[Relative incidence and frequency of malignant epithelial tumors of the uterus in the statistics of the I.O.P.M. of Milan in the decade 1958-1967].
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Biomedical subjects
Publications and source records attributed to F Rilke.
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The T1 surface antigen (CD5,p67) expression on blood lymphocytes (PBL) and lymphoid cells from lymph node biopsies (LN) from 31 patients with B-cell chronic lymphocytic leukemia (B-CLL) and 79 with B non-Hodgkin lymphoma (B-NHL), was detected in 25 B-CLL (80 per cent) and in 11 B-NHL (13 per cent) belonging to the following histologic subtypes: lymphocytic of CLL type (DLWD) one case, lymphoplasmacytoid (DLWD) four cases, centrocytic (DLPD) five cases, immunoblastic (DH) one case. All B-CLL and the T1 + B-NHL were also tested with monoclonal antibodies against the Common Acute Lymphoblastic Leukemia Antigen, B cells (FMC7, FMC8, BA1, Y29-55), T cells (OKT11a), HLA-DR and HLA-DQ monomorphic determinants. All the B-CLL and the T1+ B-NHL were CALLA-, BA1+, Y29.55+. FMC7+ cells were detected in large numbers six B-CLL (three T1+ and three T1-) and in four centrocytic lymphomas. FMC8 reacted with 70 per cent of leukemias (where it stained 30 per cent of neoplastic cells) and with 8/9 T+ B-NHL. HLA-DR and HLA-DQ molecules were detected in 100 per cent and 90 per cent of cases respectively. In vitro treatment of HLA-DQ- or T1- B-CLL with phorbol ester TPA led to the expression of these antigens as well as of the receptors for Interleukin 2 and MLR3 activation antigen. Surface membrane Ig (SIg) was detected in 79 per cent of cases, its density measured by FACS analysis varied, even markedly, from case to case. Among the B-CLL, cells with high SIg content were either T1+ or T1- and more likely FMC7+. The SIg- cases were seven B-CLL (five T1+ and two T1-) and two B-NHL, in which, however, cytoplasmic IgM was detected. This study reveals the existence of four major B-CLL subgroups: T1- SIg-, T1+ SIg+, T1+ SIg+, T1- SIg+. It also indicates that the T1 antigen may be transitionally present during B-cell differentiation and that its expression may precede that of SIg as supported by the in vitro studies. In addition, the finding that some B-NHL are T1+ suggests that they derive similarly to the B-CLL from a common progenitor.
The relation between the [3H]-thymidine labelling index (3H-Thy LI), which evaluates the S-phase cells, and the monoclonal antibody Ki-67 (MoAb Ki-67), which recognizes a nuclear antigen expressed during the cell cycle, was defined in 35 non-Hodgkin's lymphomas (NHL). Significantly higher median values of [3H]-Thy LI and Ki-67-positive cells were observed for high-grade than for low-grade malignancy tumours according to the Kiel classification, but with wide and overlapping values for the two morphologic subgroups. A significant correlation was observed between [3H]-Thy LI and Ki-67-positive cells (P less than 0.0001; r = 0.62). However, the ratio between the two cell kinetic variables on individual tumours was not constant. It sharply increased with decreasing [3H]-Thy LI values and was much higher in low-grade NHL than in high-grade NHL. Follow-up studies are needed to establish the role of the tumour growth fraction as evaluated by MoAb Ki-67 as a prognostic indicator in NHL.
Cell kinetics ([3H]-thymidine labelling index, [3H]-Thy LI) were determined on pathologic lymph nodes from 175 untreated adult patients. [3H]-Thy LI significantly differed in low-grade and high-grade malignancy groups according to the Kiel classification (median values, 1.8 per cent and 10.4 per cent, respectively) and in low, intermediate, high grade according to the Working Formulation (median values: 1.7 per cent, 4.8 per cent and 14.2 per cent, respectively) but was unrelated to pathologic stage or patient's age. Cell kinetics, histopathology, pathologic stage and patient's age were significant discriminants of 6-year survival. Multivariate analysis was performed by Cox's proportional hazard model to investigate the role of [3H]-Thy LI after making allowance for the other prognostic factors. When [3H]-Thy LI was added to the model, a large increase (chi square = 29.94) contributed by the cell kinetic variable in identifying patients at different risk was revealed.
The phenotypic features of 44 cases of sporadic Burkitt's lymphoma (BL) were investigated by monoclonal antibodies (MoAbs). The majority of cases were positive for HLA-DR (97 per cent), CD19 (100 per cent), CD20 (92 per cent) and CD37 (83 per cent) pan-B markers, in accordance with the B-cell derivation of the tumour; the B-cell restricted markers CD21, CD22 and FMC7 reacted with 28 per cent, 66 per cent and 75 per cent of cases, respectively. Of the mantle zone B-cell specific MoAbs, CD1c was always negative, whereas CD23 and 2.7 were positive with one and two cases, respectively. CD39 was weakly reactive on two specimens, one of which was CD23+. The germinal centre specific MoAbs CD10 and CD77 (Burkitt's lymphoma antigen) displayed a heterogeneous pattern of reactivity and allowed to identify 4 subgroups: CD10+/CD77+ (44 per cent), CD10+/CD77- (15 per cent), CD10-/CD77+ (36 per cent) and CD10-/CD77- (5 per cent). Of 15 cases tested for the expression of CD11a and CD18 lymphocyte-function-associated (LFA-1) antigens and their ligand ICAM-1 (CD54), seven were positive and six negative for the three markers, while the other two cases expressed alternatively the two molecules. Analysis of the putative normal BL cell counterpart, identified with the CD77 marker in normal lymphoid tissues, showed that all CD77+ B-cells were constitutively CD11a+/CD18+, suggesting that BLs are likely to arise from a LFA-1 positive B-cell and may down-regulate these molecules during neoplastic transformation.
