Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed the correlations between chromosome abnormalities and clinical and histopathologic characteristics in 77 cases of renal cell carcinoma (RCC). Chromosome changes such as +5,+7,+8,+10,+18,+X,+Y, and -Y have been excluded from the analysis because they also occur in nonneoplastic kidney tissue and cytogenetic analysis indicates that these anomalies are not involved in tumor progression. The most frequent specific chromosome abnormalities in this sample were 3p rearrangements, trisomy 17, and hyperdiploidy and were not related to tumor stage or grade or to development of distant metastases.
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PMID:Clonal chromosome changes in renal carcinoma do not correlate with clinical stages and histopathologic grades. 133 79

Chromosomal analysis of two pulmonary metastases from a 25-year-old male with alveolar soft-part sarcoma of the right lower extremity revealed multiple and complex chromosomal abnormalities. The rearrangements included deletions and translocations affecting chromosomes 1, 2, 3, 10, 11, 14, 15, and 16. Trisomy of chromosome 12 and loss of chromosome 17 was also observed.
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PMID:Multiple and complex abnormalities in a case of alveolar soft-part sarcoma. 193 19

Cytogenetic analysis was performed on 11 benign and borderline ovarian tumors. Trisomy 12, identified as a sole abnormality in 6 tumors, is likely a specific karyotypic change in different benign and borderline tumors and may well be a primary chromosomal lesion in these tumors. The possible association between amplification of the proto-oncogene K-ras-2 which is located on chromosome 12 and trisomy 12 was investigated. DNA blotting analysis of 64 tumors indicates that trisomy 12 does not seem to be related to K-ras-2 amplification in ovarian tumors. K-ras-2 amplification was observed in 3 high-grade tumors from 3 patients with metastases.
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PMID:Trisomy 12 and K-ras-2 amplification in human ovarian tumors. 207 Dec 29

Of 8 tumors surgically extirpated from 8 patients with renal cell carcinoma, 7 were successfully processed in short-term culture by collagenase method, and 130 metaphases were extracted from these 7 tumors and were subjected to chromosomal analysis according to the G banding technique. As for karyotype, 4, 2 and 1 cases were mainly diploid, hypodiploid and aneuploid, respectively. The highest incidence of chromosome aberration was marked by #3 chromosome (5 of 7 cases of which 4 and 1 showed monosomy as clonal aberration and trisomy as non-clonal aberration, respectively). The commonest gain of chromosome was noted for #7 trisomy (4 of 7 cases). Two cases had already had metastases at the time of surgery, each showing #7 trisomy. Marker chromosome was noted in 6 of 7 cases. Structural chromosome aberration had a lesser incidence compared with numerical aberration; only clonal aberrations were long-arm aberrations (2q+, 6q+) of #2 and #6 chromosomes. Short-arm aberrations (3p-, 8p-) of #3 and #8 chromosomes were noted in one case each. 3p deletion, which is reported to be predominant in the literature, was noted only in one case. This was observed in triploid cells. However, all of metaphases showing 2q+ and 6q+ had concomitant #3 monosomy, and excess portions of #2 and #6 chromosomes were in good agreement with the band pattern of #3 chromosomal long-arm. Therefore, translocation of 3q12-qter in #2 and #6 chromosomes is supposed to lead to 3p deletion. A similar mechanism seems to be involved in the formation of marker chromosomes, suggesting the involvement of deleted #3 chromosome in marker chromosomes.
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PMID:[Chromosome analysis of renal cell carcinoma]. 223 31

We report a case of an immature malignant ovarian teratoma with peritoneal implants diagnosed in an 18-year-old woman. The tumor was brought into remission after surgery (three laparotomies) and adjuvant chemotherapy. A residual peritoneal implant showed a mature epithelial and glial configuration. Histologically, the neuroectodermal component was dominant in the original tumor as well as in the metastases, being confirmed by immunohistochemistry and electron microscopy. A stem cell line has been obtained with cell culture, having a germ cell character and a yolk sac configuration. This line possessed a trisomy 12 and a translocation (7;9) similar to other chromosomal abnormalities described in immature teratomas of the testes and ovaries.
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PMID:Trisomy 12 and translocation (7;9) in an ovarian immature teratoma. 276 76

Subcutaneous (s.c.) inoculation of the 85-4LN subline, derived from a lymph nodal metastasis of the Epstein-Barr virus (EBV) transformed human chronic lymphocytic leukemia (CLL) B cell line, EBV-CLL (1), produced progressively growing lethal tumors in 31/35 nonirradiated (88.6%) and 22/25 (88%) of whole-body irradiated (440 rad) nude mice. In contrast, EBV-CLL(1) could produce progressive tumors only in irradiated nude mice. All 85-4LN cells had Epstein-Barr virus nuclear antigen and reacted with pan B and anti-la antibodies. The morphology and ultrastructural features was consistent with the lymphoblastoid nature of the cells. In all s.c. tumor bearing mice, there was enlargement of the spleen and draining lymph nodes. Karyological studies revealed human cells in the spleen and draining nodes in all the mice investigated. Metastases in nonlymphoid organs were seen in 1/8 irradiated and 8/12 nonirradiated mice. The subline contained 77% cells with 47,XY, +12 and 23% cells with 45,XY karyotype. The clone with trisomy 12 did not have any growth advantage either in s.c. transplants or in splenic/lymph nodal metastases. Treatment with the maximum permissible doses of methotrexate (MTX) or chlorambucil (CBL) revealed xenografts to be more sensitive to MTX than CBL. A clone with a 1g+ marker, i.e., 46,XY,Dup(1) (q11----q32) appeared to be associated with resistance to CBL. We have not seen any previous report on the growth and dissemination of human CLL B cells in nonirradiated nude mice. The 85-4LN subline, thus, provides a model for studying the progression, dissemination and therapeutic response of human CLL-B cells.
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PMID:Progression of a human B cell chronic lymphocytic leukemia line in nude mice. 284 46

