Nicholas D. Camarda
A5041454060- Cancer Genomics and Diagnostics
- Pancreatic and Hepatic Oncology Research
- Pregnancy and preeclampsia studies
- Hormonal Regulation and Hypertension
- Birth, Development, and Health
- Apelin-related biomedical research
- Atherosclerosis and Cardiovascular Diseases
- Blood disorders and treatments
- Epigenetics and DNA Methylation
- Acute Myeloid Leukemia Research
- Lung Cancer Treatments and Mutations
- Renal cell carcinoma treatment
- Inflammation biomarkers and pathways
- Genetics, Bioinformatics, and Biomedical Research
- Chemotherapy-induced cardiotoxicity and mitigation
- Angiogenesis and VEGF in Cancer
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Biomedical and Engineering Education
- Radiomics and Machine Learning in Medical Imaging
- Diversity and Career in Medicine
- Advances in Oncology and Radiotherapy
- Gene expression and cancer classification
- Biotin and Related Studies
- Receptor Mechanisms and Signaling
- Pneumocystis jirovecii pneumonia detection and treatment
Tufts Medical Center
2021-2024
Tufts University
2020-2024
Dana-Farber Cancer Institute
2017-2021
ORCID
2020
Harvard University
2020
Dana-Farber Brigham Cancer Center
2018
Brigham and Women's Hospital
2018
Molecular Oncology (United States)
2018
Broad Institute
2018
Eli and Edythe Broad Foundation
2018
Clinically relevant subtypes exist for pancreatic ductal adenocarcinoma (PDAC), but molecular characterization is not yet standard in clinical care. We implemented a biopsy protocol to perform time-sensitive whole-exome sequencing and RNA patients with advanced PDAC. Therapeutically genomic alterations were identified 48% (34/71) pathogenic/likely pathogenic germline 18% (13/71) of patients. Overall, 30% (21/71) enrolled experienced change management as result data. Twenty-six had and/or...
Abstract To understand the mechanisms that mediate germline genetic leukemia predisposition, we studied inherited ribosomopathy Shwachman-Diamond syndrome (SDS), a bone marrow failure disorder with high risk of myeloid malignancies at an early age. define mechanistic basis clonal hematopoiesis in SDS, investigate somatic mutations acquired by patients SDS followed longitudinally. Here report multiple independent hematopoietic clones arise life, most commonly harboring heterozygous EIF6 or...
Preeclampsia is a syndrome of high blood pressure (BP) with end organ damage in late pregnancy that associated circulating soluble VEGF receptor (sFlt1 [soluble Fms-like tyrosine kinase 1]). Women exposed to preeclampsia have substantially increased risk hypertension after pregnancy, but the mechanism remains unknown, leaving missed interventional opportunity. After preeclampsia, women enhanced sensitivity hypertensive stress. Since smooth muscle cell mineralocorticoid receptors (SMC-MR) are...
After half a century of evidence suggesting the existence mineralocorticoid receptors (MR) in vasculature, advent technology to specifically knockout MR from smooth muscle cells (SMCs) mice has elucidated contributions SMC-MR cardiovascular function and disease, independent kidney. This review summarizes latest understanding molecular mechanisms by which contributes (1) regulation vasomotor blood pressure contribute systemic pulmonary hypertension; (2) vascular remodeling response...
Women with a history of preeclampsia have evidence premature atherosclerosis and increased risk myocardial infarction stroke compared women who had normotensive pregnancy. Whether this is due to common factors or direct impact prior exposure has never been tested in mouse model.
The United States Medical Licensing Examination (USMLE) consists of Step 1, 2 Clinical Knowledge, Skills, and 3. To be licensed to practice medicine in the States, medical students must pass all parts USMLE. However, addition that pass/fail grade, are currently given a numerical score for Residency program directors have come use 1 efficiently screen growing number residency applicants. As result, deleterious environment undergraduate education has been created, importance matching their...
