Biomedical subjects

Y Soini

Publications and source records attributed to Y Soini.

At least 127 records · Page 7Linked to original sources

PubMed1993

Tenascin immunoreactivity in normal and pathological bone marrow.

AIMS: To determine the distribution of tenascin in normal and pathological bone marrow. METHODS: 48 different bone marrow lesions were studied immunohistochemically using a monoclonal antibody to tenascin. RESULTS: Tenascin immunoreactivity was found in lesions with increased fibrosis and high numbers of reticular fibres. The strongest immunoreactivity was found in myelofibrosis. Bone marrow from acute and chronic myeloid and lymphatic leukaemias showed weak or moderate immunoreactivity. In hyperplasias inconsistent reticular tenascin immunoreactivity was found; in normal bone marrow, only a few scattered positive fibres were occasionally seen. CONCLUSIONS: Tenascin was generally observed in conditions in which megakaryocytic hyperplasia was a feature. This is in line with the notion that tenascin synthesis in bone marrow fibroblasts is stimulated by TGF-beta which is synthesised by the megakaryocytic lineage. Tenascin also contains EGF-like repeats. It might therefore function as a growth promoter and in this way could also stimulate synthesis of other matrix components. On the other hand, tenascin could function as an adhesive molecule to some cells of the bone marrow. The presence of tenascin in many pathological states of the bone marrow suggests that it may have a role in their pathogenesis and that it also could be a potential marker of disease.

Antibodies, Monoclonal↗

PubMed1993

Expression of 72 kilodalton and 92 kilodalton type IV collagenase in malignant fibrous histiocytomas and dermatofibromas.

BACKGROUND: In previous studies, it has been shown that the stromal cells of epithelial tumors are capable of synthesizing 72 and 92 kilodalton (kd) type IV collagenase mRNA. The mRNA synthesis of these collagenases in mesenchymal tumors has not been extensively studied, however. This study was undertaken to explore the synthesis of 72 and 92 kd type IV collagenase mRNAs in malignant and benign fibrous histiocytomas and its correlation with the known biologic behavior of these tumors. EXPERIMENTAL DESIGN: The synthesis of 72 kd and 92 kd type IV collagenase mRNA was studied in 10 malignant fibrous histiocytomas (MFHs) and 7 dermatofibromas using in situ hybridization methods. The tumors were also studied with a commercial monoclonal antibody to the 72 kd type IV collagenase. Additionally, three dermatofibromas were studied with an antibody to the 92 kd type IV collagenase. The media of three cell lines (MFH, dermatofibroma and skin fibroblast cell line) were also analyzed by zymography assay. RESULTS: The results revealed mRNA for the 72 kd and 92 kd collagenases in tumor cells of both MFHs and dermatofibromas. Also intracytoplasmic immunoreactivity for the 72 kd type IV collagenase could be seen in all the tumors. In the zymography assay, 72 kd type IV collagenase activity was detected in the culture media of all the cell lines tested, but activity for the 92 kd enzyme was only seen in the MFH. However, immunoreactivity for the antibody to the 92 kd type IV collagenase was also seen in dermatofibromas. CONCLUSIONS: The findings indicate that MFHs and dermatofibromas produce type IV collagenases. The synthesis of the mRNAs for both 72 kd and 92 kd type IV collagenase was quantitatively similar in MFHs and dermatofibromas indicating that there is no correlation between the biologic behavior of the tumors and the synthesis of these substances. Therefore, additional factors other than synthesis of type IV collagenases by tumor cells, must be involved in the process of spread and invasion of tumor cells into the neighbouring tissues.

Aged↗

PubMed1993

Concurrent p53 expression in bronchial dysplasias and squamous cell lung carcinomas.

