A5049538257- Cancer Genomics and Diagnostics
- BRCA gene mutations in cancer
- Single-cell and spatial transcriptomics
- Glioma Diagnosis and Treatment
- Muscle Physiology and Disorders
- Muscle metabolism and nutrition
- DNA Repair Mechanisms
- Probiotics and Fermented Foods
- Aquaculture disease management and microbiota
- Genomics and Phylogenetic Studies
- Genetics, Bioinformatics, and Biomedical Research
- Spaceflight effects on biology
- RNA regulation and disease
- Pancreatic and Hepatic Oncology Research
- Lymphoma Diagnosis and Treatment
- Chromatin Remodeling and Cancer
- Gene expression and cancer classification
- PARP inhibition in cancer therapy
- Immune Cell Function and Interaction
- Lung Cancer Treatments and Mutations
- HIV/AIDS drug development and treatment
- Cancer Cells and Metastasis
- Telomeres, Telomerase, and Senescence
- T-cell and B-cell Immunology
- Cancer-related molecular mechanisms research
Jackson Laboratory
2019-2024
Cellular senescence is a form of adaptive cellular physiology associated with aging. causes proinflammatory phenotype that impairs tissue regeneration, has been linked to stress, and implicated in several human neurodegenerative diseases. We had previously determined neural progenitor cells (NPCs) derived from induced pluripotent stem cell (iPSC) lines patients primary progressive multiple sclerosis (PPMS) failed promote oligodendrocyte (OPC) maturation, whereas NPCs age-matched control did...
Significance Among the major health challenges for astronauts during prolonged space travel are loss of muscle mass and bone mass. Here, we investigated effects targeting signaling pathway mediated by secreted molecules, myostatin activin A, in mice sent to International Space Station. We show that this has significant beneficial protecting against both microgravity, suggesting strategy may be effective preventing or treating not only on missions but also people with disuse atrophy Earth,...
Triple-negative breast cancer (TNBC) and ovarian carcinomas (OvCas) with BRCA1 promoter methylation (BRCA1meth) respond more poorly to alkylating agents compared those bearing mutations in BRCA2 (BRCAmut). This is a conundrum given the biologically equivalent homologous recombination deficiency (HRD) induced by these genetic epigenetic BRCA perturbations. We dissected this problem through detailed genomic analyses of TNBC OvCa cohorts experimentation patient-derived xenografts genetically...
Brain tumors are the leading cause of cancer-related deaths in children. Tailored therapies need preclinical brain tumor models representing a wide range molecular subtypes. Here, we adapted previously established tissue-model to fresh patient cells with goal establishing3D vitro culture conditions for each type.Wereported our findings from 11 pediatric cases, consisting three medulloblastoma (MB) patients, ependymoma (EPN) one glioblastoma (GBM) patient, and four juvenile pilocytic...
The standard of care in oncology has been genomic profiling tumor tissue biopsies for the treatment and management disease, which can prove to be quite challenging terms cost, invasiveness procedure, potential risk patient. As number available drugs continues increase, so too does demand technologies testing applications that identify alterations targetable by these new therapies. Liquid use a blood draw from diseased patient may offset many disadvantages invasive procedure. However, as with...
Significance Maintenance of skeletal muscle and bone is regulated by key signaling proteins belonging to the transforming growth factor family. Here, we present genetic studies in mice showing that follistatin, which normally blocks activities these proteins, acts locally an exquisitely dose-dependent manner control growth. Moreover, our targeting receptors for reveal enormous capacity kept check this system. These findings have implications strategies target pathway clinical applications...
Abstract Genetic variants associated with autoimmune diseases are highly enriched within putative cis -regulatory regions of CD4 + T cells, suggesting that they alter disease risk via changes in gene regulation. However, very few genetic have been shown to affect cell expression or function. We tested >18,000 disease-associated for allele-specific using massively parallel reporter assays primary human cells. The 545 expression-modulating (emVars) identified greatly enrich likely causal...
Abstract Background: BRCA deficient Triple negative breast cancers (TNBC) are effectively treated with platinum agents but, upon relapse, resistance is common. A number of genes have been shown to mediate chemoresistance in vitro, but none clinically useful due the heterogeneous mechanisms vivo tumor chemo-resilience. Methods: We attacked this problem by recapitulating generation cisplatin 50 mice bearing a sensitive TNBC patient derived xenograft (PDX) TM00099, BRCA1 type 1 tandem...
Abstract Background. Homologous recombination deficiency (HRD), induced by germline and somatic BRCA1 or BRCA2 gene mutations (BRCAmut) promoter methylation (BRCA1meth), has been associated with better response to platinum agents in both triple negative breast cancer (TNBC) ovarian carcinoma (OvCa). A major conundrum arising from recent studies is why patients BRCA1meth cancers do more poorly compared those BRCAmut given the biologically equivalent HRD states. Here, we address this question...
SUMMARY Loss of homologous recombination repair (HRR) via germline and somatic BRCA1 or BRCA2 gene mutations promoter methylation has been associated with better response to platinum agents PARP inhibitors, in both triple negative breast cancer (TNBC) ovarian carcinoma (OvCa). A major conundrum arising from recent clinical studies is why cancers ( meth) respond more poorly as compared those bearing BRCA mut), given the biologically equivalent HRR deficiency states. We dissected this problem...