Radiation-induced esophagitis is a common toxicity of radiation therapy of the chest, characterized by disruption of the epithelium due to damage to the underlying basal cells. The frequency of radiation-induced esophagitis correlates with the dose of radiation the esophagus receives and the volume that is treated with that dose. Modern radiation techniques are decreasing the size of the treatment field, potentially reducing the incidence and severity of esophagitis; however, it remains an important concern in patients with lung cancer treated with chemoradiotherapy. The pathogenesis of esophagitis is similar to that of head and neck mucositis, but there have been very few trials of treatments for the prevention of radiation-induced esophagitis. Current research is limited to several natural products which have shown activity in small randomized trials. However, several agents are currently being tested in clinical trials for the treatment of radiation-induced esophagitis. A successful agent to reduce/prevent esophagitis may allow higher doses of radiation to be delivered to the cancer and increase the curability of localized lung cancer. This review highlights the current understanding and limitations of data in radiation-induced esophagitis and current and potential future approaches to treatment.
Novel drugs and continuous therapy have improved outcomes in patients with multiple myeloma (MM); however, current therapies are largely non-curative with diminishing durations of response with subsequent therapies. Cellular therapies including chimeric antigen receptor T (CAR-T) cells have started to illustrate deeper and longer durations of relapse in the relapsed/refractory population. Current research seeks to expand on the durability of response, novel combinations, and targets, as well as the timing of CAR-T cells in the treatment schema. This review summarizes the updates in cellular therapy for MM.
Abnormal activation of mesenchymal epithelial transition (MET) receptor tyrosine kinase is associated with oncogenesis. Various underlying mechanisms, including alteration, amplification, gene rearrangement, and exon skipping in the transcript account for abnormal MET signaling. One of the critical alterations in MET leading to non-small cell lung carcinoma (NSCLC) is MET exon 14 (METex14) skipping, a driver mutation, which accounts for approximately 3–4% of lung adenocarcinoma. METex14 skipping results in the formation of a functionally active and stable truncated receptor lacking the juxtamembrane regulatory domain responsible for MET ubiquitination. Several MET kinase inhibitors have been developed targeting MET receptors, and many are in clinical trials. The US Food and Drug Administration has recently approved capmatinib (Tabrecta; Novartis, Basel, Switzerland) for the treatment of NSCLC with METex14 skipping alteration. We review the current understanding of the implications of aberrant MET activation in NSCLC harboring METex14 skipping alteration, available diagnostic options, potential therapies in the pipeline, and the future clinical landscape for such alterations.
