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

A 19-year-old woman presented with a large mediastinal mass, histologically shown to be malignant lymphoma of lymphoblastic type (LBL). Immunophenotypic and gene rearrangement analysis unequivocally demonstrated that the neoplasm was of B-cell lineage. The neoplastic cells expressed terminal deoxynucleotidyl transferase, the pan-B cell antigens CD19, CD20, and CD22, and were negative for immunoglobulins and numerous T-cell antigens tested. Southern blot analysis showed rearrangement of one allele of the immunoglobulin heavy chain gene while the immunoglobulin kappa and T-cell receptor beta chain genes were in the germline configuration. Thus, the immunophenotypic and molecular findings in this case correspond to an early stage of B-cell differentiation, the pre-pre B-cell stage as has been named by others. In contrast with LBL of immature T-cell lineage, precursor B-cell LBLs involving the mediastinum are truly rare. Occasional cases have been reported that have arisen elsewhere and subsequently involved the mediastinum at time of relapse or tumor progression. Well-documented examples of immature B-cell LBL arising in the mediastinum are virtually unreported. The site and cell population giving rise to this neoplasm is unknown. However, origin from precursors of normal thymic medullary B cells is proposed as one possibility.
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PMID:Mediastinal lymphoblastic lymphoma with an immature B-cell immunophenotype. 131 99

Recently, the failure of interleukin 4 (IL4) autocrine growing CT4S cells to grow in vivo has been demonstrated. Because it could not be excluded that the cells produce insufficient amounts of IL4 to support their growth in vivo, subclones were established which are unresponsive to exogenous IL4 and therefore have acquired full growth autonomy. From the fact that the subclones likewise did not give rise to tumors when injected into nude mice, one may conclude that the IL4 production of autocrine growing CT4S prevents their growth in vivo. To test this hypothesis, a retroviral vector containing the IL4 gene under the control of the immunoglobulin heavy chain (Igh) enhancer/promoter was constructed and used to infect the myeloma cell line J558L. An IL4 producing clone was established (J558L-XEPIL4) and the tumor progression in comparison to the parental clone J558L was monitored in nude mice. The IL4 production significantly delayed the growth of J558L-XEPIL4 in vivo. Tumor suppression was much more evident when J558L-XEPIL4 cells were injected into syngeneic BALB/c mice. These results may explain why autocrine growing CT4S do not grow in vivo and suggest the involvement of functional T lymphocytes in the effectiveness of the host dependent anti-tumor action of IL4.
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PMID:Lack of tumorigenicity of interleukin 4 autocrine growing cells seems related to the anti-tumor function of interleukin 4. 227 62

Clonal selections occurring during the progression of Moloney murine leukemia virus (MuLV)-induced T-cell lymphomas in mice were examined in primary and transplanted tumors by monitoring various molecular markers: proviral integration patterns, MuLV insertions near c-myc and pim-1, and rearrangements of the immunoglobulin heavy chain and beta-chain T-cell receptor genes. The results were as follows. Moloney MuLV frequently induced oligoclonal tumors with proviral insertions near c-myc or pim-1 in the independent clones. Moloney MuLV acted as a highly efficient insertional mutagen, able to activate different (putative) oncogenes in one cell lineage. Clonal selections during tumor progression were frequently marked by the acquisition of new proviral integrations. Independent tumor cell clones exhibited a homing preference upon transplantation in syngeneic hosts and were differently affected by the route of transplantation.
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PMID:Tumor progression in murine leukemia virus-induced T-cell lymphomas: monitoring clonal selections with viral and cellular probes. 309 54