We analyzed the p53 protein immunohistochemically in bronchial dysplasias or squamous cell carcinomas in situ and in squamous cell lung carcinomas occurring in the same patients. The polyclonal antibody used (CM-1) is directed against the wild-type p53 protein, but also recognizes the mutated p53 in formalin-fixed and paraffin-embedded sections. To study the integrity of basement membranes (BMs) and the possible invasion of the dysplastic epithelium, immunostainings for the BM proteins laminin and type IV collagen were used. Nine of the 17 dysplasias showed p53 protein expression (53%); it was significantly more often seen in severe dysplasias and carcinomas in situ than in mild or moderate dysplasias (P = 0.04). The p53 antigenicity was generally located in the basal part of the epithelium. The BMs beneath mildly dysplastic epithelia were continuous. In contrast, those under moderately or severely dysplastic epithelia showed occasional disruptions. p53 protein expression was also found in dysplastic epithelium above a continuous BM suggesting an ominous process before signs of invasion. Twelve of the 17 squamous cell carcinomas showed p53 protein expression (71%). There was a significant concurrent p53 expression in bronchial dysplasias and their related squamous cell carcinomas (P = 0.009), so that all nine cases of p53 positive bronchial dysplasia also showed p53 positivity in the associated squamous cell carcinomas. These findings indicate that p53 protein expression is possible in premalignant bronchial lesions, and suggests that the p53 expression could, at least in some cases, be an early event in the development of a squamous cell carcinoma of the lung.

Aged↗

PubMed1993

Genes of laminin B1 chain, alpha 1 (IV) chain of type IV collagen, and 72-kd type IV collagenase are mainly expressed by the stromal cells of lung carcinomas.

In this study, we analyzed the expression of messenger (m)RNAs for laminin B1 chain, alpha 1 (IV) chain of type IV collagen, and 72-kd type IV collagenase in 15 primary lung carcinomas and in two metastatic adenocarcinomas to the lung. The results show that the mRNA synthesis for these proteins mainly occurs in the stromal fibroblasts and endothelial cells. In a proportion of tumors, mRNAs for laminin B1 chain and 72-kd type IV collagenase could also be observed in carcinoma cells, but the amount of mRNAs was considerably lower in them than in the stromal cells. There were no convincing signals for the presence of the alpha 1 (IV) chain of type IV collagen mRNA in any of the carcinoma cells. A simultaneous expression or lack of expression of signals for laminin B1 chain and 72-kd type IV collagenase mRNAs could be observed in carcinoma cells of 12 cases, suggesting that the activation of these two genes may be somehow connected. There was no association between the mRNA expression and the differentiation degree or the size of the tumors. The occurrence of the mRNA synthesis for the 72-kd type IV collagenase in stromal fibroblasts and endothelial cells indicates that the stromal cells of tumors have a more pronounced impact on the spread of the neoplastic disease than previously thought. The results further show that in their ability to synthesize these proteins the stromal cells of tumors resemble those of developing embryonic tissues. This resemblance is probably connected with the constant remodeling of extracellular matrix in response to the proliferative activity of carcinoma cells.

Aged↗

PubMed1992

p53 immunohistochemistry in malignant fibrous histiocytomas and other mesenchymal tumours.

In this study we analysed by immunohistochemistry the expression of p53 protein in 14 malignant fibrous histocytomas (MFHs), 22 other types of sarcoma (eight leiomyosarcomas, four rhabdomyosarcomas, four liposarcomas, two fibrosarcomas, two chondrosarcomas, one malignant schwannoma, and one dermatofibrosarcoma protuberans), and 25 non-malignant mesenchymal lesions (eight dermatofibromas, four cases of nodular fasciitis, three leiomyomas, three fibromatoses, two epithelioid.leiomyomas, two neurofibromas, one schwannoma, one myositis ossificans, and one giant cell tumour of tendon sheath). Four MFHs and nine other types of sarcoma (four leiomyosarcomas, two chondrosarcomas, one liposarcoma, one fibrosarcoma, and one dermatofibrosarcoma protuberans) showed nuclear positivity for p53. Of the benign soft tissue lesions, p53 positivity was observed in two fibromatoses, one nodular fasciitis, and one dermatofibroma. The number of p53-positive cells in these benign lesions was considerably smaller than that in most of the p53-positive sarcomas. The p53 positivity in MFHs and other types of sarcoma indicates that p53 gene alterations may play a part in the neoplastic transformation of these tumours. The occurrence of p53 positivity in benign mesenchymal lesions suggests that sometimes p53 protein may accumulate in cells without an associated malignancy. Because of this, p53 immunoreactivity cannot, by itself, be used as a criterion of malignancy. According to our results, p53 positivity in over 1 per cent of tumour cells in mesenchymal lesions favours malignancy.

