Objective: To evaluate whether quantification of lung GGN shape is useful in predicting pathological categorization of lung adenocarcinoma and guiding the clinic. Methods: 98 patients with primary lung adenocarcinoma were pathologically confirmed and CT was performed preoperatively, and all lesions were pathologically ≤ 30 mm in size. On CT images, we measured the maximum area of the lesion’s cross-section (MA). The longest diameter of the tumor (LD) was marked with points A and B, and the perpendicular diameter (PD) was marked with points C and D, which was the longest diameter perpendicular to AB. and D, which was the longest diameter perpendicular to AB. We took angles A and B as big angle A (BiA) and small angle A (SmA). We measured the MA, LD, and PD, and for analysis we derived the LD/PD ratio and the BiA/SmA ratio. The data were analysed using the chi-square test, t-test, ROC analysis, and binary logistic regression analysis. Results: Precursor glandular lesions (PGL) and microinvasive adenocarcinoma (MIA) were distinguished from invasive adenocarcinoma (IAC) by the BiA/SmA ratio and LD, two independent factors (p = 0.007, p = 0.018). Lung adenocarcinoma pathological categorization was indicated by the BiA/SmA ratio of 1.35 and the LD of 11.56 mm with sensitivity of 81.36% and 71.79%, respectively; specificity of 71.79% and 74.36%, respectively; and AUC of 0.8357 (95% CI: 0.7558–0.9157, p < 0.001), 0.8666 (95% CI: 0.7866–0.9465, p < 0.001), respectively. In predicting the pathological categorization of lung adenocarcinoma, the area under the ROC curve of the BiA/SmA ratio combined with LD was 0.9231 (95% CI: 0.8700-0.9762, p < 0.001), with a sensitivity of 81.36% and a specificity of 89.74%. Conclusions: Quantification of lung GGN morphology by the BiA/SmA ratio combined with LD could be helpful in predicting pathological classification of lung adenocarcinoma.

Colorectal cancer (CRC) is one of the most common causes of cancer-associated death worldwide, and a rapid increase in the incidence and mortality of CRC h

Oxaliplatin is a first-line chemotherapeutic agent for cancer treatment, but the monotherapy effect is limited.Oxaliplatin-induced peripheral neurotoxicity (OIPN) is a dose-limiting clinical problem, leading to decreased quality of life or even treatment discontinuation. Fibroblast growth factor 1 (FGF1) was initially identified in the pituitary gland and the brain as a substance that promotes mitosis in fibroblasts, however, dysregulated FGF1 expression is associated with human pathologies, particularly cancer. Our study aimed to propose a combination therapeutic strategy to overcome the suboptimal efficacy and neurotoxic side effects of oxaliplatin monotherapy. We first performed transcriptomic sequencing and then constructed FGF1 knockdown and overexpression cell lines to elucidate FGF1's role in tumor progression and its impact on oxaliplatin's chemotherapeutic effect. Furthermore, behavioral experiments in tumor-bearing mice and transmission electron microscopy (TEM) of sciatic nerves were used to evaluate the role of FGF1 in OIPN. Finally, mechanistic studies using Western blotting (WB) and immunohistochemistry (IHC) elucidated the molecular pathways regulated by FGF1. Our study found that FGF1 expression was increased in hepatocellular carcinoma and lung cancer cells and the dorsal root ganglia (DRG) of tumor-bearing mice after oxaliplatin treatment. FGF1 overexpression promoted tumor growth and exacerbated neuronal damage. Conversely, knockdown of FGF1 not only enhanced the anti-tumor efficacy of oxaliplatin but also markedly reduced oxaliplatin-induced neurotoxicity. Mechanistic investigations revealed that FGF1 promotes cancer progression and exacerbates neurological damage by acting on the FGFR pathway. Strikingly, the combination of oxaliplatin and FGFR inhibitors inhibited tumor growth to a greater extent and provided obvious relief from the neurotoxicity produced by oxaliplatin. FGF1 promotes tumor progression and impairs oxaliplatin's therapeutic efficacy by activating the FGFR signaling pathway, while also inducing neuropathic injury. Notably, combining oxaliplatin with FGFR inhibitors enhances antitumor efficacy and alleviates oxaliplatin-induced peripheral neuropathy (OIPN) symptoms.

The mitochondrial transcription elongation factor (TEFM) is a pivotal regulator of mitochondrial DNA (mtDNA) replication and transcription. While cytoplasm