Publications by authors named "Asha Dhanarajan"

Introduction: We present a case report of hearing loss in a patient with Waldenstrom macroglobulinemia (WM) receiving treatment with bortezomib.

Case Presentation: Our patient developed sudden bilateral sensorineural hearing loss after receiving three doses of bortezomib. His hearing loss was irreversible and resulted in a cochlear implant.

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Background And Objective: Gastric cancer is the fifth most common cancer worldwide and the fourth leading cause of cancer-related death. Unfortunately, patients often present with advanced disease at diagnosis, which is directly related to its high mortality. Numerous trials, as early as the 1980's, have shown that cytotoxic chemotherapy improves survival.

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Lenvatinib is a clinically effective multikinase inhibitor approved for first-line therapy of advanced hepatocellular carcinoma (HCC). Although resistance against lenvatinib often emerges and limits its antitumor activity, the underlying molecular mechanisms involved in endogenous and acquired resistance remain elusive. In this study, we identified focal adhesion kinase (FAK) as a critical contributor to lenvatinib resistance in HCC.

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Background: Liver tumors are commonly encountered in oncology. The study aimed to assess the impact of magnetic resonance imaging (MRI)-guided stereotactic body radiation therapy (SBRT) (MRgSBRT) on disease-related outcomes and the toxicity profile.

Methods: Patients who received MRgSBRT from 2019 to 2021 for primary and metastatic liver tumors were included in this analysis.

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Purpose Of Review: Multiple new tyrosine kinase inhibitors, immunotherapies and anti-angiogenic therapies are now available for the treatment of advanced hepatocellular carcinoma (HCC). In this article, we reviewed the evidence supporting these new therapies.

Recent Findings: The combination of atezolizumab and bevacizumab has become a new standard of care for initial systemic therapy in eligible patients, replacing sorafenib in the first line for many patients.

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Lenvatinib is a multikinase inhibitor approved as a first-line therapy for advanced hepatocellular carcinoma (HCC). However, the development of drug resistance is common, and the underlying mechanisms governing this resistance are largely unknown. In this study, we established two lenvatinib-resistant (LR) HCC cell lines and identified integrin subunit beta 8 (ITGB8) as a critical contributor to lenvatinib resistance in HCC.

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Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer and cancer-related mortality worldwide. Studies have suggested that aspirin (ASA) and statins may be associated with a decrease in incident HCC.

Goals: We aimed to evaluate the effect of ASA and statin use on the incidence of HCC in a prospective cohort of patients with liver cirrhosis and to identify if there was an increased risk of esophageal variceal hemorrhage (VH) in patients with ASA use.

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Hepatocellular carcinoma (HCC) remains one of the deadliest malignancies worldwide. One major obstacle to treatment is a lack of effective molecular-targeted therapies. In this study, we find that EphA2 expression and signaling are enriched in human HCC and associated with poor prognosis.

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Background & Aims: We investigated whether ABL proto-oncogene 1, non-receptor tyrosine kinase (ABL1) is involved in development of hepatocellular carcinoma (HCC).

Methods: We analyzed clinical and gene expression data from The Cancer Genome Atlas. Albumin-Cre (Hep) mice and mice with hepatocyte-specific disruption of Abl1 (Hep mice) were given hydrodynamic injections of plasmids encoding the Sleeping Beauty transposase and transposons with the MET gene and a catenin β1 gene with an N-terminal truncation, which induces development of liver tumors.

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There is an urgent need to understand the molecular signaling pathways that drive or mediate the development of hepatocellular carcinoma (HCC). The focal adhesion kinase (FAK) gene protein tyrosine kinase 2 is amplified in 16.4% of The Cancer Genome Atlas HCC specimens, and its amplification leads to increased FAK mRNA expression.

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