Genes, p53↗

PubMed1992

Low p53 protein expression in salivary gland tumours compared with lung carcinomas.

Fifty-one salivary gland tumours (23 pleomorphic adenomas, 5 Warthin's tumours, 12 mucoepidermoid carcinomas, 7 adenoid cystic carcinomas, 3 undifferentiated carcinomas and 1 acinic cell tumour) and 27 lung carcinomas (18 squamous cell carcinomas) were analysed immunohistochemically for the expression of p53 nuclear phosphoprotein. Eight out of 51 (16%) salivary gland tumours were p53 positive. Three of these were benign and 5 malignant. All 3 benign salivary gland tumours were pleomorphic adenomas and expressed only occasional nuclear positivity with less than 1% of tumour cells positive. Of the 5 p53-positive malignant tumours, 3 were mucoepidermoid carcinomas and 2 undifferentiated carcinomas. The malignant salivary gland tumours expressed more than 1% of positive nuclei in every case. Seventeen lung carcinomas were p53 positive (63%). Thirteen of these were squamous cell carcinomas, 3 were adenocarcinomas and 1 small cell lung carcinoma. The results show that mutations of the p53 gene may be infrequent in salivary gland tumours when compared with lung carcinomas. The relatively indolent course of some histological types of malignant salivary gland tumours could be associated with the preservation of the non-mutated p53 gene in most of these tumours. The presence of p53 positivity in some pleomorphic adenomas might, on one hand, suggest that p53 gene alterations are also present in these tumours; on the other hand, the accumulation of the p53 protein in these tumours might also be due to some unknown mechanism, not necessarily related to p53 gene mutation.

Adenocarcinoma↗

PubMed1992

Tenascin in salivary gland tumours.

The distribution of tenascin immunoreactivity was analysed in salivary gland tissue and in various benign and malignant tumours of the salivary gland. In the non-neoplastic tissue, tenascin was seen in the areas of basement membranes of the ductal epithelium. No immunoreactivity could be observed in the serous or mucous glands. In pleomorphic adenomas, tenascin immunoreactivity could be seen in the stromal compartment. It was more pronounced in the dense stromal areas and chondroid elements than in the myxoid area. In Warthin's tumours, strong tenascin immunoreactivity could be observed in the basement membrane zone of the epithelial component. In the lymphatic component, faint reticular staining could be seen. In adenoid cystic carcinomas, acinic cell tumours and mucoepidermoid carcinomas, tenascin showed a linear stromal distribution. No intracytoplasmic immunoreactivity could be seen in any of the cases. The widespread tenascin positivity in salivary gland tumours suggests that tenascin may play a role in the induction and progression of salivary gland tumours, presumably by interfering with the normal parenchymal-mesenchymal interaction.

Adenoma↗

PubMed1992

Comparative analysis of p53 protein immunoreactivity in prostatic, lung and breast carcinomas.

