Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study mechanisms involved in evolution of soft tissue sarcomas, we compared DNA ploidy and karyotypes at different stages of their disease in two patients with myxoid liposarcomas (MLS), one with a fibrosarcoma (FS), and two with rhabdomyosarcomas (RMS). None of the MLS samples revealed clearcut histologic changes in later samples as compared to their primaries, and the DNA ploidy in all samples was diploid. In one patient karyotypes at four different times during the 19 yr of his disease all revealed a t(11;12) (p15;q13), but additional clonal chromosomal abnormalities occurred only in later recurrences. In another patient the karyotypes obtained in the 26th and 28th yr of his disease were similar and included the t(12;16) (q13;p11), characteristic of MLS. A comparison with karyotypes of six other MLS patients at different disease stages suggests that the presence of a t(12;16) may correlate with less aggressive clinical behavior. The histology of the FS remained low-grade and the DNA ploidy diploid. The karyotype, however, showed evolution. In both MLS and FS, chromosomal changes thus seem to be a more sensitive marker for tumor progression than histologic changes or DNA ploidy. In one embryonal RMS, karyotypes obtained 7 and 11 yr after the primary diagnosis were different but clearly had a common "progenitor." In one alveolar RMS, the primary and the synchronous lung and lymph node metastases all revealed a t(2;13). The findings in RMS suggest that polyploidization is an early event in tumor evolution, especially in the alveolar subtype, which may be followed by additional chromosomal changes. In addition, DNA ploidy was measured in eight other RMSs. Among the RMSs the embryonal subtype was characterized by DNA aneuploidy, whereas three of the alveolar cases were in the tetraploid range and one was peridiploid. In local recurrences and in metastases changes in DNA index were observed in half the cases.
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PMID:DNA ploidy and karyotype in recurrent and metastatic soft tissue sarcomas. 134 14

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

A case of diffuse large cell lymphoma with t(2p-;8q+) is reported. Immunologically the lymphoma cells were shown to be of B-cell origin and positive for surface gamma and kappa chains, B4, CALLA, and Ia1 markers. Karyotypically three major clones were detected: 47,XX, + 12,t(2;8)(p11-13;q24) (52%); 47,XX, + 12 (26%); and 46,XX,t(2;8)(p11-13;q24) (15%). A t(2p-;8q +) has been exclusively reported in cases of Burkitt's lymphoma or Burkitt-type acute lymphocytic leukemia. The present case is the first one with t(2p-;8q +) observed in non-Burkitt-type lymphoid malignancy of the B-cell lineage. The t(2p-;8q +) may play a primary role in the early stage of transformation of B cells, and trisomy 12 may provide them secondarily with an advantage for tumor progression. The phenotypic pictures provided by 8q24 rearrangements seem to be heterogeneous, as previously suggested.
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PMID:A variant Burkitt-type translocation (2p-;8q+) in a patient with diffuse large cell lymphoma. 379 Nov 76

Recurrent pleural effusions from a 45-year-old man who was diagnosed as having non-Hodgkin's lymphoma of immunoblastic type were studied cytogenetically. The majority of the metaphases were tetraploid, but there were also lymphoma cells observed with pseudodiploid chromosome constitutions. Cytogenetic analysis by G-banding revealed the existence of at least two cell populations. The karyotype of the minor pseudodiploid clone, which exhibited partial trisomy of 1q11qter and monosomy of 6p11pter as sole abnormalities, was 46,XY,der(6)t(1;6)(q11;p11). The karyotype of the major clone was 92,XXYY,-1,der(6)t(1;6)(q11;p11)x2, +9. The ancestral diploid clone, carrier of the balanced translocation involving chromosomes 1 and 6, was not observed even in the first pleural effusion harvest. The high proportion of tetraploid cells in the recurrent effusions was an indication that these cells were favorably selected in the environment of the somatic cavity. Our cytogenetic findings suggest that partial trisomy of 1q may be a crucial secondary chromosomal abnormality in highly malignant non-Hodgkin's lymphoma. This genetic imbalance was predetermined from the primary abnormality and may be responsible for further tumor progression, as suggested from the clonal evolution in this particular case and, therefore, may be associated with the aggressive biologic behavior of malignant cells.
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PMID:Clonal evolution of an immunoblastic type non-Hodgkin's lymphoma with der(6)t(1;6)(q11;p11) as its primary cytogenetic abnormality. 785 Jul 53

