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Article: ERBB2 mutation: A promising target in non-squamous cervical cancer

TitleERBB2 mutation: A promising target in non-squamous cervical cancer
Authors
Issue Date2018
Citation
Gynecologic Oncology, 2018 How to Cite?
AbstractOBJECTIVE: ERBB2 mutations have been found in a subset of invasive cervical cancer (ICC). Nevertheless, the prevalence, mutation spectrum, clinicopathological relevance, human papillomavirus (HPV)-genotype association and prognostic significance of ERBB2-mutated ICCs have not been well established. METHODS: In this study, ICC samples (N=1015) were assessed for mutations in ERBB2, KRAS, and PIK3CA by cDNA-based Sanger sequencing. RESULTS: Somatic ERBB2 mutations were detected in 3.15% patients. The ERBB2 mutation rate was significantly higher in adenocarcinoma (4.52%, 7/155), adenosquamous carcinoma (7.59%, 6/79) and neuroendocrine carcinoma (10.34%, 3/29) than that in squamous carcinoma (2.14%, 16/749) (P=0.004, Fisher exact test). In addition, 18.75% of the patients carrying ERBB2 mutations concomitantly harbored PIK3CA or KRAS mutations. Patients with ERBB2-mutated ICCs tended to have a worse prognosis than those with wild-type or PIK3CA-mutated ICCs but a better prognosis than those with KRAS-mutated ICCs. CONCLUSIONS: This study provided a promising rationale for the clinical investigation of tyrosine kinase inhibitors for the treatment of cervical cancer with ERBB2 mutations. Patients with non-squamous cell carcinomas have priority as candidates for ERBB2-targeted therapy. Concurrent PIK3CA/RAS mutations should be considered in the design of clinical trials.
Persistent Identifierhttp://hdl.handle.net/10722/250579
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXiang, L-
dc.contributor.authorJiang, W-
dc.contributor.authorYe, S-
dc.contributor.authorHe, T-
dc.contributor.authorPei, X-
dc.contributor.authorLi, J-
dc.contributor.authorChan, DW-
dc.contributor.authorNgan, HYS-
dc.contributor.authorLi, F-
dc.contributor.authorTao, P-
dc.contributor.authorShen, X-
dc.contributor.authorZhou, X-
dc.contributor.authorWu, X-
dc.contributor.authorYang, G-
dc.contributor.authorYang, H-
dc.date.accessioned2018-01-18T04:29:16Z-
dc.date.available2018-01-18T04:29:16Z-
dc.date.issued2018-
dc.identifier.citationGynecologic Oncology, 2018-
dc.identifier.urihttp://hdl.handle.net/10722/250579-
dc.description.abstractOBJECTIVE: ERBB2 mutations have been found in a subset of invasive cervical cancer (ICC). Nevertheless, the prevalence, mutation spectrum, clinicopathological relevance, human papillomavirus (HPV)-genotype association and prognostic significance of ERBB2-mutated ICCs have not been well established. METHODS: In this study, ICC samples (N=1015) were assessed for mutations in ERBB2, KRAS, and PIK3CA by cDNA-based Sanger sequencing. RESULTS: Somatic ERBB2 mutations were detected in 3.15% patients. The ERBB2 mutation rate was significantly higher in adenocarcinoma (4.52%, 7/155), adenosquamous carcinoma (7.59%, 6/79) and neuroendocrine carcinoma (10.34%, 3/29) than that in squamous carcinoma (2.14%, 16/749) (P=0.004, Fisher exact test). In addition, 18.75% of the patients carrying ERBB2 mutations concomitantly harbored PIK3CA or KRAS mutations. Patients with ERBB2-mutated ICCs tended to have a worse prognosis than those with wild-type or PIK3CA-mutated ICCs but a better prognosis than those with KRAS-mutated ICCs. CONCLUSIONS: This study provided a promising rationale for the clinical investigation of tyrosine kinase inhibitors for the treatment of cervical cancer with ERBB2 mutations. Patients with non-squamous cell carcinomas have priority as candidates for ERBB2-targeted therapy. Concurrent PIK3CA/RAS mutations should be considered in the design of clinical trials.-
dc.languageeng-
dc.relation.ispartofGynecologic Oncology-
dc.titleERBB2 mutation: A promising target in non-squamous cervical cancer-
dc.typeArticle-
dc.identifier.emailChan, DW: dwchan@hku.hk-
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hk-
dc.identifier.authorityChan, DW=rp00543-
dc.identifier.authorityNgan, HYS=rp00346-
dc.identifier.doi10.1016/j.ygyno.2017.12.023-
dc.identifier.hkuros284014-
dc.identifier.isiWOS:000425574100013-

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