In this study we analysed the expression of p53 protein in a total of 143 carcinomas immunohistochemically. These consisted of 34 prostatic adenocarcinomas, 59 lung and 50 breast carcinomas. In 28 cases, an average of 2-3 additional sections from different tumour areas were analysed. Forty-nine of the 143 carcinomas (34%) showed typical nuclear immunoreactivity by immunohistochemical staining with the p53 antibody CM-1. Two of the 34 prostatic carcinomas (6%) were p53 positive while 25 of the 59 lung carcinomas (43%) and 22 of the 50 breast carcinomas (44%) showed positivity for p53. By grade: 49% of grade III tumours, 36% of grade II and 5% of grade I tumours were p53 positive. There were significantly more p53-positive cases in grade II-III tumours than in grade I tumours (P = 0.001) when all tumours were taken into account. Further, there were significantly more p53-positive cases in grade III than in grade I-II tumours (P = 0.001). In lung tumours there were significantly more p53-positive cases in grade II-III tumours than in grade I tumours (P = 0.018). Similarly, there were significantly more p53-positive tumours in grade III breast tumours than in grade I-II tumours (P = 0.003). The low incidence of p53 positivity in prostate carcinomas suggests that mutations of the p53 gene are not as frequent in the neoplastic transformation of these tumours as in lung or breast carcinomas. The association of p53 positivity with tumours of higher grade suggests that p53 mutations lead to tumours of a more aggressive type. The analysis of tumours by multiple sections indicates that p53 positivity is not evenly distributed in tumour tissue. Therefore, analysis of additional tumour areas may reveal positivity some cases, which is not evident if only one section is studied.

Adenocarcinoma↗

PubMed1992

Tenascin in reactive lymph nodes and in malignant lymphomas.

Tenascin is an extracellular matrix protein which accumulates in the stroma of various malignant and some benign neoplasms. This has been verified in several immunohistochemical studies. The distribution of tenascin immunoreactivity in lymphatic tissues and neoplasias, however, has not been thoroughly studied. In this investigation we analyzed tenascin immunoreactivity in several benign and malignant lymphatic lesions, including both Hodgkin's and non-Hodgkin's lymphomas. In benign lymph nodes, faint reticular immunoreactivity could be observed in the lymphatic tissue. In benign reactive hyperplasias, a stronger reticular pattern of tenascin immunoreactivity was observed in the interfollicular and medullary areas, while the lymphoid follicles contained only a few positive fibers. A similar immunoreactivity was observed in malignant follicular lymphomas. In diffuse lymphomas, a diffuse meshwork of positively stained fibers was seen. This was also the case for the three cases of Hodgkin's disease of the lymphocyte-predominance nodular subtype. There was no difference in the intensity of the immunoreactivity between benign and malignant disorders. However, in Hodgkin's disease of the nodular sclerosis and lymphocyte-depletion subtypes, a much more pronounced immunoreactivity could be observed in the fibrous septa and the cords. This suggests that the tumor cells are possibly capable of synthesizing growth factors which stimulate fibroblasts to synthesize tenascin. The results indicate that tenascin does not accumulate in the stroma of malignant lymphoid neoplasms with the exclusion of some subtypes of Hodgkin's disease. The distribution of tenascin immunoreactivity in lymphatic tissue is similar to that of the reticular fibers suggesting that the molecules are associated with these structures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1992

Immunohistochemical evaluation of the cytoarchitecture of benign and malignant breast lesions.

Fifty-three breast lesions, which had been fixed in formalin and embedded in paraffin, were immunohistochemically analyzed with monoclonal antibodies to cytokeratin subtypes 1, 5, 10, 14 (34BE12), muscle-specific actins (HHF35) and antiserum to S100 protein, all of which have been used as markers for myoepithelial cells. With these antibodies, a continuous myoepithelial cell layer could generally be seen around the benign ducts and acini. In in situ carcinomas, such a layer could still be observed, though it was usually discontinuous and sometimes absent. In infiltrating carcinomas, no myoepithelial cell layer could be observed. In intraductal hyperplasias, scattered HHF35, 34BE12 and S100-positive cells could be seen amongst the proliferating intraductal cells. In in situ and infiltrating carcinomas, however, such cells could also be observed. This was seen especially with antibodies 34BE12 and S100, and to a lesser extent also with HHF35. Morphologically these cells seemed to belong to the malignant cell population. Although myoepithelial cell preservation is an important morphological parameter in the histological evaluation of breast lesions, the results suggest that the myoepithelial cell markers 34BE12, HHF35 and S100 cannot be used in the differential diagnosis between benign and malignant breast lesions in a straightforward manner. This is because in situ carcinomas have a more or less preserved myoepithelial cell layer, and because many infiltrating and in situ carcinomas contain a subpopulation of neoplastic cells expressing these markers, possibly signifying myoepithelial cell differentiation.

