Clinical and computed tomography characteristics of non‐small cell lung cancer with ALK gene rearrangement: Comparison with EGFR mutation and ALK/EGFR‐negative lung cancer

Abstract

Background The study was conducted to evaluate the clinical and computed tomography (CT) findings of non‐small cell lung cancer (NSCLC) patients to distinguish between ALK gene rearrangement, EGFR mutation, and non‐ ALK / EGFR (no genetic abnormalities). Methods We enrolled 201 patients with primary NSCLC who had undergone molecular testing for both ALK gene rearrangement and EGFR mutation. The clinical features and CT findings of the main lesion and associated pulmonary abnormalities were investigated. Results Female gender ( P = 0.0043 vs. non‐ ALK / EGFR ), young age ( P = 0.0156 vs. EGFR ), and a light or never smoking history ( P = 0.0039 vs. non‐ ALK / EGFR ) were significant clinical characteristics of NSCLC with ALK gene rearrangement. The significant CT characteristics compared to NSCLC with EGFR mutation were a large mass ( P = 0.0155), solid mass ( P = 0.0048), and no air bronchogram ( P = 0.0148). A central location ( P = 0.0322) and lymphadenopathy ( P = 0.0353) were also more frequently observed. Coexisting emphysema was significantly less frequent in NSCLC patients with ALK gene rearrangement ( P = 0.0135) than non‐ ALK / EGFR . Conclusions NSCLC with ALK gene rearrangement was more likely to develop in younger women with a light or never smoking history. The characteristic CT findings of NSCLC with ALK gene rearrangement were a large solid mass, less air bronchogram, a central location, and lymphadenopathy.

Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts

“…The association of immunohistochemical STIM1 staining with the clinicopathological parameters of the patients was analyzed using the χ [2] test with a P-value of <0.05 considered to indicate statistically significant differences. The other data were analyzed using Student's t-test, with P ≤ 0.05 considered statistically significant.…”

“…Human carcinogenesis predominantly involves a disordered balance of cell proliferation, differentiation and apoptosis. A number of studies have provided evidence supporting that altered Ca [2]+ signaling contributes to tumorigenesis and tumor progression [23,24]. STIM1, the Ca [2]+ storage sensor protein with a single transmembrane domain localized to the ER, is the key component of SOCE.…”

“…A number of studies have provided evidence supporting that altered Ca [2]+ signaling contributes to tumorigenesis and tumor progression [23,24]. STIM1, the Ca [2]+ storage sensor protein with a single transmembrane domain localized to the ER, is the key component of SOCE. Also, STIM1 is a key activator of store-operated channels (SOCs) that allow extracellular Ca [2]+ influx into cells [25].…”

“…STIM1, the Ca [2]+ storage sensor protein with a single transmembrane domain localized to the ER, is the key component of SOCE. Also, STIM1 is a key activator of store-operated channels (SOCs) that allow extracellular Ca [2]+ influx into cells [25]. The present study demonstrated that STIM1 was overexpressed in NSCLC tissues and the expression of STIM1 protein was associated with advanced NSCLC T stage.…”

“…Lung cancer is the leading cause of cancer-related mortality in both men and women worldwide [1]. Histologically, non-small-cell lung cancer (NSCLC) accounts for~80% of lung cancer cases and is a heterogeneous clinical entity with the major histological subtypes comprising squamous cell carcinoma, adenocarcinoma and largecell carcinoma [2]. The overall 5-year survival remains of NSCLC is poor, and evenfor patients with early-stage disease who undergocuratively intended surgery, the postoperative recur-rence rate is high compared to other types of cancer [3].…”