We report a case of CD7+ stem cell lymphoma. A 47-year-old man presented with general malaise and lumbago in April 1997. The patient exhibited swollen left cervical lymph-nodes and an intra-abdominal bulky mass. He was referred to us because lymph-node biopsy specimens indicated a diagnosis of diffuse type malignant lymphoma. An abdominal CT scan disclosed large retroperitoneal, para-aortic, and mesenteric root masses. Bone marrow involvement was shown by bone marrow biopsy specimens, though no circulating blasts were detected at presentation. The patient was treated with high-dose CHOP therapy without any benefit. Though ESHAP therapy was performed as salvage chemotherapy, the abdominal masses did not shrink at all. The patient died of tumor progression in November 1997. In the terminal stage, the lymphoma cells emerged in the peripheral blood and thus became available for analysis. The cells expressed CD5, 7, 34, 38, 71, but were negative for CD1, 2, 3, 4, 8, 10, 13, 14, 16, 19, 20, 21, 25, HLA-DR, and EMA. An immunoglobulin heavy chain gene rearrangement band was detected by Southern blot analysis. However, no T cell receptor lambda or beta chain gene rearrangement bands were detected.
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PMID:[Chemotherapy-resistant CD7-positive stem cell lymphoma presenting with intra-abdominal mass]. 1002 52

The molecular genetic hallmark of mantle cell lymphomas (MCL) is the reciprocal translocation t(11;14)(q13;q32) which juxtaposes the bcl-1 proto-oncogene to one of the joining segments of the immunoglobulin heavy chain gene. This translocation is very common in MCL and occurs in up to 70% of these malignancies. Due to the aggressive nature of MCL, markers identifying tumor progression and clinical outcomes are necessary. In this study we examined whether a corroborative relation exists between p53 mutations, bcl-1 translocation, and the proliferative fraction in MCL. We evaluated the proliferative fraction, p53 gene status, and bcl-1 translocation in 21 patients with confirmed MCL. Controls consisted of normal DNA and 7 B-cell lymphomas. Immunohistochemical detection of Ki-67 was used to assess proliferative activity while molecular techniques were used to detect p53 mutations and the bcl-1 gene translocation. Reactivity to the monoclonal antibody Ki-67 on neoplastic cells ranged from 5% to 40% in typical MCL cases. The bcl-1 gene translocation was detected by PCR in 48% (10/21) of MCLs while no rearrangements were detected by PCR in case control DNA. Screening exons 5-8 of the p53 gene for mutations did not identify a single mutation in any of the MCL cases. No correlation was found between p53 mutations, the presence of a bcl-1 translocation, and the proliferative activity of neoplastic MCL cells. We conclude that these markers may demonstrate independent events which occur during the pathogenesis of MCL.
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PMID:Proliferative fraction, bcl-1 gene translocation, and p53 mutation status as markers in mantle cell lymphoma. 1008 8

We describe here the first well-characterized case of "composite" lymphoma of the spleen in which the two components were a low-grade and a high-grade B-cell non-Hodgkin's lymphomas. The patient was an elderly man with prominent splenomegaly and multiple hypoechogenic lesions of the spleen. A splenectomy was performed, and the macroscopic and histological findings showed the simultaneous presence of a "low-grade" B-cell lymphoma, lymphoplasmacytoid (immunocytoma) and a "high-grade" B-cell lymphoma (immunoblastic), which were spatially separated. The two lesions expressed the same immunoglobulin light chain (lambda), but the Southern blot analysis showed different patterns of immunoglobulin heavy chain (IgH) clonal rearrangement. PCR analysis followed by direct sequencing of the IgH-amplified rearrangement products provided molecular-genetic evidence that the two components of the composite lymphoma had the same clonal origin. Since both EBV LMP-1 and p53 were negative by immunohistochemistry, it is unlikely that EBV and p53 were involved in the neoplastic progression in this case. PCR analysis and direct sequencing of IgH-amplified rearrangement products are useful tools to investigate clonality in cases in which Southern blot analysis cannot be performed or does not provide conclusive findings.
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PMID:"Composite" lymphoma, lymphoplasmacytoid and diffuse large B-cell lymphoma of the spleen: molecular-genetic evidence of a common clonal origin. 1052 9