Actins↗

PubMed1992

p53 expression in lymphatic malignancies.

AIMS: To investigate the expression of p53 protein in malignant and benign lymphoid tissues. METHODS: Tissue from 42 non-Hodgkin's lymphomas, 10 Hodgkin's lymphomas, three atypical hyperplasias and five benign reactive hyperplasias was studied immunohistochemically for the expression of p53 protein. RESULTS: Of the 42 non-Hodgkin's lymphomas, 13 (31%) were positive for p53 in some of the tumour cells. In two cases the proportion of positive cells was more than 10% and in four cases it was between 1-5%. These six cases consisted of three Burkitt's lymphomas, one immunoblastic lymphoma, one centroblastic diffuse lymphoma and one angioimmunoblastic lymphoma. In seven cases the proportion of p53 positive tumour cells was less than 1%. These cases comprised three centroblastic diffuse, three centroblastic polymorphic diffuse, and one angioimmunoblastic type lymphoma. In three out of 10 (30%) Hodgkin's lymphomas, a proportion of the Reed-Sternberg cells were p53 positive. One of these was a mixed cellular subtype and two nodular sclerosing subtypes. p53 protein was not expressed in the three atypical hyperplasias or the five benign reactive hyperplasias of the lymph nodes. CONCLUSIONS: The presence of p53 positivity in non-Hodgkin's and Hodgkin's lymphomas indicates that mutations of the p53 gene may play a part in the development of these tumours. The concentration of p53 positivity in high grade lymphomas suggests that p53 is involved in the transformation of low grade lymphomas to more aggressive types. Because no p53 positivity was observed in benign lesions of the lymph nodes, positive p53 immunohistochemical staining in a lymphoid lesion suggests malignancy.

Hodgkin Disease↗

PubMed1992

Evidence by in situ hybridization that c-erbB-2 proto-oncogene expression is a marker of malignancy and is expressed in lung adenocarcinomas.

In order to identify potential markers of malignancy in diagnostic respiratory cytopathology, c-myc and c-erbB-2 proto-oncogene expression was studied in fine needle aspirates from 14 consecutive fresh operation tissue samples (after surgical removal) representing lung tumors and a variety of other cell samples by in situ hybridization of 35S-labeled antisense and sense RNA c-myc and c-erbB-2 specific proto-oncogene probes. All 14 lung tumors showed c-myc expression and eight also showed c-erbB-2 expression. On average, the c-myc expression was about 4 times higher than that of c-erbB-2 (P less than 0.001). c-erbB-2 expression, confirmed also as a cytoplasmic membrane-bound reactivity by immunohistochemical stainings for c-erbB-2 oncoprotein, was significantly related to adenocarcinoma (P less than 0.025), whereas increasing tumor size correlated significantly with increasing c-myc expression (P less than 0.05). On average, all the tumor cell lines showed 2-fold expression of c-myc compared with the lung tumors (P less than 0.025). c-erbB-2 expression was found in six of 11 cell lines. High c-myc proto-oncogene expression was also found in broncho-epithelial cells and alveolar macrophages, and a low expression was found in lymphocytes but not in neutrophils, while none of these cells showed c-erbB-2 proto-oncogene expression. Our results demonstrate extensive c-myc proto-oncogene expression in both malignant and non-neoplastic proliferating cells, but not in terminally differentiated cells such as neutrophils. Therefore c-myc expression must also be related to general cell proliferation and not only malignancy per se. In marked contrast, c-erbB-2 proto-oncogene expression was found only in adenocarcinoma cells, and thus can be used as a marker for malignancy in diagnostic respiratory cytopathology.

