Editorial: Impact of tumor microenvironment on lung cancer (original) (raw)

Editorial on the Research Topic Impact of tumor microenvironment on lung cancer Lung cancer is the leading cause of cancer-related mortality worldwide. In 2022 the Cancer Statistics Center calculated an estimated four new cases and one death per minute from lung cancer solely in the United States (http://cancerstatisticscenter.cancer.org). Lung cancer displays poor survival rates caused by recurrence and metastatic spreading. The anatomical and cellular features of healthy lungs that serve respiratory and defensive purposes, restructure during carcinogenesis to give rise to the tumor microenvironment (TME). This tumor-intermingled "organ" that acts in symbiosis with the cancer cells nourishes their aggressiveness and resistance (1), thus representing a target-rich milieu to hunt for anticancer options. Despite major efforts the complex pro-tumorigenic interactions occurring within the TME landscape (2, 3) are still substantially uncharted, thus precluding design of thoroughly eradicating strategies. Therefore, research must sturdily focus on discovering biomarkers to facilitate early diagnoses, improve clinical predictions and stratification parameters, as well as identifying new avenues to target cancer cells vulnerabilities and to modulate the protumorigenic TME. Within the TME, the immune infiltrating system and the stromal cells have emerged as therapeutic, diagnostic and prognostic tools in NSCLC (4-6). In this Research Topic, several novel biomarker signatures were presented, contributing to the ever-growing puzzle describing the entire complexity of pulmonary TMEs. A 14-TMErelated gene signature was identified to exhibit significant prognostic potential for patients affected by malignant pleural mesothelioma (MPMs), a rare but highly aggressive thoracic malignancy [Xu et al.]. Similarly, analyses from 450 NSCLC cases identified key immune cell types associated with recurrence of stage IA-B NSCLC within 40 months after surgical resection, contributing to develop an immune-related gene panel that predicts relapse-free survival (RFS) [Wang et al.]. Focusing on the immune-related genes differentially expressed in lung adenocarcinomas (LuADs) displaying high and low immune/stromal scores, Colony-stimulating factor 2 receptor beta (CSF2RB) was identified as a hub gene within LuAD-TMEs [Zhu et al.]. Low CSF2RB expression was associated with poor survival and CSF2RB was identified as an independent risk factor for prognosis, independent of whether patients received chemotherapy or radiotherapy. More importantly, a high expression of CSF2RB was related to early T, N, and clinical stages. Further studies are expected to Frontiers in Oncology frontiersin.org 01