A5042265453- Cancer Genomics and Diagnostics
- Gastric Cancer Management and Outcomes
- Pancreatic and Hepatic Oncology Research
- Lung Cancer Treatments and Mutations
- Esophageal Cancer Research and Treatment
- Colorectal Cancer Treatments and Studies
- Metastasis and carcinoma case studies
- Radiomics and Machine Learning in Medical Imaging
- Cancer Immunotherapy and Biomarkers
- Genetic factors in colorectal cancer
- Gastrointestinal Tumor Research and Treatment
- DNA Repair Mechanisms
- Genetics and Neurodevelopmental Disorders
- Cancer, Lipids, and Metabolism
- Acute Myeloid Leukemia Research
- Fibroblast Growth Factor Research
- Ferroptosis and cancer prognosis
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Oral and gingival health research
- Blood groups and transfusion
- Neuroblastoma Research and Treatments
- Colorectal and Anal Carcinomas
- Medical Imaging Techniques and Applications
- Histiocytic Disorders and Treatments
- Renal Diseases and Glomerulopathies
Memorial Sloan Kettering Cancer Center
2015-2025
Cornell University
2019-2024
Kettering University
2020
Marshfield Clinic
2009-2013
St. Luke's-Roosevelt Hospital Center
2006-2012
The watch-and-wait (WW) strategy aims to spare patients with rectal cancer unnecessary resection.To analyze the outcomes of WW among who had a clinical complete response neoadjuvant therapy.This retrospective case series analysis conducted at comprehensive center in New York included received diagnosis adenocarcinoma between January 1, 2006, and 31, 2015. median follow-up was 43 months. Data analyses were from June 2016, October 2018.Patients after completing therapy agreed active...
Genomic methods can identify homologous recombination deficiency (HRD). Rigorous evaluation of their outcome association to DNA damage response-targeted therapies like platinum in pancreatic ductal adenocarcinoma (PDAC) is essential maximizing therapeutic outcome.
<title>Abstract</title> Detection of circulating tumor DNA (ctDNA) signals the presence occult residual disease following complete surgical resection a and identifies patients at high risk for recurrence. This study aimed to evaluate whether highly effective therapy, such as PD-1 blockade in mismatch repair deficient (MMRd) tumors, could reduce recurrence ctDNA positive curative intent surgery. To test this hypothesis, we designed prospective identify who were tumors investigate course would...
Subset analyses from phase III evaluation of epidermal growth factor receptor inhibition (EGFRi) suggest improved outcomes in patients with EGFR-amplified gastroesophageal adenocarcinoma (GEA), but large-scale are lacking. This multi-institutional analysis sought to determine the role EGFRi largest cohort GEA date.A total 60 15 tertiary cancer centers six countries met inclusion criteria. These criteria required histologically confirmed metastatic or unresectable setting EGFR amplification...
To determine the safety and efficacy of adding anti-PD-L1 antibody durvalumab to induction FOLFOX preoperative chemotherapy in locally advanced esophageal adenocarcinoma.
Abstract Purpose: Targeted therapies have improved outcomes for patients with metastatic colorectal cancer, but their impact is limited by rapid emergence of resistance. We hypothesized that an understanding the underlying genetic mechanisms and intrinsic tumor features mediate resistance to therapy will guide new therapeutic strategies ultimately allow prevention Experimental Design: assembled a series 52 paired pretreatment progression samples who received targeting EGFR (n = 17), BRAF...
Importance Clonal hematopoiesis (CH) has been associated with development of atherosclerosis and leukemia worse survival among patients cancer; however, the association cancer therapy efficacy, in particular immune checkpoint blockade (ICB), toxicity not yet established. Given widespread use ICB critical role hematopoietic stem cell–derived lymphocytes play mediating antitumor responses, CH may be therapeutic efficacy hematologic toxicity. Objective To determine between outcomes, toxicity,...
Histiocytic sarcoma (HS) is a very rare hematopoietic neoplasm that has been reported in association with other hematological malignancies. Presentation of HS the central nervous system even less common. Diagnosis requires presence histiocytic markers and systematic exclusion cell lineages. Primary tumors are aggressive generally have poor outcomes. There no standard treatment guidelines due to lack clinical trials limited number case reports. Here we present unique two primary lesions...
Abstract Purpose: VEGFR2-directed therapy is commonly used to treat metastatic esophagogastric cancer, but disease progresses in most patients within months. Therapeutic resistance likely mediated part by co-occurring amplifications of the genes for multiple oncogenic receptor tyrosine kinases (RTK). We therefore tested efficacy combined inhibition VEGFR1-3, PDGFα/β, and FGFR1-3 using nintedanib. Patients Methods: with adenocarcinoma progression on first-line chemotherapy were treated...
Satya S. Bhupathi, MD, MPH*, Sreelatha Chalasani, MPH* and Roxann Rokey, FACC, FASE† Department of General Internal Medicine, Marshfield Clinic, Marshfield, Wisconsin USA Cardiology, Corresponding Author: MPH, 1000 North Oak Avenue, WI 54449, Tel.: 715-387-5537, Fax: 715-389-5757, E-mail: chalasani.sreelatha{at}marshfieldclinic.org
4132 Background: HRD is an emerging biomarker for platinum therapy in PDAC. The clinical implications regarding differences outcome between germline and somatic advanced PDAC treated with 1L unexplored. Methods: We evaluated overall survival (OS) (stage III/IV) based on their pathogenic (gHRD) (sHRD) using integrated genomic profiling from MSK-IMPACT use. defined by alterations the following genes: BRCA1/2, PALB2, ARID1A/B/2, ATR, ATRX, ATM, BAP1, RAD50/51C/D, BRIP1, NBN, CHECK1/2, FANCA/C,...