Adenocarcinoma↗

PubMed1991

Tumor cells of malignant fibrous histiocytomas express mRNA for laminin.

In situ hybridization was used on routinely processed paraffin-embedded tissue sections to study the synthesis of the basement membrane (BM) proteins laminin and type IV collagen in 14 cases of malignant fibrous histiocytoma (MFH). Complementary RNA probes coding for the pro-alpha 1 (IV) chain of human type IV collagen and the B1 chain of human laminin were used to detect the respective mRNAs. The results were correlated with the immunohistochemical reactivity of tumor cells to specific antibodies against the P1 fragment of laminin and the 7S domain of type IV collagen. Signals for the presence of laminin mRNA in atypical neoplastic tumor cells could be detected in 11 MFHs. None of the tumors could be shown to contain signals for type IV collagen mRNA in their cells, although such signals were detected in the endothelial cells of tumor capillaries. In the corresponding immunohistochemical stainings, nine MFHs showed intracytoplasmic staining of tumor cells for laminin and one tumor showed weak staining for type IV collagen in the neoplastic cells. The results show that the laminin immunoreactivity found in MFHs is due to synthesis in the tumor cells and not to endogenous uptake of this protein. Synthesis of laminin in the majority of MFHs is in accordance with the notion that these tumors originate from primitive mesenchymal cells in soft tissues.

Aged↗

PubMed1990

Immunohistochemistry of markers of histiomonocytic cells in malignant fibrous histiocytomas. A monoclonal antibody study.

Nine cases of malignant fibrous histiocytomas (MFH) were examined immunohistochemically in frozen sections with six different monoclonal antibodies to histiomonocytic and related cells (EBM11, HAM-56, KB90, antibodies to dendritic reticulum cells, HLADR and LCA). Ten other soft tissue sarcomas, two desmoid tumors, twelve carcinomas, three seminomas and four lymphomas were studied for comparison. All cases of MFH showed positivity for histiomonocytic cell antigens. In six cases, the positive cells could be clearly interpreted to be infiltrating non-neoplastic cells. However, immunoreactivity for multiple histiocytic markers (EBM11, HAM-56, KB90, HLADR) was seen in tumor cells in three cases of MFH. In one of these cases, the positivity could be verified with KP1, an antibody to histiomonocytic cells applied in formalin fixed and paraffin embedded tissue. None of the tumors was positive with the antibody to dendritic reticulum cells or LCA. In the series of non-histiocytic tumors, no cases showed widespread positivity for multiple histiocytic markers. Our results suggest that in relation to true histiomonocytic differentiation MFH might be a heterogeneous group of tumors. The widespread immunoreactivity for multiple histiocytic markers in some cases may indicate a true histiomonocytic differentiation in some MFHs.

Antibodies, Monoclonal↗

PubMed1990

Cell differentiation in benign cutaneous fibrous histiocytomas. An immunohistochemical study with antibodies to histiomonocytic cells and intermediate filament proteins.

Seven benign cutaneous fibrous histiocytomas (BFHs) were investigated immunohistochemically by using a panel of antibodies to histiomonocytic cells and intermediate filament proteins. Immunoreactivity with antimacrophage antibodies was observed in all tumors in a significant but varying proportion of the tumor cells. All tumors were also positive for vimentin. In addition, two of the BFHs were positive for cytokeratin and one for desmin. The results suggest that BFHs either display a true histiomonocytic trait or, alternatively, contain a prominent histiomonocytic infiltration. Some BFHs may be related to smooth muscle cells as indicated by desmin positivity. The occasional occurrence of cytokeratin in BFHs could also be explained by smooth muscle cell differentiation.

