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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amplification and rearrangement of cellular proto-oncogenes are two of the several possible genetic alterations implicated in carcinogenesis and tumor progression. Although morphologically similar tumors may be heterogeneous at the level of the genome, some tumor types have shown relatively frequent and consistent abnormalities of specific oncogenes. In order to determine the frequency of oncogene amplification and rearrangement in several types of human sarcomas and to determine if histologically similar tumors have common genetic alterations, we analyzed 26 primary sarcomas by Southern hybridization. The oncogene probes utilized were N- and H-ras, sis, EGF-R (erb-B-1), neu (erb-B-2), fos, N- and c-myc, mos, and yes. The tumors studied included: five rhabdomyosarcomas (one alveolar, four embryonal), six malignant fibrous histiocytomas, six leiomyosarcomas, four liposarcomas, two Ewing's sarcomas, one osteosarcoma, and two fibrosarcomas. Oncogene abnormalities were identified in three tumors. One rhabdomyosarcoma showed 12-fold amplification and concurrent rearrangement of sis. This particular tumor also revealed rearrangement of H-ras and 15-fold amplification of c-myc. A second rhabdomyosarcoma revealed rearrangement of neu. A liposarcoma had a sis rearrangement. These findings suggest that many sarcomas show no common structural oncogene abnormalities. The presence of differing oncogene alterations within the rhabdomyosarcoma group indicates genetic heterogeneity among histologically similar sarcomas. The finding of a sis rearrangement in both a liposarcoma and a rhabdomyosarcoma, however, may suggest common oncogenesis among different tumor types.
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PMID:Genomic alterations in sarcomas: a histologic correlative study with use of oncogene panels. 149 46

A myxoid liposarcoma showed macroscopic, histologic, and cytogenetic heterogeneity. In one of three myxoid nodules and in the surrounding lipoma-like tumor tissue, the translocation t(12;16)(q13;p11), known to be specific for myxoid liposarcoma, was found as the sole chromosomal abnormality. In the other two nodules, additional rearrangements involving chromosomes 1, 12, and 16 were found. These aberrations were probably secondary to the primary t(12;16), and are cytogenetic evidence of clonal evolution. The complex chromosome aberrations were present in those tumor parts that had more malignant histology, indicating that the acquisition of secondary chromosomal aberrations parallels the histologic manifestations of tumor progression.
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PMID:Chromosomal evolution and tumor progression in a myxoid liposarcoma. 219 80

Well documented examples of primary malignant giant cell tumor of bone (giant cell tumor and concurrent sarcoma arising de novo) are exceedingly rare in the literature. We report a case arising in the left ischium of a 44-yr-old man. He had no previous history of radiation therapy or multiple resections. Histologically, the tumor was a typical giant cell tumor of bone juxtaposed to a malignant fibrous histiocytoma (MFH). The juxtaposition of a high grade sarcoma (MFH) and a locally aggressive nonmalignant neoplasm such as giant cell tumor is analogous to several other tumors of bone and soft tissue in which a low grade malignant or locally aggressive tumor can be associated with MFH or fibrosarcoma de novo, namely chondrosarcoma, chordoma, liposarcoma, and well differentiated intraosseous and parosteal osteosarcoma. The presence of a high grade malignant component in each of the aforementioned neoplasms generally portends a more ominous prognosis, although this is not invariably true. Recognition of the phenomenon of "dedifferentiation" (or tumor progression) in some bone tumors and sarcomas is important to ensure appropriate treatment. Distinction from secondary malignant giant cell tumors which are usually radiation induced is also important, since the latter have a much worse prognosis than those with dedifferentiation occurring de novo.
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PMID:Primary malignant giant cell tumor of bone: "dedifferentiated" giant cell tumor. 255 83

We report the cytogenetic findings in three mixed liposarcoma following short-term cultures. During the course of cytogenetic investigation of various types of liposarcomas, we observed an interstitial deletion of the long arm of chromosome 6 together with the translocation (12;16)(q13;p11) in three tumors. Translocation (12;16) is associated with myxoid and mixed (myxoid/round cell) liposarcomas, although deletion of chromosome 6 has been observed in only a few of these tumors. Our findings suggest that del(6), as an additional change in myxoid liposarcoma, is probably related to tumor progression.
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PMID:Deletion 6q in three cases of mixed-type liposarcoma in addition to t(12;16)(q13;p11) 788 98