Abstract Background Angiogenesis is critical to gastroesophageal adenocarcinoma growth and metastasis. Regorafenib a multikinase inhibitor targeting angiogenic stromal receptor tyrosine kinases. We evaluated whether regorafenib augments the antitumor effect of first-line chemotherapy in metastatic esophagogastric cancer. Materials Methods Patients with previously untreated received 5-fluorouracil, leucovorin, oxaliplatin (mFOLFOX6) every 14 days 160 mg daily on 4 10 each 14-day cycle. The...
4029 Background: Induction FOLFOX followed by PET-directed CRT prior to surgery demonstrated positive results in the CALGB 80803 study. We investigated safety and efficacy of adding D, an anti-PD-L1 antibody, CRT. Methods: Patients (pts) with locally advanced esophageal/GEJ adenocarcinoma were enrolled. Pts received 2 cycles mFOLFOX6 repeat PET/CT. PET responders (≥35% reduction SUV (PETr)) 5-FU/capecitabine oxaliplatin RT 50.4Gy, while induction non-responders (PETnr) carboplatin/paclitaxel...
Sreelatha Chalasani, MD, MPH, Hemender Singh Vats, Tarit K. Banerjee, FACP and Alan McKenzie, MD Department of General Internal Medicine, Marshfield Clinic, 1000 North Oak Avenue, Marshfield, Wisconsin 54449 FACP, Hematology/Oncology, Endocrinology, Reprint Requests: WI 54449, Tel: 715-387-5537, Fax: 715-389-3808, E-mail: vats.hemender{at}marshfieldclinic.org
226 Background: Based on the positive results of CALGB 80803 study (J Clin Oncol 2017;35:1 [abstr]), we have added D to induction FOLFOX and pre-op CRT. Methods: Patients (Pts) had T any N+ or T3-4N M0 esophageal Siewert Type I-III GEJ adenocarcinoma staged by EUS, PET/CT CT. Pts received mFOLFOX6 ×2 prior repeat PET/CT. PET responders (PETr) 5-FU capecitabine oxaliplatin with RT 50.4Gy, while non-responders (PETnr) carboplatin/paclitaxel RT. All 1,500 mg q4W starting 2 wks during...
4053 Background: REGO is a VEGFR2, FGFR2 and PDGFR small-molecule inhibitor with survival benefit in metastatic colorectal cancer. We performed phase II trial of first-line FOLFOX+REGO EG Methods: Patients (pts) previously untreated adenocarcinoma measurable or evaluable disease received mFOLFOX6 q14d oral 160 mg daily on days 4 to10 18 to 24 q28d. The primary objective was improve historical 6-month progression-free (PFS) from 40% 61% REGO. With target accrual 36 pts 5% type I error rate,...
Sreelatha Chalasani, MD*, Shankar S. Bettadahalli, MD†, Satya V. Bhupathi, MD* and Vijay H. Aswani, MD, PhD‡⇑ *Department of Internal/Hospital Medicine, Marshfield Clinic, Marshfield, Wisconsin, USA †Department Endocrinology, ‡Department Internal Medicine & Pediatrics (Med/Peds), Corresponding Author: PhD, Department Pediatrics, 1000 North Oak Avenue, Mail stop: 1F3, WI 54449 USA, Tel: 715-387-5600, Fax: 715-389-3322, Email: aswani.vijay{at}marshfieldclinic.org
e15791 Background: Tumors with mismatch repair-deficiency (MMRD) have a high mutational burden and good responses to immunotherapy (Le, NEJM, 2015). We describe the natural course, clinicopathological, genomic status of MMRD PDAC patients (pts) at Memorial Sloan Kettering Cancer Center (MSKCC). Methods: MSKCC institutional registry ICD billing database queried from 2006-2016 for pts genetically confirmed mutations in repair (MMR) genes. Mutation # determined via MSK-IMPACT, targeted tumor...
Abstract Background: Not infrequently, an apparent second pancreas ductal adenocarcinoma (PDAC) is identified either synchronously or metachronously. To date, it remains unclear whether these individual PDACs represent intrapancreatic metastases a new primary PDAC. Here, we sought to understand the clinicogenomic features of this patient population provide insights on underlying biology and management implications. Methods: Memorial Sloan Kettering Cancer Center (MSK) institutional databases...
<div>AbstractPurpose:<p>Targeted therapies have improved outcomes for patients with metastatic colorectal cancer, but their impact is limited by rapid emergence of resistance. We hypothesized that an understanding the underlying genetic mechanisms and intrinsic tumor features mediate resistance to therapy will guide new therapeutic strategies ultimately allow prevention resistance.</p>Experimental Design:<p>We assembled a series 52 paired pretreatment progression...
<p>Supplementary tables and figures</p>
<div>AbstractPurpose:<p>Targeted therapies have improved outcomes for patients with metastatic colorectal cancer, but their impact is limited by rapid emergence of resistance. We hypothesized that an understanding the underlying genetic mechanisms and intrinsic tumor features mediate resistance to therapy will guide new therapeutic strategies ultimately allow prevention resistance.</p>Experimental Design:<p>We assembled a series 52 paired pretreatment progression...
<p>Supplementary tables and figures</p>