Adult↗

PubMed1989

Immunoreactivity for laminin and type IV collagen in malignant and benign fibrous histiocytoma.

Sixteen malignant fibrous histiocytomas (MFH) and ten benign fibrous histiocytomas of the skin were studied immunohistochemically for the distribution of two basement membrane (BM) proteins, laminin and type IV collagen, in order to evaluate their cellular nature. Linear staining for both proteins was present in the vascular BMs. Intracytoplasmic laminin was observed in the neoplastic fibroblast-like and pleomorphic giant cells in 11 MFHs. Two MFHs also showed similar staining for type IV collagen. In the giant cell subtype of MFH, the reactive giant cells were totally negative whereas the neoplastic cells were strongly positive for laminin. Extracellular fibres staining positively for both BM proteins were seen in two MFHs. Except for the capillary network, the benign fibrous histiocytomas were negative for laminin and type IV collagen. On the basis of the present results, we favour the concept that MFHs are primitive mesenchymal tumours, some of which may show histogenetic relationships with tumours of BM forming mesenchymal cells.

Adolescent↗

PubMed1989

Alpha-1-antitrypsin and lysozyme. Their limited significance in fibrohistiocytic tumors.

A wide range of tumors were immunohistochemically analyzed for alpha-1-antitrypsin (AAT) and lysozyme in order to evaluate their specificity as histiocytic markers and their significance in the diagnostic and histogenetic evaluation of fibrohistiocytic tumors. Besides histiocytic lesions, AAT immunoreactivity was commonly found in different types of carcinomas and sarcomas, and strong immunoreactivity was found in carcinoid tumors, malignant melanomas, and schwannomas, which, however, had negative results for lysozyme. The AAT immunoreactivity could be abolished with the absorption of the antibody with purified AAT also in nonhistiocytic tumors. The neoplastic pleomorphic cells in malignant fibrous histiocytomas (MFHs) usually had strongly positive results for AAT, whereas only entrapped histocytes had positive results for lysozyme and for two monoclonal antibodies to histomonocytic cells. The results show that AAT has a relatively low specificity as a histiocytic marker, and one should be careful in concluding the histiocytic nature of tumors, such as MFHs, based on AAT immunostaining. It seems also questionable whether AAT can be used as a diagnostic marker for MFH. The reason for the widespread AAT immunoreactivity in various tumors may be that AAT is taken up from serum to various types of nonhistiocytic tumor cells.

Biomarkers, Tumor↗

PubMed1989

Malignant fibrous histiocytoma. Heterogeneous patterns of intermediate filament proteins by immunohistochemistry.

Patterns of intermediate filament expression of 10 malignant fibrous histiocytomas (MFHs) were immunohistochemically evaluated using acetone-fixed frozen sections. Seven cases represented the storiform-pleomorphic subtype, 2 were of myxoid type, and 1 was of giant-cell type. All cases had been studied by electron microscopy, and no proof for the diagnoses of liposarcoma, rhabdomyosarcoma, and leiomyosarcoma could be obtained. All tumors showed prominent vimentin immunoreactivity in the tumor cells. Cytokeratin-positive neoplastic cells were found in 2 cases, and in the majority of tumor cells in 1 of these. The 68k neurofilament-positive cells were found in 2 cases. Desmin was not found beyond doubt in the neoplastic cells in any cases, and all cases were negative for glial fibrillary acidic protein. The expression of several types of intermediate filament indicates divergent differentiation properties in MFH and may suggest the heterogeneity of this entity, but more cases should be studied to elaborate any possible consistent patterns of intermediate filament expression in different types of MFH. The expression of multiple types of intermediate filament proteins in MFH can alternatively signify random activation of the corresponding genes in the primitive tumor cells. The complex patterns of intermediate filament proteins in morphologically defined MFHs should be taken into account in the practical immunohistologic analysis of tumors.

Cell Differentiation↗