推定的癌症干细胞(CSC)标记已经从黑色素瘤小鼠和体外模型中出现,但它们在石蜡包埋的患者样本中的表达相对于临床结果仍未被研究。而不是肿瘤块的细胞,可以想象,CSC驱动肿瘤进展。因此,完全根除可防止黑色素瘤复发.因为肿瘤细胞增殖升高是侵袭性疾病的既定指标,本研究旨在探讨黑色素瘤复发与假定的表达CD271,CD166或CD20的CSC增殖之间的相关性.此外,在奈维研究了这些标记的表达,黑色素瘤,和他们的复发。在黑色素瘤患者中,30例复发(病例)和30例无复发(对照)的肿瘤厚度相匹配,溃疡,克拉克级别,子类型,site,性别,和年龄。患者的一个石蜡包埋切片\'原发性黑色素瘤(n=60),复发(n=21),和痣(n=17)的Ki-67/MART1免疫组织化学双重染色和CD271,CD166和CD20的单一染色。他们的整个幻灯片图像被对齐为虚拟四重染色。图像分析确定了每个推定的干细胞标志物和肿瘤体积的增殖指数,以及肿瘤区域和表皮中的标志物百分比水平。在病例与对照中,中位真皮增殖指数(无/mm2)CD271为211vs103(p=0.04),CD166为512vs227(p=0.3),CD20为184vs97(p=0.3),肿瘤体积为95vs103(p=0.6)。额外的兴趣,表皮CD271+角质形成细胞在痣中总计8.8%,在黑色素瘤中总计0.98%(p=0.0007)。即使在表皮(p=0.002)和真皮(p=0.006)中CD166也观察到痣和黑色素瘤之间的差异,它们在视觉上不太明显。CD20+MART1+细胞在一半的黑色素瘤中缺失,还有所有的naevi和复发.总之,在这项特殊的病例对照研究中,高水平的CD271+Ki-67+MART1+细胞与黑色素瘤复发相关,而不是与常见的Ki-67指标相关.随着进一步的调查,这些细胞可能是潜在的治疗靶点。尤其是,表皮CD271+角质形成细胞的丢失似乎是黑色素瘤发展所必需的;因此,识别可以作为额外研究的诊断工具。
Putative cancer stem cell (CSC) markers have arisen from melanoma mouse and in vitro models, but their expression in paraffin embedded patient samples relative to clinical outcome remains largely unexplored. Rather than cells of the tumour bulk, conceivably, CSC drive tumour progression. Accordingly, complete eradication may prevent melanoma relapse. Because elevated tumour-cell proliferation is an established indicator of aggressive disease, this study aimed to investigate the correlation between melanoma recurrence and proliferation of putative CSC that express CD271, CD166, or CD20. Additionally, the expression of these markers was studied in naevi, melanomas, and their recurrence. In melanoma patients, 30 with relapse (cases) and 30 without (controls) were matched for tumour thickness, ulceration, Clark level, subtype, site, gender, and age. One paraffin-embedded section of the patients\' primary melanoma (n = 60), relapse (n = 21), and naevus (n = 17) were immunohistochemically double-stained for Ki-67/MART1 and single-stained for CD271, CD166, and CD20. Their whole slide images were aligned as virtual quadruple stains. Image analysis established proliferation indices of each putative stem cell marker and the tumour bulk in addition to the markers\' percentage level in tumour areas and the epidermis. In cases vs controls, median dermal proliferation indices (no./mm2) were 211 vs 103 (p = 0.04) for CD271, 512 vs 227 (p = 0.3) for CD166, 184 vs 97 (p = 0.3) for CD20, and 95 vs 103 (p = 0.6) for the tumour bulk. Of additional interest, epidermal CD271+ keratinocytes totalled 8.8% in naevi and 0.98% in melanomas (p = 0.0007). Even though differences between naevi and melanomas also were observed for CD166 in both the epidermis (p = 0.002) and dermis (p = 0.006), they were visually less apparent. CD20+MART1+ cells were absent in half of the melanomas, and all naevi and relapses. In conclusion, high levels of CD271+Ki-67+MART1+ cells were linked to melanoma relapse as opposed to common Ki-67 indices in this particular
case-control study. With further investigation, such cells could be potential targets of therapy. Especially, loss of epidermal CD271+ keratinocytes seemed necessary for melanoma development; hence, identification may serve as a diagnostic tool with additional research.