Fifty-nine cases of atypical lipomatous tumors (ALT) of soft tissue (atypical lipomas, well-differentiated liposarcomas) were studied morphologically and cytogenetically as part of an international collaborative study. Forty-nine cases were deeply seated (including retroperitoneum), and 10 were superficial. Clonal chromosomal abnormalities were found in 55 cases (93%). Supernumerary ring or giant marker chromosomes (RGCs), the sole consistent alteration, were found in 37 ALTs (63%). They were more common in tumors that were large (p < 0.001), deeply seated (p < 0.005), that contained lipoblasts (p < 0.05), and that had marked cytologic atypia (p < 0.05). In a relatively short follow-up period (average, 3 years), only three of 59 cases recurred, one resulting in the patient's death. All three cases had RGCs. Also, five of the six cases that underwent dedifferentiation had RGCs, indicating that RGCs are associated not only with low-grade malignant behavior (in the form of local recurrence) but also with the potential for tumor progression. When the karyotypic profile of ALT was compared with that of 233 other types of adipose tissue tumors similarly analyzed by the authors, a statistically highly significant correlation (p < 0.0001) was found between ALT and RGCs. These results support the existence of ALT as a distinct tumor subtype that is different from ordinary lipoma and from spindle or pleomorphic lipoma, albeit histogenetically closely related to them. It also supports the proposed pathogenetic link between ALT and dedifferentiated liposarcoma. The association between chromosomal and morphologic findings indicates the potential role of karyotypic analysis in the differential diagnosis of ALT with ordinary lipoma, spindle or pleomorphic lipoma, hibernoma, and myxoid liposarcoma.
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PMID:Combined morphologic and karyotypic study of 59 atypical lipomatous tumors. Evaluation of their relationship and differential diagnosis with other adipose tissue tumors (a report of the CHAMP Study Group). 882 23

Authors operated on 6339 malignant breast tumors at the Department of Surgery, National Institute on Oncology between 1980 and 1994. The records of 14 patients with sarcomas of the breast were analyzed. These included 2 malignant phyllodes tumors, 3 malignant fibrous histiocytomas, 2-2 fibrosarcomas and carcinosarcomas and liposarcoma, angiosarcoma, leiomyosarcoma, osteosarcoma and dermatofibrosarcoma protuberans one of each. During this period 5 patients died, 9 are living without evidence of tumor. Analysing these 14 cases authors present their policy in surgical therapy of breast sarcomas compared with literature data. They emphasise the importance of wide resection margins for prevention of tumor progression. The above mentioned principle is valid for local recurrences so radicalization of the previous conservative breast surgery may be necessary in selected cases. Intraoperative histological examination is recommended to verify that the resection margins are tumor free. Axillary block dissection is not necessary except in cases when palpable, firm lymph nodes are present in the region. Depending on the histological grade adjuvant radiotherapy could be considered but its effectiveness is not proven.
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PMID:[Experience in the treatment of breast sarcomas]. 907 52

Myxoid and round cell liposarcoma represents a morphological spectrum in which tumor progression from low-grade myxoid to high-grade round cell areas is frequently observed. A distinctive t(12;16)(q13;p11) reciprocal translocation rearranges the CHOP gene localized to 12q13 in most cases. Data concerning the occurrence of cell cycle aberrations in this subset of mesenchymal malignancies are very limited. Therefore, we analyzed a histologically homogeneous series of 21 cases of myxoid and round cell liposarcoma. The p53 pathway was studied by investigating the TP53 gene and protein, mdm2 protein, and p21Waf1 protein. The Rb-cyclin D pathway was analyzed by studying the pRb protein, the p16MTS1 gene, cyclin D1, cyclin D3, p27Kip1, cdk4, and cdk6 proteins. In contrast with the rare involvement of the TP53 gene in well differentiated liposarcoma, aberrations of the TP53 gene were observed in approximately 30% of cases of myxoid and round cell liposarcoma. Notably, mdm2 overexpression was seen in 56% of cases and correlated with histological grade, therefore indicating a possible role in tumor progression. Abnormalities involving the Rb-cyclin D pathway were observed in more than 90% of cases. pRb loss was present in one-third of cases and, at variance with that observed in other subsets of sarcoma, overexpression of cyclin Ds represented a rare event. Interestingly, upregulation of either cdk4 or cdk6 was demonstrated in 85% of cases.
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PMID:Molecular aberrations of the G1-S checkpoint in myxoid and round cell liposarcoma. 940 3

