关键词: adenoid cystic carcinoma ktn1-prkd1 myb-nf1b polymorphous adenocarcinoma ppp2r2a::prkd1 salivary duct carcinoma salivary gland tumors

来  源:   DOI:10.7759/cureus.61639   PDF(Pubmed)

Abstract:
Salivary gland tumors (SGT) encompass a wide range of neoplasms, each with its own unique histological type and clinical presentation. This review hones in on prevalent subtypes of SGTs, including adenoid cystic carcinoma (ACC), salivary duct carcinoma (SDC), and polymorphous adenocarcinoma (PAC). The articles, identified through specific keywords, were meticulously screened in databases like PubMed, Scopus, Google Scholar, and Web of Science from 2018 to 2023. Eight articles delved into genetic modifications among the selected SGT types. A fusion protein known as MYB-NF1B is typically associated with ACC, promoting cell proliferation while inhibiting apoptosis. The presence of MYB modifications in ACCs is a beacon of hope, as it is linked to a more favorable prognosis. In contrast, SDCs often exhibit HER2 expression. The invasive nature of SGTs contributes to their resistance to treatment. In the case of PAC, the role of PRKD1 is particularly noteworthy. PRKD1, integrated with other genes from the PRKD1/2/3 cluster, helps to differentiate PAC from other diseases. Furthermore, the genetic profiles of KTN1-PRKD1) and PPP2R2A:PRKD1 are distinct. The significant genetic variability among SGTs necessitates meticulous examination. This field is in a constant state of evolution, with new discoveries reshaping our understanding. Genetics is a key player in deciphering SGTs and tailoring treatments. This complex neoplasm demands ongoing research to uncover all genetic influences, thereby enhancing diagnostic methodologies, therapeutic strategies, and patient outcomes.
摘要:
唾液腺肿瘤(SGT)包括广泛的肿瘤,每个都有自己独特的组织学类型和临床表现。这篇综述磨练了SGT的流行亚型,包括腺样囊性癌(ACC),涎管癌(SDC),和多形性腺癌(PAC)。文章,通过特定关键字识别,在PubMed等数据库中精心筛选,Scopus,谷歌学者,和WebofScience从2018年到2023年。八篇文章深入研究了所选SGT类型之间的遗传修饰。一种称为MYB-NF1B的融合蛋白通常与ACC相关,促进细胞增殖,同时抑制细胞凋亡。ACC中MYB修改的存在是希望的灯塔,因为它与更有利的预后有关。相比之下,SDC通常表现出HER2表达。SGT的侵入性有助于它们对治疗的抗性。在PAC的情况下,PRKD1的作用尤其值得注意。PRKD1,与PRKD1/2/3簇的其他基因整合,有助于区分PAC与其他疾病。此外,KTN1-PRKD1)和PPP2R2A:PRKD1的遗传图谱不同。SGT之间的显着遗传变异性需要细致的检查。这个领域处于不断发展的状态,新的发现重塑了我们的理解。遗传学是破译SGT和定制治疗的关键参与者。这种复杂的肿瘤需要持续的研究来揭示所有的遗传影响,从而增强诊断方法,治疗策略,和患者结果。
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