Biomarker expression and druggable gene alterations for development of an appropriate therapeutic protocol for pulmonary adenosquamous carcinoma

Watanabe, Yukio; Shiraishi, Kouya; Takahashi, Fumiaki; Yoshida, Akihiko; Suzuki, Kenji; Asamura, Hisao; Takeuchi, Masahiro; Furuta, Koh; Tsuta, Koji

doi:10.1111/his.12556

Cited by 5 publications

(1 citation statement)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because EGFR mutation is the most common genomic anomaly in ASC, some studies ( 4 , 15 ) have focused on the efficiency of EGFR-TKIs in EGFR-positive ASC patients and found that ASC patients had similar efficacy to EGFR TKI compared with adenocarcinoma. Despite the presence of ALK-positive cases and molecular profiling studies of ASC ( 2 , 4 , 16 , 17 ), only a small number of ALK-TKI therapies for EML4-ALK fusion ASC patients have been reported ( 5 ), no non-classical ALK fusions have been reported in ASC. Echinoderm microtubule-associated protein-like 4 (EML4)-ALK is the canonical and most common ALK gene arrangement found in NSCLC, by which multiple EML4 breakpoints fuse in frame with the kinase domain of ALK ( 18 ).…”

Section: Discussionmentioning

confidence: 99%

Case report: Dramatic response to alectinib in a lung adenosquamous carcinoma patient harbouring a novel CPE-ALK fusion

Qin

Tan

et al. 2022

Front. Oncol.

View full text Add to dashboard Cite

Lung Adenosquamous carcinoma (ASC) is a rare histological subtype of lung cancer accounting for 0.4%–4% of all lung cancers. ASC is generally considered to be an aggressive cancer with poor prognosis. There is no specific standard treatment for ASC, and current treatment of ASC is relied on the guideline for non-small cell lung cancer (NSCLC). To date, only sporadic canonical EML4-ALK fusions have been reported in ASC patients, and the efficiency of ALK-TKI is still unclear in non-canonical ALK fusion positive ASC patients. Here we describe the case of a stage IV ASC patient harboring a novel CPE-ALK fusion detected via 74 genes panel analysis. Interestingly, the TP53 was wild-type and no another somatic mutation was found within 74 genes. In addition, immunohistochemical staining (IHC) also supports an oncogenic role for the CPE-ALK fusion. Based on these findings, the patient received alectinib 600 mg twice daily. After 4 months on treatment the patients achieved a radiological partial response (PR) and his symptoms were significantly relieved. Imaging showed that lesions of the patient were reduced, and the clinical evaluation was partial response (PR). To the best of our knowledge, this is the first report of a dramatic tumor response to alectinib in a patient with ASC harboring a CPE-ALK fusion. In addition, targeted NGS analysis may improve detection of ALK fusion in routine practice.

show abstract