Almonertinib as a neoadjuvant therapy for patients with a superior pulmonary sulcus tumor with activated EGFR mutation: A case report.

A superior pulmonary sulcus tumor, also known as a Pancoast tumor, invades tissues or organs at the entrance of the thorax, such as the brachial plexus, upper ribs, vertebrae, subclavian vessels and stellate ganglia. Induction concurrent chemoradiotherapy followed by radical surgical resection is the preferred treatment. The present study reported the case of a 52-year-old male who presented at Hubei Cancer Hospital, Tongji Medical College (Wuhan, Hubei) with left chest pain and an abnormal chest computed tomography scan showing a mass of 81x43 mm in the left upper chest wall that invaded the first, second and third anterior ribs.

G protein-coupled estrogen receptor (GPER) mediates NSCLC progression induced by 17β-estradiol (E2) and selective agonist G1.

Estrogen classically drives lung cancer development via estrogen receptor β (ERβ). However, fulvestrant, an anti-estrogen-based endocrine therapeutic treatment, shows limited effects for non-small cell lung cancer (NSCLC) in phase II clinical trials. G protein-coupled estrogen receptor (GPER), a third estrogen receptor that binds to estrogen, has been found to be activated by fulvestrant, stimulating the progression of breast, endometrial, and ovarian cancers.

Crosstalk between IGF-1R and other tumor promoting pathways.

Insulin-like growth factor 1 receptor (IGF-1R) is important in cancer pathogenesis and progression. While its signaling pathway is an interesting therapeutic target, recent clinical trials have exhibited limited effects; however, significant crosstalks between IGF- 1R and other signaling pathways have garnered increasing attention. These complex networks include interactions between IGF-1R and receptor tyrosine kinases (RTKs), including insulin receptor (IR), epidermal growth factor receptor (EGFR), vascular endothelial growth factor receptor (VEGFR), mesenchymal-epithelial transition factor (MET), platelet-derived growth factor receptor (PDGFR), and fibroblast growth factor receptor (FGFR).

Estrogen and insulin-like growth factor 1 synergistically promote the development of lung adenocarcinoma in mice.

Estrogen receptor (ER) and insulin-like growth factor-1 receptor (IGF-1R) signaling are implicated in lung cancer progression. Based on their previous findings, the authors sought to investigate whether estrogen and IGF-1 act synergistically to promote lung adenocarcinoma (LADE) development in mice. LADE was induced with urethane in ovariectomized Kunming mice.