Abstract Vascular endothelial growth factor receptor inhibitors (VEGFRis) improve cancer survival but are associated with treatment-limiting hypertension, often attributed to cell (EC) dysfunction. Using phosphoproteomic profiling of VEGFRi-treated ECs, drugs were screened for mitigators VEGFRi-induced EC dysfunction and validated in primary aortic mice, canine patients. VEGFRi treatment significantly raised systolic blood pressure (SBP) increased markers renal mice α-Adrenergic-antagonists...
ABSTRACT The canonical paradigm of GPCR signaling recognizes G proteins and β-arrestins as the two primary transducers that promote signaling. Recent evidence suggests atypical chemokine receptor 3 (ACKR3) does not couple to proteins, are dispensable for some its functions. Here, we employed proximity labeling identify interact with ACKR3 in cells devoid β-arrestin. We identified involved endocytic machinery evaluated a subset conserved across several GPCR-based experiments. discovered bone...
Abstract Shwachman-Diamond syndrome (SDS) is an inherited bone marrow failure with predisposition to developing leukemia. We found that multiple independent somatic hematopoietic clones arise early in life, most commonly harboring heterozygous mutations EIF6 or TP53 . cause functional compensation for the germline deficiency by alleviating SDS ribosome joining defect, improving translation, and reducing p53 activation. decrease checkpoint activation without affecting assembly. link...
Objective: Animal models of atherosclerosis are used extensively to interrogate molecular mechanisms in serial fashion. We tested whether a novel systems biology approach integration preclinical data identifies pathways and regulators human disease. Approach Results: Of 716 articles published ATVB from 1995 2019 using the apolipoprotein E knockout mouse study atherosclerosis, were extracted 360 unique studies which gene was experimentally perturbed impact plaque size or composition analyzed...
Introduction: Vascular endothelial growth factor receptor inhibitors (VEGFRis) are a class of tyrosine kinase (TKIs) used to treat human and canine cancers, but these drugs also cause hypertension (HTN) cell (EC) dysfunction. Purpose: We combined phosphoproteomic analysis in ECs with cross-species in-vitro in-vivo approach identify mitigating therapies for VEGFRi-induced EC dysfunction HTN. Methods Results: developed sorafenib-induced HTN mouse model showing increased blood pressure,...
Abstract BACKGROUND Vascular endothelial growth factor receptor inhibitors (VEGFRis) improve cancer patient survival by inhibiting tumor angiogenesis. However, VEGFRis induce treatment-limiting hypertension which has been associated with impaired vascular cell (EC) function and kidney damage. The mineralocorticoid (MR) regulates blood pressure (BP) via its effects on the vasculature kidney. Thus, we interrogated role of MR in EC dysfunction, renal impairment, a mouse model VEGFRi-induced...
Abstract Pancreatic ductal adenocarcinoma (PDAC) is currently the fourth-leading cause of cancer-related death in United States and projected to become second leading by 2030. Most patients present with advanced disease die within 12 months diagnosis. Recent genomic studies primary pancreatic cancer resection specimens have identified several molecular alterations subtypes that may guide precision medicine approaches clinical management. However, landscape metastatic PDAC has been less well...
Abstract Although lung adenocarcinomas frequently metastasize to the brain, treatment options for adenocarcinoma brain metastases are limited. We discovered novel candidate drivers of progression by using case-control analyses compare whole-exome sequencing data from a cohort 73 control 503 primary adenocarcinomas. identified 3 genomic regions with significantly more frequent amplifications in compared cohort: MYC (12% vs 6%), YAP1 (7% 0.8%) and MMP13 (10% 0.6%). also CDKN2A/B as region...
<p>MAF file for copy number variations identified in the cohort</p>
<p>Supplementary Figure S1: Overview of workflow and data generation. Supplementary S2: Analysis neoplastic cellularity. S3: Recurrent copy number alterations. S4: Mutational signature analysis. S5: PDAC gene expression signatures. S6: Clinically relevant alterations in the cohort.</p>
<p>MAF file for mutations identified in the cohort</p>
<p>Supplementary Experimental Methods</p>