Morphological and immunophenotypic variations in malignant melanoma

A variety of cytomorphological features, architectural patterns and stromal changes may be observed in malignant melanomas. Hence, melanomas may mimic carcinomas, sarcomas, benign stromal tumours, lymphomas, plasmacytomas and germ cell tumours. Melanomas may be composed of large pleomorphic cells, small cells, spindle cells and may contain clear, signet-ring, pseudolipoblastic, rhabdoid, plasmacytoid or balloon cells. Various inclusions and phagocytosed material may be present in their cytoplasm. Nuclei may show bi- or multi-nucleation, lobation, inclusions, grooving and angulation. Architectural variations include fasciculation, whorling, nesting, trabeculation, pseudoglandular/pseudopapillary/pseudofollicular, pseudorosetting and angiocentric patterns. Myxoid or desmoplastic changes and very rarely pseudoangiosarcomatous change, granulomatous inflammation or osteoclastic giant cell response may be seen in the stroma. The stromal blood vessels may exhibit a haemangiopericytomatous pattern, proliferation of glomeruloid blood vessels and perivascular hyalinization. Occasionally, differentiation to nonmelanocytic structures (Schwannian, fibro-/myofibroblastic, osteocartilaginous, smooth muscle, rhabdomyoblastic, ganglionic and ganglioneuroblastic) may be observed. Typically melanomas are S100 protein, NKIC3, HMB-45, Melan-A and tyrosinase positive but some melanomas may exhibit an aberrant immunophenotype and may express cytokeratins, desmin, smooth muscle actin, KP1 (CD68), CEA, EMA and VS38. Very rarely, neurofilament protein and GFAP positivity may be seen.     

Expression of the neural cell adhesion molecule (CD56) by human myeloma cells.

Recent studies in multiple myeloma indicate that molecules associated with different haematopoietic lineages may be expressed aberrantly by myeloma cells. In order to investigate this phenomenon further, we studied the immunophenotype of bone marrow cells from 21 patients with multiple myeloma using a panel of monoclonal antibodies against T,B, myelomonocytic, and natural killer (NK)-cell antigens. Leu-19/NKH1 (CD56), a molecule identical to N-CAM, which is normally expressed by neuroectodermal and NK cells, was found in 13 patients (62%). Dual-parameter flow cytometry was used to correlate N-CAM positivity with DNA aneuploidy or cytoplasmic immunoglobulin expression as markers of myeloma cells. When N-CAM was found positive, other haematopoietic antigens were expressed only in three out of 13 cases (23%). In contrast, myeloma cells not expressing N-CAM frequently exhibited pre-B cell markers, myeloid antigen, and HLA-DR, respectively (seven out of eight cases, 88%). Six out of eight N-CAM-negative myelomas were of the IgG lambda isotype, otherwise no clearcut association with basic clinical and laboratory parameters was noted. We conclude that N-CAM expression is a common finding in multiple myeloma. Whether its expression and the observed antigenic heterogeneity is just a manifestation of malignancy or N-CAM may play a role in the biology of multiple myeloma regarding tumour cell spread, remains to be explained.     

后肾腺瘤临床病理及免疫组化观察分析

目的 探讨后肾腺瘤(metanephrie adenoma,MA)的病理特征及鉴别诊断方法.方法 应用常规病理、免疫组化方法观察本所近年诊断的2例MA手术切除标本,结合相关临床资料(从病史中摘取)分析其病理特点.结果 2例大体均为类圆形厌白色肿块,大小各约1、4 cm,有薄层包膜,与周同组织分界清楚.组织学上具有独特的形态结构特点:瘤细胞较小,核大质少,无异型性,呈规则的小管、小团状及肾小球样等结构排列.免疫组化分析:Vimentin阳性,WT1阳性或部分阳性,CK灶性阳性,CD57有1例散在和小灶性阳性,另1例片状强刚性,EMA、CK7、CgA、CD10均为阴性.2例均发生于中老年女性,其中1例在同一肾脏的另一部位还有肾细胞癌.结论 作为WHO分类中一种少见的良性肾肿瘤类型,MA在形态学上具有独特的组织结构特点,免疫表型表现为WT1、CD57、Vimentin、CK多有表达,其中Vimentin恒定出现,WT1、ED57、CK表达强度和范围各有小同,而EMA、CK7、CgA、CD10多无表达;要注意与Wlims瘤、肾乳头状细胞癌、后肾腺纤维瘤等进行鉴别.     

急性白血病患者免疫学表型分析

采用间接免疫荧光技术对４９例急性白血病患者进行免疫学表型分析，结果为２４例急性淋巴细胞白血病（ＡＬＬ）中，共发现Ｔ－ＡＬＬ和Ｃ－ＡＬＬ各８例，Ｎ－ＡＬＬ６例，前Ｂ－ＡＬＬ和Ｂ－ＡＬＬ各１例；２５例急性非淋巴细胞白血病中，有２例Ｍ-４和３例Ｍ-５表达ＣＤ-（１４）。２４例ＡＬＬ均不表达ＣＤ-（１３）或ＣＤ-（３３）。     

The immunophenotype of T-lymphoblastic lymphoma in children and adolescents: a Children's Oncology Group report

T-lymphoblastic leukaemia (T-ALL) and T-lymphoblastic lymphoma (T-LBL) are neoplasms derived from immature lymphoid cells of T-cell lineage. These neoplasms are biologically similar, but significant differences may exist between the two given their clinical differences. Although ample data regarding the immunophenotypic characterization T-ALL are available, there is a paucity of such data in children and adolescents with T-LBL. We used flow cytometry and/or immunohistochemistry to characterize the immunophenotypic profile of 180 children and adolescents with newly diagnosed T-LBL enrolled in the Children's Oncology Group 5971 study. Multiple T-cell, B-cell, myeloid, and other markers were evaluated. We identified diagnostically useful immunophenotypic features of T-LBL as well as distinct immunophenotypic subgroups, although none of these was statistically related to event-free or overall survival in this retrospective analysis. Further studies of biologically and immunophenotypically distinct subgroups of T-LBL, such as the early T-cell precursor phenotype, are warranted.