Pawelek John M
Department of Dermatology and the Yale Cancer Center, Yale School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520-8059, USA.
Cell Adh Migr. 2007 Jan-Mar;1(1):2-6. Epub 2007 Jan 15.
Cutaneous malignant melanoma (CMM) begins in the epidermis as the clonal emergence of melanocytes having a deregulated mitotic cycle. In a manner not yet understood, some descendents of these cells loosen their adhesions in situ and migrate into the dermis, thus initiating the processes of invasion and metastasis. These cells look and act much like macrophage-melanoma hybrids created in the lab or arising in mice. But genetic proof for hybrids in human melanoma is still lacking. Nonetheless, should tumor cell hybridization account for the invasive phenotype, this would surely evoke new therapeutic approaches regarding mechanisms of cell fusion and hybrid-specific molecular signatures. Here are described some of the remarkable phenotypic similarities between experimental macrophage-melanoma hybrids and CMM. The results suggest that invasive and metastatic CMM might well arise through fusion and genomic hybridization between melanoma cells and migratory bone marrow-derived cells.
皮肤恶性黑色素瘤(CMM)起源于表皮,是有丝分裂周期失调的黑素细胞的克隆性出现。这些细胞的一些后代以一种尚不清楚的方式在原位松解其黏附并迁移至真皮,从而启动侵袭和转移过程。这些细胞的外观和行为很像在实验室中产生或在小鼠体内出现的巨噬细胞-黑色素瘤杂交细胞。但人类黑色素瘤中杂交细胞的遗传学证据仍然缺乏。尽管如此,如果肿瘤细胞杂交是侵袭性表型的原因,这肯定会引发关于细胞融合机制和杂交特异性分子特征的新治疗方法。本文描述了实验性巨噬细胞-黑色素瘤杂交细胞与CMM之间一些显著的表型相似性。结果表明,侵袭性和转移性CMM很可能是通过黑色素瘤细胞与迁移的骨髓来源细胞之间的融合和基因组杂交产生的。