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An typical nuclear structure consisting of a cribriform and condensed chromatin pattern with hyperchromasia, a small nucleolus and a moderately increased nuclear-cytoplasmic ratio was observed in the epithelial cells of the crypts and in the stromal and muscular cells of 51 out of 70 oncologically negative biopsies of the rectal mucosa. The subsequent retrieval of all clinical and histologia data revealed that the 51 cases included 39 of adenocarcinoma of the large intestine either present (15 cases) at a variable distance from the false negative biopsy or removed previously (24 cases), 7 of extra-intestinal malignant tumor (parotid gland, urinary bladder, endometrium, breast, stomach, metastatic, anus) and 5 with benign conditions of the large intestine. Of the remaining 19 cases whose biopsies did not reveal the atypical nuclear structure 16 had benign lesions of the large intestine and nowhere evidence of malignancy, two had an adenocarcinoma of the large bowel (one present and one removed previously) and one a carcinoma of the anus. In the rectal biopsies examined the atypical nuclear structure was detected in 93.9% of the cases with a malignant tumor either present or removed previously and in 19% of the cases with benign conditions. The morphologic evidence indicated that the atypical nuclear structure was compatible with a possible distrubance of the mitotic cycle since the findings were restricted to the generative compartment of rectal epithelium. The results are discussed in connection with their possible practical use as a diagnostic aid in the evaluation and interpretation of false negative and negative rectal biopsies as well as with their possible significance in the biology of tumor-bearing hosts.
The recent identification among non-Hodgkin's malignant lymphomas of a high-grade malignancy entity of possible thymic origin and defined as lymphoblastic convoluted-cell lymphoma allowed the morphologic and radiological diagnosis of nine cases of this disease. Males outnumbered females (6/9) and the age ranged from 6 to 54 years. The histologic diagnosis relied upon the characteristic non cohesive cellularity as well as upon the peculiar cribriform nuclear structure, the convoluted appearance of the nuclei, the anisokaryosis, the paucity of the cytoplasm and the minimal size of the nucleoli. The anatomical distribution of the disease was ascertained in the lymph nodes, spleen, liver and several other extranodal sites. Bone marrow invasion was observed in seven cases and presence of lymphoma cells in the peripheral blood in six. A thymic mediastinal mass was present radiologically in seven cases and lymphography was positive in five. Follow-up data revealed death of four patients within 10 months and survival of two up to 17 months. The cellular morphology of the malignant lymphoma seems to be sufficiently diagnostic. This entity deserves an autonomous position within the classifications of malignant lymphomas as it appears in the functional one proposed by Lukes and Collins (21) as well as in the Kiel classification (13).
A soft tissue malignant fibrous histiocytoma was studied by light and electron microscopy. The presence of fibroblast-like cells, histiocyte-like cells, undifferentiated stem cells, and xanthomatous cells was confirmed. Fibroblast- and histiocyte-like multinucleated giant cells were also observed. The observation of lysosomes in some fibroblast-like cells, the features of undifferentiated stem cells, and the presence of cells and intermediate characteristics common to xanthomatous, histiocytic, and stem cells suggest a strict relationship among these cellular types.
AIMS: Circumstantial evidence suggests that genetic changes may lead to tumor progression within the myxoid liposarcoma tumors (MLTs) carrying non-random chromosomal translocation t(12;16). METHODS: To address this subject an immunophenotypic analysis, applying antibodies against proteins encoded by TP53, MDM2 and CDK4 genes, complemented by molecular analysis of eight suitable cases, was performed on 104 consecutive cases. Chromosomal translocations were assessed either by cytogenetic analysis or by RT-PCR in 9 suitable cases and chimeric transcripts were found in all cases but two pleomorphic liposarcomas. RESULTS: Based on immunophenotyping and tumor site, the case material consisted of three groups. The first one was made up of 92 non-retroperitoneal cases carrying a null p53, mdm2, cdk4 immunophenotype, which remained unchanged over the time of recurrences and along the gamut of histologic subtypes. The second group was represented by five p53+, mdm2-, cdk4- non-retroperitoneal cases, 4 of which were further analysed by PCR-SSCP for p53 mutation. The immunophenotypic profile of these cases, complemented by the molecular findings, supported a role of TP53 in tumor progression in three high-grade MLTs. The third group, consisting of 7 retroperitoneal cases, showed a heterogeneous immunophenotype, sharing immunophenotypic and molecular features with the well-differentiated/evoluted (dedifferentiated) liposarcoma group. CONCLUSIONS: TP53 mutations seem to play a role in tumor progression in a few cases of MLTs (2.8%) showing more aggressive histologic characteristics. The unexpected finding that a number of retroperitoneal LMTs display the immunophenotypic profile of the well differentiated/evoluted (dedifferentiated) liposarcomas, deserves further investigation.