Honma S, Tsukada S, Honda S, Nakamura M, Takakuwa K, Maruhashi T, Kodama S, Kanazawa K, Takahashi T, Tanaka K
Department of Obstetrics and Gynecology, Niigata University School of Medicine, Japan.
Int J Cancer. 1994 Jun 1;57(5):650-5. doi: 10.1002/ijc.2910570507.
To determine possible correlations between the selective loss of HLA-class-I allelic forms on neoplastic cells and their biological-clinical characteristics, 89 squamous-cell carcinomas of the uterine cervix were evaluated immunohistochemically using monomorphic and polymorphic antibodies against HLA-A, -B, and -C molecules and analyzed clinico-pathologically. Four of the carcinomas exhibited a lack of detectable class-I heavy-chain expression associated with beta 2-microglobulin. In 19 of 42 HLA-A2-positive patients, tumor cells revealed loss of the HLA-A2 allelic product. Loss of HLA-B7 and/or 40 (B7/40) allelic product(s) on tumor cells was observed in 12 of 25 HLA-B7/40-positive cases. These alterations did not correlate with patient age, clinical stage (FIGO) of the disease, histological sub-type (WHO) or depth of cervical invasion. However, a statistically significant correlation was observed between lymph-node metastases and selective loss of HLA-B7/40 allelic product(s), but not with HLA-A2 allelic product on cancer cells of the primary lesion. Our results indicate that selective loss of certain HLA-class-I alleles on neoplastic cells can influence the nodal metastatic potential and suggest that these 2 class-I molecules may have different immune functions as restriction elements in T-cell-mediated cytotoxicity.
为了确定肿瘤细胞上HLA - I类等位基因形式的选择性缺失与其生物学 - 临床特征之间可能存在的相关性,我们使用针对HLA - A、-B和 -C分子的单克隆和多克隆抗体,对89例子宫颈鳞状细胞癌进行了免疫组织化学评估,并进行了临床病理分析。其中4例癌表现出与β2 - 微球蛋白相关的可检测到的I类重链表达缺失。在42例HLA - A2阳性患者中的19例中,肿瘤细胞显示HLA - A2等位基因产物缺失。在25例HLA - B7/40阳性病例中的12例中,观察到肿瘤细胞上HLA - B7和/或40(B7/40)等位基因产物缺失。这些改变与患者年龄、疾病的临床分期(FIGO)、组织学亚型(WHO)或宫颈浸润深度均无相关性。然而,在淋巴结转移与HLA - B7/40等位基因产物的选择性缺失之间观察到具有统计学意义的相关性,但与原发性病变癌细胞上的HLA - A2等位基因产物无关。我们的结果表明,肿瘤细胞上某些HLA - I类等位基因的选择性缺失可影响淋巴结转移潜能,并提示这两种I类分子作为T细胞介导的细胞毒性中的限制元件可能具有不同的免疫功能。