A5025797727- Lung Cancer Research Studies
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Metastasis and carcinoma case studies
- Cancer Cells and Metastasis
- Lung Cancer Treatments and Mutations
- RNA Research and Splicing
- Wnt/β-catenin signaling in development and cancer
- Epigenetics and DNA Methylation
- BRCA gene mutations in cancer
- Cancer therapeutics and mechanisms
- Virus-based gene therapy research
- Monoclonal and Polyclonal Antibodies Research
- Neuroendocrine Tumor Research Advances
- Nutrition, Genetics, and Disease
- CRISPR and Genetic Engineering
- PARP inhibition in cancer therapy
- DNA Repair Mechanisms
- Cancer Genomics and Diagnostics
- Genomics and Chromatin Dynamics
- Cancer-related gene regulation
- interferon and immune responses
The University of Texas Southwestern Medical Center
2023-2025
Children's Medical Center
2023-2025
Southwestern Medical Center
2025
Duke-NUS Medical School
2020-2023
Abstract Small cell lung cancer (SCLC) presents as a highly chemosensitive malignancy but acquires cross-resistance after relapse. This transformation is nearly inevitable in patients has been difficult to capture laboratory models. Here, we present preclinical system that recapitulates acquired cross-resistance, developed from 51 patient-derived xenograft (PDX) Each model was tested vivo against three clinical regimens: cisplatin plus etoposide, olaparib temozolomide, and topotecan. These...
Article4 March 2021Open Access Transparent process WNT inhibition creates a BRCA-like state in Wnt-addicted cancer Amanpreet Kaur Program Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore, Singapore Search for more papers by this author Jun Yi Stanley Lim Sugunavathi Sepramaniam Experimental Drug Development Centre, A*Star, Siddhi Patnaik Nathan Harmston Science Division, Yale-NUS College, May Ann Lee Enrico Petretto Center Computational Biology Cardiovascular Metabolic...
Abstract Extrachromosomal DNA (ecDNA) is a prevalent driver of cancer, whose random segregation promotes aggressive tumors. Acentric ecDNAs attach to chromosomes during mitosis for segregation. However, the molecular mechanism governing ecDNA-chromosome mitotic interactions remains poorly understood. This study shows that histone 3 lysine 27 acetylation (H3K27ac)-marked chromatin mitosis. H3K27ac depletion resulted in ecDNA detachment from chromosomes. Diverse bromodomain proteins, which are...
Aberrant Wnt signaling drives a number of cancers through regulation diverse downstream pathways. Wnt/β-catenin achieves this in part by increasing the expression proto-oncogenes such as MYC and cyclins. However, global assessment Wnt-regulated transcriptome vivo genetically distinct demonstrates that suppresses many genes it activates. In study, we examined set are upregulated upon inhibition Wnt-addicted pancreatic colorectal cancer models. Decreasing led to marked increase gene activating...
ABSTRACT Small cell lung cancer (SCLC) presents as a highly chemosensitive malignancy but acquires cross-resistance after relapse. This transformation is nearly inevitable in patients has been difficult to capture laboratory models. Here we present pre-clinical system that recapitulates acquired SCLC, developed from 51 patient-derived xenografts (PDXs). Each model was tested for vivo sensitivity three clinical regimens: cisplatin plus etoposide, olaparib temozolomide, and topotecan. These...
ABSTRACT Wnt signaling maintains diverse adult stem cell compartments and is implicated in chemotherapy resistance cancer. PORCN inhibitors that block secretion have proven effective Wnt-addicted preclinical cancer models are clinical trials. In a survey for potential combination therapies, we found inhibition synergizes with the PARP inhibitor olaparib cancers. Mechanistically, find multiple genes homologous recombination Fanconi anemia repair pathways, including BRCA1 , FANCD2 RAD51...
<p>MYC paralog copy number and ecDNA status in SCLC cell lines, PDX models biopsy samples derived before treatment or after relapse.</p>
<p>Comparison gene expression and H3K27ac between MGH1518 serial models</p>
<p>Genomic analysis of chromosome 17 focal amplification in MGH1531-5BX and ecDNA junction mutations MGH1518-3A.</p>
<p>Comparison of chemotherapy regimen delta-AUC and comparison average by PDX source.</p>
<p>Method to compare ecMYC level with resistance drug-induced DNA damage.</p>
<p>Acquired ecMYCN amplification in MGH1578 serial models and lineage oncogene expression compared with ecDNA status across the PDX panel.</p>
<p>Reconstruction of ecDNAs containing MYC paralogs and MYCL FISH in MGH1501-1A metaphase chromosomes.</p>
<p>Levels of ecMYC in untreated and treated MGH1518-3A xenografts</p>
<p>Calculation of delta-AUC and comparison EC with EP in PDX models.</p>
<p>MYC paralog amplifications that were detected or omitted by segmented copy number analysis, and patient survival compared with ecDNA status of PDX models.</p>
<p>Untreated PDX growth curves.</p>
<p>Frequency of amplified oncogenes across PDX panel, similarity ecMYC/L/N structures, and regression analysis average drug response versus MYC paralog copy number, expression amplicon type.</p>
<p>Reconstruction of ecDNAs that do not contain MYC paralogs.</p>
<p>Genomic analysis of chromosome 8 focal amplification in MGH1518-3A</p>
<div>Abstract<p>Small cell lung cancer (SCLC) presents as a highly chemosensitive malignancy but acquires cross-resistance after relapse. This transformation is nearly inevitable in patients has been difficult to capture laboratory models. Here, we present preclinical system that recapitulates acquired cross-resistance, developed from 51 patient-derived xenograft (PDX) Each model was tested <i>in vivo</i> against three clinical regimens: cisplatin plus etoposide,...
<p>Reconstruction of ecDNAs containing MYC paralogs and MYCL FISH in MGH1501-1A metaphase chromosomes.</p>
<p>MYC paralog copy number and ecDNA status in SCLC cell lines, PDX models biopsy samples derived before treatment or after relapse.</p>