In a case of retroperitoneal dedifferentiated mixed-type liposarcoma, a dedifferentiated component was observed in the so-called mixed-type liposarcoma consisting of well-differentiated and myxoid components. The proliferative activity was compared among the different components of the tumor by immunohistochemical study using the proliferating cell nuclear antigen (PCNA) and MIB-1 monoclonal antibodies. The dedifferentiated component showed higher positivity than the well-differentiated and myxoid components, and tumor progression was most advanced in the dedifferentiated component. In the chronological examination of each component, the labeling indices of PCNA and MIB-1 were significantly higher at the third recurrence than in the primary lesion in all types, indicating that the proliferative activity of the tumor cells increased gradually. Considering the surgical treatment of liposarcoma, an extended resection encompassing normal adjacent tissues is required in cases containing the dedifferentiated component in comparison to the cases containing only well-differentiated or myxoid components.
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PMID:Case of retroperitoneal dedifferentiated mixed-type liposarcoma: comparison of proliferative activity in specimens from four operations. 1047 74

To broaden the knowledge of myxoid morphology in liposarcoma, eight cases of unusual liposarcoma with combined well-differentiated and myxoid malignant fibrous histiocytoma (MFH)-like myxoid areas are reported. The tumors arose as huge retroperitoneal masses in elderly patients, except for one that occurred in the spermatic cord. Three cases had local recurrences, and one of the seven patients who were followed up had died of the tumor. Grossly, the tumors were mostly confluent and multinodular and showed a glistening myxoid appearance in variable proportions, which merged gradually into or were juxtaposed to yellow fatty or sclerotic whitish areas. Microscopically, in addition to areas of well-differentiated lipoma-like or sclerosing liposarcoma, all the tumors contained myxoid portions characterized by scattered multinucleated or bizarre giant cells and a prominent plexiform vascular pattern that resembled myxoid MFH or myxofibrosarcoma. The myxoid areas were associated with discernible lipogenesis. High-grade dedifferentiation was present in one tumor. Cytogenetically, in one case, the myxoid lesion had nonrandom chromosomal aberrations, such as ring and marker chromosomes, characteristic of a well-differentiated variant of liposarcoma. In a nested reverse transcription-polymerase chain reaction analysis using archival paraffin-embedded tissue, it was seen that none of the eight tumors with myxoid MFH-like features had TLS/FUS-CHOP fusion transcripts characteristic of myxoid and round cell liposarcomas. These clinicopathologic and molecular features suggest that the current myxoid tumors are more closely related to well-differentiated liposarcoma rather than to ordinary myxoid liposarcoma despite their unequivocal myxoid morphology. Missense point mutations of the p53 gene were detected in two (25%) cases by single-strand conformation polymorphism and sequence analyses. Immunohistochemical expressions of p53 and mdm2 were observed in 75% of the cases, in which immunoreactive tumor cells were seen more often in the myxoid MFH-like areas. Thus, altered p53 pathways, such as p53 gene mutation and mdm2-mediated inactivation of p53, may play a pathogenetic role in this form of tumor progression showing myxoid MFH-like morphology in liposarcoma, as has been suggested in dedifferentiated liposarcoma.
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PMID:Retroperitoneal liposarcoma with combined well-differentiated and myxoid malignant fibrous histiocytoma-like myxoid areas. 1058 1

A mixed myxoid/round cell liposarcoma was macrodissected in its 2 histologic components and investigated for genetic differences between its low-grade myxoid and the high-grade round-cell region. For both, we failed to detect p53 gene mutations, loss of heterozygosity at the p53 or Rb genes, and p53 protein expression. The round-cell component showed a high telomerase activity, and an elevated c-myc mRNA and protein expression. The myxoid component was characterized by a lack of telomerase activity and low c-myc mRNA expression, and immunohistochemistry failed to detect the c-myc protein. There was a higher Mib-1 proliferation index in the round-cell portion. The same specific translocation t(12;16) and the fusion transcript type II in both components confirmed the close relationship between myxoid and round-cell liposarcomas. Telomerase activity and increased c-myc expression seem to be helpful molecular markers for characterizing tumor progression in myxoid liposarcoma.
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PMID:Myxoid liposarcoma with transition to round-cell lesion-cell cycle regulator genes and telomerase activity characterizing tumor progression: a case report. 1066 32


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