The hypothesis of tumor progression proposed by Nowell [P. C. Nowell, Science (Wash. DC), 194: 23-28, 1976] states that one mechanism for the development of the metastatic phenotype could be the induction of chromosomal instability. We have developed a new experimental system for studying the induction of the metastatic phenotype using early passage fibroblasts which become metastatic in nude mice after transformation with the Harvey ras oncogene [R. J. Muschel et al., Am. J. Pathol., 121: 1-8, 1985; R. Pozzatti et al., Science (Wash. DC), 232: 223-227, 1986]. Since the early passage fibroblasts themselves are diploid, we reasoned that this might be a system in which karyotypic change after tumor formation or metastasis might easily be evaluated. Thus, we performed cytogenetic analysis on multiple metastases and tumors which had been derived from cells transformed with the cellular Harvey ras1 oncogene and compared their karyotypes. The karyotypes of the cells isolated from 5 tumors and 14 metastases were, as far as we could determine, identical to those of the injected cells. This could easily be evaluated because of the two clones studied one was diploid; the other has a trisomy of chromosome 4 without any other detectable abnormality. These results suggest that in this system using nude mice, selection for a necessary or even advantageous chromosomal aberration does not occur during tumor formation or metastasis. Furthermore, they indicate that the presence of the ras gene itself does not induce chromosomal rearrangements or aneuploidy and that a cell can be both tumorigenic and metastatic yet remain diploid.
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PMID:Karyotypic analysis of diploid or near diploid metastatic Harvey ras transformed rat embryo fibroblasts. 373 Oct 77

To evaluate the significance of karyotypic evolution of tumor cells with an 8;14 translocation [t(8;14)(q24;q32)], we examined the clinicopathologic features and immunologic phenotypes of nine Japanese patients with various types of B-cell malignancy with the translocation. All these patients had structural rearrangements of the long arm of chromosome No. I (Iq) in a stem line or the subline of tumor cells with a t(8;14). The rearrangements were composed of a translocation involving Iq with other chromosomes and a tandem duplication of Iq, and they were exclusively associated with a partial trisomy for Iq. Two patients with diffuse large-cell lymphoma, whose tumor cells did not express surface immunoglobulins (s-Ig), had the Iq translocation in their highly complex karyotypes. Tumor cells from the other seven patients expressed s-Ig and the karyotypes were relatively simple. Among these patients, the Iq translocation was found in two patients with Burkitt's lymphoma, and the Iq duplication were observed in a stem line or the sublines from four patients with Burkitt's lymphoma-leukemia and one each with small non-cleaved-cell or diffuse large-cell lymphoma. Except for one patient in the stage of IE, these patients had a poor prognosis because of the clinical conversion of extranodal metastases in the earlier disease phase. These findings are compatible with those of Western patients with a t(8;14). Therefore, tumor cells marked primarily with a t(8;14) could have "major routes" in the karyotypic evolution, for which potentials should be recognized as clinical risk factors, and the morphologic presentation and the expression of surface immunoglobulins may be associated with the process of karyotypic evolution.
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PMID:Karyotype evolution in B-cell lymphoid malignancy with an 8;14 translocation. 660 42

Trypsin G banding was performed on metaphase chromosomes from 14 cell lines derived from primary tumors or metastases of 11 patients with testicular cancer. Most of the cell lines, 11 of 14, have a modal number between 51 and 61. All lines have numerical and structural changes involving chromosome 1 with trisomy of the q arm being the common aberration. Break points in chromosome 1 were nonrandom, being concentrated in the regions of p12, q12, p36, and p22, which resulted in morphologically identical marker chromosomes in different cases. These changes probably are not artifacts of cell culture. In one instance, three lines derived from the same patient, one from tissue removed at operation, and two from separate metastases removed at autopsy nearly 3 years later after unsuccessful radiotherapy and chemotherapy had identical chromosome compositions. In another case, lines derived from a primary tumor and a metastasis from the same patient also had identical marker chromosomes. The consistent involvement of chromosome 1 in aberrations may be associated with the highly malignant nature of testicular cancers.
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PMID:Nonrandom abnormalities in chromosome 1 in human testicular cancers. 747 Oct 97

We used the fluorescence in situ hybridization (FISH) method to show that chromosome 7 trisomy is associated with the progression of human prostate cancer. Thirty-six specimens including 15 primary prostate carcinomas, 16 metastatic lesions, and 5 normal prostate tissues, as well as 2 prostate carcinoma cell lines of different tumorigenic potential, were examined for chromosome 7 aneuploidy. Our results showed that the androgen-unresponsive tumorigenic cell line PC-3 exhibited a significantly higher ratio of chromosome 7 to total chromosome number than the androgen-responsive nontumorigenic cell line LNCaP (P = 0.001). In prostate specimens, the frequency of trisomy 7 cells was significantly increased (P < 0.05) in the advanced stage tumors (C and DI) but not in the early (B) stage tumors or normal prostatic tissue. Furthermore, metastases showed a higher frequency of trisomy 7 cells than primary tumors (P = 0.005). In 2 patients with paired primary and metastatic tumors, trisomy 7 cells increased from 4-7% in the primary tumors to 42-45% in the metastatic tumor cells in the bone marrow. Therefore, our data suggest that trisomy 7 may be a common feature associated with local and metastatic progression and serve as a novel marker for human prostate cancer progression.
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PMID:Trisomy 7: a potential cytogenetic marker of human prostate cancer progression. 750 96


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