Abstract Cytogenetic analysis of short‐term cultures from 25 malignant fibrous histiocytomas (MFH) revealed clonal chromosome abnormalities in 17 tumors: ten storiform‐pleomorphic and seven myxoid MFH. Telomeric associations, rings, and dicentric chromosomes were present in 11 tumors and cytogenetic signs of gene amplification (homogeneously staining regions and double minute chromosomes) in four. The breakpoint distribution of the numerous structural rearrangements was nonrandom. The chromosome bands most frequently affected were 19p13 (in eight tumors; eight rearrangements gave rise to 19p+ markers, some of which looked similar, and an r(19) was found in one case), 11p11 (in seven tumors; three translocations and four deletions), 1q11 (in seven tumors; one translocation and six deletions), and 3p12 (in six tumors; all deletions). Other bands involved at least four times were 1p36, 5p15, and 20q13. Of particular clinical interest was the observation that tumors with 19p+ seemed to have a pronounced tendency to recur locally (local recurrence in five of eight tumors with 19p+ compared to one of nine in tumors without this aberration; observation period 4–16 months).
In a cytometric DNA study of high-grade osteosarcoma, the relationship between DNA content and morphology was analyzed. The investigation, based on microspectrophotometry of tissue sections and flow cytometry (FCM), included both primary lesions and recurrences. FCM analysis, applied to a consecutive series of 47 primary osteosarcomas, disclosed that 2 were diploid and 45 were nondiploid, 8 of which were tetraploid. Multiple aneuploid peaks were detected in 13 tumors. Among the nondiploid tumors, there was no clear relationship between the peak DNA value(s) and the histologic subtype (osteoblastic, chondroblastic, fibroblastic) or grade (III-IV). The proliferative activity, as reflected by the percentage of S-phase cells, could be determined in 38 of the 47 tumors analyzed by FCM. The percentage was higher for aneuploid than for tetraploid lesions; however, the distribution of S-phase cells was not related to the histologic subtype or the grade of the tumors. To assess the reliability of a single sample for FCM, the DNA content of biopsy and surgical specimens was compared in 20 tumors; there was complete agreement in all cases with respect to the classification of the lesion as diploid, tetraploid or aneuploid. Analysis by FCM or microspectrophotometry of 12 local recurrences and 16 metastases and the corresponding 19 primary tumors showed that an aneuploid characteristic of the primary lesion was retained during progression of the disease. In 12 tumors analyzed by microspectrophotometry in tissue sections, comparison of chondroblastic and osteoblastic/fibroblastic areas within the same lesion consistently disclosed hyperploidy in both areas.(ABSTRACT TRUNCATED AT 250 WORDS)
Research Articles| August 29 2011 Reverse Transcriptase Polymerase Chain Reaction on Fine Needle Aspirates for Rapid Detection of Translocations in Synovial Sarcoma Subject Area: Pathology and Cell Biology Gunnar Nilsson; Gunnar Nilsson From the Department of Cellular and Molecular Tumor Pathology, Cancer Center Karolinska and the Department of Pediatric Hematology and Oncology; Unit of Cytology, Department of Pathology; and Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden. Search for other works by this author on: This Site PubMed Google Scholar Min Wang; Min Wang From the Department of Cellular and Molecular Tumor Pathology, Cancer Center Karolinska and the Department of Pediatric Hematology and Oncology; Unit of Cytology, Department of Pathology; and Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden. Search for other works by this author on: This Site PubMed Google Scholar Johan Wejde; Johan Wejde From the Department of Cellular and Molecular Tumor Pathology, Cancer Center Karolinska and the Department of Pediatric Hematology and Oncology; Unit of Cytology, Department of Pathology; and Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden. Search for other works by this author on: This Site PubMed Google Scholar Lena Kanter; Lena Kanter From the Department of Cellular and Molecular Tumor Pathology, Cancer Center Karolinska and the Department of Pediatric Hematology and Oncology; Unit of Cytology, Department of Pathology; and Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden. Search for other works by this author on: This Site PubMed Google Scholar Jonas Karlén; Jonas Karlén From the Department of Cellular and Molecular Tumor Pathology, Cancer Center Karolinska and the Department of Pediatric Hematology and Oncology; Unit of Cytology, Department of Pathology; and Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden. Search for other works by this author on: This Site PubMed Google Scholar Edneia Tani; Edneia Tani From the Department of Cellular and Molecular Tumor Pathology, Cancer