Locati Laura D, Perrone Federica, Cortelazzi Barbara, Lo Vullo Salvatore, Bossi Paolo, Dagrada Gianpaolo, Quattrone Pasquale, Bergamini Cristiana, Potepan Paolo, Civelli Enrico, Fallai Carlo, Pilotti Silvana, Licitra Lisa
Head and Neck Medical Oncology Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Laboratory of Experimental Molecular Pathology, Department of Pathology, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Head Neck. 2016 May;38(5):724-31. doi: 10.1002/hed.23940. Epub 2015 Jun 25.
Androgen deprivation therapy has some clinical activity in selected salivary gland cancer histotypes, with androgen receptor expression.
We retrospectively analyzed patients with androgen receptor-expressing recurrent/metastatic salivary gland cancer, treated with androgen deprivation therapy. Protein expression of androgen receptor and ErbB family members was investigated. Progression-free survival (PFS) and overall survival (OS) were the main endpoints.
Seventeen patients were identified. No significant toxicities were reported. Overall response rate was 64.7%; 3-year PFS and 5-year OS were 11.8% and 19.3%, respectively. Androgen receptor overexpression may be sustained by gain of chromosome X (58%) and TP53 mutation (44%). No association between response to androgen deprivation therapy and epidermal growth factor receptor (EGFR), human epidermal growth factor receptor (HER)2, HER3 expression, PIK3CA mutations, or phosphatase and tensin homolog (PTEN) deletion was identified.
We confirm the activity of androgen deprivation therapy in androgen receptor-expressing recurrent/metastatic salivary gland cancers. The hypothesis that an androgen receptor increased gene copy number may represent a possible mechanism of primary resistance should be further investigated.
雄激素剥夺疗法在某些具有雄激素受体表达的唾液腺癌组织类型中具有一定临床活性。
我们回顾性分析了接受雄激素剥夺疗法治疗的雄激素受体表达阳性的复发性/转移性唾液腺癌患者。研究了雄激素受体和表皮生长因子受体(ErbB)家族成员的蛋白表达。无进展生存期(PFS)和总生存期(OS)是主要终点。
共纳入17例患者。未报告明显毒性。总体缓解率为64.7%;3年PFS和5年OS分别为11.8%和19.3%。雄激素受体过表达可能由X染色体增益(58%)和TP53突变(44%)维持。未发现雄激素剥夺疗法的反应与表皮生长因子受体(EGFR)、人表皮生长因子受体(HER)2、HER3表达、PIK3CA突变或磷酸酶和张力蛋白同源物(PTEN)缺失之间存在关联。
我们证实了雄激素剥夺疗法在雄激素受体表达阳性的复发性/转移性唾液腺癌中的活性。雄激素受体基因拷贝数增加可能代表原发性耐药的一种可能机制这一假设应进一步研究。