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

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

Neoplastic transformation, cancer progression, and metastasis are determined by a series of well-defined changes that take place in target tissue cells. Genetic alterations associated with human prostate carcinogenesis are not well defined. Some chromosomal changes, including gain of chromosomes 7, 12, 17, and X and loss of heterozygosity in chromosomes 8p, 10q, 16q, 17p, and 18q, have been reported. We examined five newly established and eight previously established prostate cancer cell lines before and after subcutis and orthotopic injection into nude mice and observed that structural alterations of chromosome 5 were present in all of the cell lines except the parental LNCaP. The fluorescence in situ hybridization preparations with the use of whole chromosome 5 DNA painting probe confirmed our Giemsa-banding data. Alterations of chromosome 5 consisted of t(1;5)(p36;q15), t(5;?)(p11;?), del(5)(q23q35) in the SP2964(= ARCaP) cell line; t(5;8)(p15;q12), i(5)(p10), t(5;15)(q11;p11) in the SP3031 cell line; t(5;?;15) (q15;?;p11), t(5;7;14)(q31;p11-q32;q11), in the SP3173 and SP3241 cell lines (derived from the same patient); del(5)(q23-33) and t(5;7;14)(q31;p11-q32;q11) in the SP3316 cell line; t(3;5)(q21;q35) in the SP2884 cell line; t(5;5)(p15;q11) in the SP2356 cell line; i(5)(p10),t(5;?)(q23;?) in the DU-145 cell line; and i(5)(p10), t(5;?)(q11;?) and t(2;5)(q15;q15) in the PC-3 cell line. Because, in most cases, alteration of chromosome 5 resulted in the partial or complete loss of 5q, we conjectured that 5q might contain one or more tumor-suppressor genes for human prostate cancer development.
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PMID:Structural alterations of chromosome 5 in twelve human prostate cancer cell lines. 979 73

We describe a case of testicular B cell lymphoma with deletion of chromosome 5, del(5)(p11), as a sole structural abnormality. Histopathological diagnosis of the tumor was a high-grade lymphoma of the diffuse type containing cells positive for B cell specific antigen (CD20) and negative for the leukocyte common antigen (CD45). Deletion 5p may define the region of a tumor suppressor gene that could be associated with tumor progression and invasiveness and may serve as an indicator of poor prognosis in testicular lymphomas.
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PMID:Deletion 5p11 accompanied by multiple numerical changes in testicular lymphoma. 1173 24

We present karyotypes of 15 meningiomas with structural aberrations of chromosome 7, which were taken from a consecutive series of 400 cytogenetically characterized meningiomas. Twelve of these tumors (80%) displayed partial or complete monosomy 7p with a consensus deleted region of 7p12 approximately pter, in 6 of 15 cases arising from an unbalanced whole-arm t(1;7)(q11;p11), and in 4 of 15 cases from a whole-arm translocation involving other chromosomes. Other types of partial aneusomy 7 (3/15 cases) or balanced aberrations of chromosome 7 (2/15 cases) were relatively rare. In most cases (11/15), the centromeric region of chromosome 7 was involved in the rearrangements. We conclude that in meningiomas, the near-centromeric region of chromosome 7 is particularly prone to structural rearrangements most frequently resulting in monosomy 7p. The investigation of the histopathologic features of this rare cytogenetic subgroup of meningiomas showed no clear genotype/phenotype correlation. As 7 of 11 of the meningiomas with monosomy 7p belonged to World Health Organization grades II or III, which usually comprise less than 20% of all meningiomas, partial loss of 7p appears to be involved in tumor progression in meningiomas. Because monosomy 7p is typically associated with the strongly progression-associated monosomy 1p, however, monosomy 7p represents a cofactor more than a stand-alone feature of meningioma progression.
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PMID:Monosomy 7p in meningiomas: a rare constituent of tumor progression. 1281 Feb 58

Cathepsin B protein and activity are known to localize to the basal plasma membrane of colon carcinoma cells following the appearance of K-ras mutations. Using immunofluorescence and subcellular fractionation techniques and two human colon carcinoma cell lines - one with a mutated K-ras allele (HCT 116) and a daughter line in which the mutated allele has been disrupted (HKh-2)-we demonstrate that the localization of cathepsin B to caveolae on the surface of these carcinoma cells is regulated by mutant K-ras. In HCT 116 cells, a greater percentage of cathepsin B was distributed to the caveolae, and the secretion of cathepsin B and pericellular (membrane-associated and secreted) cathepsin B activity were greater than observed in HKh-2 cells. Previous studies established the light chain of annexin II tetramer, p11, as a binding site for cathepsin B on the surface of tumor cells. The deletion of active K-ras in HKh-2 cells reduced the steady-state levels of p11 and caveolin-1 and the distribution of p11 to caveolae. Based upon these results, we speculate that cathepsin B, a protease implicated in tumor progression, plays a functional role in initiating proteolytic cascades in caveolae as downstream components of this cascade (e.g., urokinase plasminogen activator and urokinase plasminogen activator receptor) are also present in HCT 116 caveolae.
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PMID:Mutant K-ras regulates cathepsin B localization on the surface of human colorectal carcinoma cells. 1496 44


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