methylation
- interferon and immune responses
- Single-cell and spatial transcriptomics
- Bacteriophages and microbial interactions
- Cancer, Hypoxia, and Metabolism
- Nanoplatforms for cancer theranostics
- Cancer Genomics and Diagnostics
- Cancer Research and Treatments
- Cancer therapeutics and mechanisms
- Circular RNAs in diseases
- Skin and Cellular Biology Research
The University of Texas MD Anderson Cancer Center
2021-2025
Harvard University
2019
Dana-Farber Cancer Institute
2019
Long Island University
2017-2018
Combinatorial clinical trials of PARP inhibitors with immunotherapies are ongoing, yet the immunomodulatory effects inhibition have been incompletely studied. Here, we sought to dissect mechanisms underlying inhibitor-induced changes in tumor microenvironment BRCA1-deficient triple-negative breast cancer (TNBC). We demonstrate that inhibitor olaparib induces CD8+ T-cell infiltration and activation vivo, depletion severely compromises antitumor efficacy. Olaparib-induced recruitment is...
Lung squamous cell carcinoma (LSCC) remains a leading cause of cancer death with few therapeutic options. We characterized the proteogenomic landscape LSCC, providing deeper exposition LSCC biology potential implications. identify NSD3 as an alternative driver in FGFR1-amplified tumors and low-p63 overexpressing target survivin. SOX2 is considered undruggable, but our analyses provide rationale for exploring chromatin modifiers such LSD1 EZH2 to SOX2-overexpressing tumors. Our data support...
CDK4/6 inhibition is now part of the standard armamentarium for patients with estrogen receptor-positive (ER+) breast cancer, so that defining mechanisms resistance a pressing issue. Here, we identify increased CDK6 expression as key determinant acquired after palbociclib treatment in ER+ cancer cells. critical cellular survival during exposure. The observed resistant cells dependent on TGF-β pathway suppression via miR-432-5p expression. Exosomal mediates transfer phenotype between...
Abstract Triple-negative breast cancer (TNBC) is a highly metastatic subtype of cancer. The epithelial-to-mesenchymal transition nonbinary process in the cascade that generates tumor cells with both epithelial and mesenchymal traits known as hybrid EM cells. Recent studies have elucidated enhanced potential cancers featuring phenotype, highlighting need to uncover molecular drivers targetable vulnerabilities state. Here, we discovered tumors are enriched CD38, an immunosuppressive molecule...
Epithelial-mesenchymal transition (EMT) empowers epithelial cells with mesenchymal and stem-like attributes, facilitating metastasis, a leading cause of cancer-related mortality. Hybrid epithelial-mesenchymal (E/M) cells, retaining both traits, exhibit heightened metastatic potential stemness. The intermediate filament, vimentin, is upregulated during EMT, enhancing the resilience invasiveness carcinoma cells. phosphorylation vimentin critical to its structure function. Here, we identify...
<div>Abstract<p>Triple-negative breast cancer (TNBC) is a highly metastatic subtype of cancer. The epithelial-to-mesenchymal transition nonbinary process in the cascade that generates tumor cells with both epithelial and mesenchymal traits known as hybrid EM cells. Recent studies have elucidated enhanced potential cancers featuring phenotype, highlighting need to uncover molecular drivers targetable vulnerabilities state. Here, we discovered tumors are enriched CD38, an...
<p>Supplementary data, tables and legends</p>
Abstract Background- Triple-negative breast cancer (TNBC) is challenging to treat due fewer clinically detectable targets and its propensity metastasize. Epithelial mesenchymal transition (EMT) a key feature of the metastatic cascade. Recent data highlights enhanced potential hybrid epithelial-mesenchymal (EM) phenotypes from partial activation EMT. However, mechanistic insights targetable vulnerabilities within EM remain elusive. We identified that tumors are enriched in CD38, an...
Abstract Combinatorial clinical trials of PARP inhibitors with immunotherapies are ongoing, yet the immunomodulatory effects inhibition have been incompletely studied. Here, we sought to dissect mechanisms underlying inhibitor-induced changes in tumor microenvironment BRCA1-deficient triple-negative breast cancer (TNBC). We demonstrate that inhibitor olaparib induces CD8+ T cell infiltration and activation vivo, depletion cells severely compromises anti-tumor efficacy. Olaparib-induced...
Combinatorial clinical trials of PARP inhibitors with immunotherapies are ongoing, yet the immunomodulatory effects inhibition have been incompletely studied. Here, we sought to dissect mechanisms underlying inhibitor-induced changes in tumor microenvironment BRCA1-deficient triple-negative breast cancer (TNBC). We demonstrate that inhibitor olaparib induces CD8+ T cell infiltration and activation vivo, depletion cells severely compromises anti-tumor efficacy. Olaparib-induced recruitment is...
Abstract Introduction: Upper Gastrointestinal Cancers (UGCs) are a leading cause of cancer-related mortality and account for approximately 1.1 million deaths worldwide. UGCs respond poorly to conventional chemotherapy due constitutive over activity multiple oncogenic signaling mechanisms, including the epidermal growth factor receptor (EGFR), ERBB2/HER-2, Aurora kinases, JAK-STAT pathways. In addition, presence mutant P53 further imparts resistance chemotherapeutic agents. Therefore, novel...
Abstract Background: The overexpression of cyclin-dependent kinases 4/6 (CDK4/6) is known to cause cell cycle dysregulation in certain cancer types, making these attractive targets for pharmacological inhibition. effectiveness first-generation non-selective kinases, such as roscovitine and flavopiridol, was hampered by toxicities, leading the development second-generation compounds like IBRANCE®/Palbociclib that specifically inhibit CDK4 6. ON 123300 a third-generation potent CDK4/6...
Abstract Background: Upper Gastrointestinal Cancers (UGCs) respond poorly to conventional chemotherapy due overactive intrinsic mechanisms that mediate cellular proliferation and drug resistance. Dysregulated cell division increased activity of cyclin-dependent kinases 4/6 (CDK4/6) is one such mechanism drives progression UGCs, making them an important therapeutic target. Palbociclib a second generation cdk4/6 specific inhibitor approved for treatment ER+ breast cancers. Since Cisplatin...
Abstract Introduction: Upper Gastrointestinal Cancers (UGCs) exhibit resistance to conventional chemotherapy due variable P53 status and constitutive overactivity of EGFR, ERBB2/HER-2, Aurora kinases, JAK2 oncogenes. UGC is a leading cause cancer related deaths worldwide development multi-kinase targeting inhibitors could pave the way for improved better therapeutic outcomes. In this study, we investigated series N4-phenylsubstituted-7H-pyrrolo[2,3-d]pyrimidin-4-amines selected promising...
Abstract Introduction: Breast cancer is the most prevalent type of in women, accounting for 12% all annual cases worldwide with deaths attributed to metastasis. It displays both inter- and intra-tumoral heterogeneity which linked epithelial-mesenchymal transition (EMT). This program involves acquisition a mesenchymal-like phenotype allowing cells disseminate from primary tumor metastasize. However, recent studies show that do not need undergo complete EMT gain invasive potential; instead,...