Surgery of enlarging lesions after stereotactic radiosurgery for brain metastases in patients with non-small cell lung cancer with oncogenic driver mutations frequently reveals radiation necrosis: case series and review.

In brain metastases, radiation necrosis (RN) is a complication that arises after single or multiple fractionated stereotactic radiosurgery (SRS/FSRS), which is challenging to distinguish from local recurrence (LR). Studies have shown increased RN incidence rates in non-small cell lung cancer (NSCLC) patients with oncogenic driver mutations (ODMs) or receiving tyrosine kinase inhibitors (TKIs). This study investigated enlarging brain lesions following SRS/FSRS, for which additional surgeries were performed to distinguish between RN and LR. We investigated seven NSCLC patients with ODMs undergoing SRS/FSRS for BM and undergoing surgery for suspicion of LR on MRI imaging. Descriptive statistics were performed. Among the seven patients, six were EGFR+, while one was ALK+. The median irradiation dose was 30 Gy (range, 20-35 Gy). The median time to develop RN after SRS/FSRS was 11.1 months (range: 6.3-31.2 months). Moreover, gradually enlarging lesions were found in all patients after 6 months post-SRS/FSR. Brain radiation necrosis was pathologically confirmed in all the patients. RN should be suspected in NSCLC patients when lesions keep enlarging after 6 months post-SRS/FSRS, especially for patients with ODMs and receiving TKIs. Further, this case series indicates that further dose reduction might be necessary to avoid RN for such patients.

Up-regulation of collagen type V alpha 2 (COL5A2) promotes malignant phenotypes in gastric cancer cell via inducing epithelial-mesenchymal transition (EMT).

Recent studies have reported that collagen type V alpha 2 (COL5A2) is a hub gene and associated with the prognosis of gastric cancer (GC) patients, playing an important role in GC. In this study, we aim to fathom out the biological roles of COL5A2 and its relevant mechanism in GC. Oncomine, gene expression profiling interactive analysis, and UALCAN were used to explore the effects of COL5A2 on GC. Cell counting kit-8 assay, colony formation assay, and transwell assay were conducted to investigate the biological behaviors of GC cell lines AGS and SGC-7901. Quantitative reverse transcription polymerase chain reaction and western blot were performed to determine gene and protein expressions. COL5A2 expression was up-regulated and negatively correlated with survival percentage of GC patients. COL5A2 expression was notably elevated in high stage and high grade of GC. Down-regulation of COL5A2 inhibited proliferation, migration, and invasion of AGS and SGC-7901 cells. COL5A2 induced epithelial-mesenchymal transition (EMT) by promoting the expressions of mesenchymal markers (SNAI1, SNAI2, TWIST, VIM, and MMP2), thereby facilitating the malignant phenotypes of GC. COL5A2 plays an oncogenic role in GC and has potential to predict the progression and prognosis of GC patients.