Arvind Dasari

Jan 8, 2025 | onclive.com | Arvind Dasari

CommentaryVideoJanuary 8, 2025Author(s):Arvind N. Dasari, MD, MS, discusses the roles for the FDA-approved agents fruquintinib and TAS-102 plus bevacizumab in the mCRC treatment paradigm.

Oct 11, 2024 | digitalcommons.library.tmc.edu | Timothy E. Newhook |Michael J. Overman |Yun Shin Chun |Arvind Dasari

OBJECTIVE: To evaluate the association of perioperative ctDNA dynamics on outcomes after hepatectomy for CLM. SUMMARY BACKGROUND DATA: Prognostication is imprecise for patients undergoing hepatectomy for CLM, and ctDNA is a promising biomarker. However, clinical implications of perioperative ctDNA dynamics are not well established.

Oct 11, 2024 | digitalcommons.library.tmc.edu | Benny Johnson |Van Morris |Xuemei Wang |Arvind Dasari

Although V600E accounts for the majority of the BRAF mutations in metastatic colorectal cancer (mCRC), non-V600 BRAF variants have been shown in recent years to represent a distinct molecular subtype. This study provides a comprehensive profile of BRAF variants in mCRC using a large genomic database of circulating tumor DNA (ctDNA) and analyzing clinical outcomes in a cohort of patients with atypical (non-V600) BRAF variants (aBRAF; class II, class III, unclassified).

Aug 30, 2024 | onclive.com | Arvind Dasari

Arvind N. Dasari, MD, MS, associate professor, the Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, discusses later-line therapies considerations in unresectable metastatic colorectal cancer (mCRC). Resistance to standard treatments including cytotoxic agents like 5-fluorouracil (5-FU), irinotecan, oxaliplatin, and targeted therapies like anti-BRAF, anti-HER2, and anti-EGFR agents is common in patients with unresectable mCRC, Dasari begins.

Aug 8, 2024 | cancernetwork.com | Scott Kopetz |Arvind Dasari |Jing Yi |Mackenzie Phillips

August 8, 2024By The panel examines challenges in interpreting circulating tumor DNA results and their impact on clinical decision-making processes. How do you factor ctDNA into treatment selection and management? How do you integrate ctDNA with radiographic or pathologic correlates? Are there challenges associated with the interpretation of ctDNA to inform your clinical decision-making? What do we know about sensitivity of ctDNA with different sites of metastatic disease?