Center Karolinska and the Department of Pediatric Hematology and Oncology; Unit of Cytology, Department of Pathology; and Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden. Search for other works by this author on: This Site PubMed Google Scholar Andris Kreicbergs; Andris Kreicbergs From the Department of Cellular and Molecular Tumor Pathology, Cancer Center Karolinska and the Department of Pediatric Hematology and Oncology; Unit of Cytology, Department of Pathology; and Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden. Search for other works by this author on: This Site PubMed Google Scholar Olle Larsson Olle Larsson From the Department of Cellular and Molecular Tumor Pathology, Cancer Center Karolinska and the Department of Pediatric Hematology and Oncology; Unit of Cytology, Department of Pathology; and Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden. Search for other works by this author on: This Site PubMed Google Scholar Acta Cytologica (1998) 42 (6): 1317–1324. https://doi.org/10.1159/000332161 Article history Published Online: August 29 2011 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Gunnar Nilsson, Min Wang, Johan Wejde, Lena Kanter, Jonas Karlén, Edneia Tani, Andris Kreicbergs, Olle Larsson; Reverse Transcriptase Polymerase Chain Reaction on Fine Needle Aspirates for Rapid Detection of Translocations in Synovial Sarcoma. Acta Cytologica 1 December 1998; 42 (6): 1317–1324. https://doi.org/10.1159/000332161 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsActa Cytologica Search Advanced Search Article PDF first page preview Close Modal Keywords: reverse transcriptase, polymerase chain reaction, aspiration biopsy, translocation (genetics), sarcoma, synovial This content is only available via PDF. 1998Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
The DNA content of osteosarcomas, and of giant cell tumors, osteoblastomas, aneurysmal bone cysts, and fibrous dysplasias was determined by cytophotometry. Of 158 tumors, 141 were histologically noncontroversial, whereas 17 posed diagnostic difficulties. In the noncontroversial group, all 41 benign tumors had a diploid (normal) DNA content. Ninety-two of 96 high-grade osteosarcomas were hyperploid (increased DNA content). The four analyzed low-grade parosteal osteosarcomas were diploid. Among 17 diagnostically controversial cases, nine were primarily diagnosed and treated as benign. Three of these patients, nevertheless, exhibited a malignant clinical course and two had local recurrence. All five proved to have hyperploid tumors. The four nonrecurrent lesions were diploid. Of eight patients primarily evaluated as malignant, one died and two developed local recurrence. These three patients had hyperploid tumors. Among the five nonrecurrent lesions, two were hyperploid and three diploid. In the diagnostically controversial group, recurrence or death was consistently related to hyperploidy. The present study shows that the vast majority of high-grade osteosarcomas are hyperploid. Benign bone tumors, which may be mixed up histologically with osteosarcoma, are diploid. Routine DNA analysis of primary bone tumors, as an adjunct to histopathologic assessment, can be employed to obtain diagnostic confirmation. In cases presenting histopathologic difficulties, ploidy determination may provide decisive diagnostic information.
Abstract We tested the chondrogenic potential of demineralized allogeneic bone matrix (DABM) in the repair of osteochondral defects. In 42 adult rabbits, a 5‐mm 2 or 15‐mm 2 defect was created bilaterally in the intercondylar groove of distal femur. DABM was inserted directly in 37 defects, whereas in 35 it was inserted after previous placement in muscle for 4, 16, or 19 days. Another 12 defects were left empty, serving as controls. Subgroups of animals were killed at 6, 12, 18, and 26 weeks. The distal femora were excised and prepared for histologic evaluation in hematoxylin‐eosin and toluidine blue. Cartilage‐like repair tissue was observed in the majority of defects. However, there was a great variability in the experimental groups without any clear relationship to type of DABM implant, defect size, or postoperative time. Even individual knees exhibited varying stages of cartilage differentiation. Overall, DABM placed in muscle for 19 days appeared to yield the best repair of the defects. The most consistent findings of the present study were bone formation in the marrow of distal femur and, notably, the absence of bone differentiation toward the joint surface. Hence, it seems that the synovial environment prevents bone formation otherwise induced by DABM in vascular tissue. Although tissue formed in articular defects supplemented with DABM is of cartilaginous differentiation, which is retained over time, it is of highly variable quality. Hence, the described approach has to be optimized before it can be applied for the purpose suggested.