We describe here two patients with mantle cell lymphoma (MCL) who after a few years, developed to the diffuse large cell lymphoma (DLCL) (anaplastic centrocytic lymphoma) growing in a diffuse sheets without the classical MCL component. In both the initial and second biopsy specimens, in each case, tumor cells were positive for cyclin D1, sIgM, sIgD, and CD5, but were negative for CD10 and CD23. In a study of immunoglobulin heavy chain (IgH) gene rearrangement, using the polymerase chain reaction (PCR) method, the products obtained from each paired biopsy tissue sample were the same size, and in one case had an identical sequence to the non-mutated VH gene. Immunohistochemistry was used to examine the expression of p53, p27Kip1 and cyclin E. Interestingly, there was clear overexpression of p53 protein in case 1 but not in case 2, compared with other typical MCL cases. The expression of p27Kip1 in the second biopsies of each case was decreased compared with those in the initial biopsies. In case 2, however, p27Kip1 was clearly expressed in the first and second biopsies, in contrast to other typical MCL cases. Thus these 2 cases demonstrate not only that the variant form of MCL may arise de novo, but also that MCL may transform to DLCL at the time of relapse. Although the mechanism of tumor progression/transformation is still poorly understood, the overexpression of p53 or p27Kip1 may be linked to a cellular mechanism involved in the development of the variant form of MCL.
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PMID:Expression of cell cycle regulating proteins in an unusual transformation of mantle cell lymphoma. 1061 57

We describe here two patients with mantle cell lymphoma (MCL) who after a few years, developed to the diffuse large cell lymphoma (DLCL)( anaplastic centrocytic lymphoma) growing in a diffuse sheets without the classical MCL component. In both the initial and second biopsy specimens, in each case, tumor cells were positive for cyclin D1, sIgM, sIgD, and CD5, but were negative for CD10 and CD23. In a study of immunoglobulin heavy chain (IgH) gene rearrangement, using the polymerase chain reaction (PCR) method, the products obtained from each paired biopsy tissue sample were the same size, and in one case had an identical sequence to the non-mutated VH gene. Immunohistochemistry was used to examine the expression of p53, p27(Kip1) and cyclin E. Interestingly, there was clear overexpression of p53 protein in case 1 but not in case 2, compared with other typical MCL cases. The expression of p27(Kip1) in the second biopsies of each case was decreased compared with those in the initial biopsies. In case 2, however, p27(Kip1) was clearly expressed in the first and second biopsies, in contrast to other typical MCL cases. Thus these 2 cases demonstrate not only that the variant form of MCL may arise de novo, but also that MCL may transform to DLCL at the time of relapse. Although the mechanism of tumor progression/transformation is still poorly understood, the overexpression of p53 or p27(Kip1) may be linked to a cellular mechanism involved in the development of the variant form of MCL.
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PMID:Expression of Cell Cycle Regulating Proteins in an Unusual Transformation of Mantle Cell Lymphoma. 1104 6

A molecular cytogenetic study was performed on the diagnostic tumor sample and three relapses from a case with blastoid mantle cell lymphoma. The clonal relatedness of the tumors was demonstrated by identical rearrangements of the immunoglobulin heavy chain gene and was supported by results from comparative genomic hybridization analyses. All samples shared the common alterations of losses of 6q, 9p, and 11q and gains of 3q, 9q, 12p, and 13q, suggesting that they were relatively early events in the tumorigenesis. Relapse 1 also showed a loss of 8p, while relapses 2 and 3 had gained the X chromosome and 7p, in addition, relapse 3 displayed gains of chromosomes 3 and 20. Taken together, the findings suggest that relapses 2 and 3 developed from the diagnostic tumor sample, while relapse 1 represents a separate lineage of tumor progression originating directly from a postulated ancestral tumor cell carrying the common chromosomal alterations identified in all tumors.
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PMID:Clonal development of a blastoid mantle cell lymphoma studied with comparative genomic hybridization. 1254 56

To assess a possible role in tumor progression, the occurrence and type of K- and N-RAS mutations were determined in purified tumor cells, including samples from patients with premalignant monoclonal gammopathy of undetermined significance (MGUS), multiple myeloma (MM), and extramedullary plasma cell (PC) tumors (ExPCTs). Immunophenotypic aberrant PCs were flow sorted from 20 MGUS, 58 MM, and 13 ExPCT patients. One RAS mutation was identified in 20 MGUS tumors (5%), in contrast to a much higher prevalence of RAS mutations in all stages of MM (about 31%). Further, oncogene analyses showed that RAS mutations are not evenly distributed among different molecular subclasses of MM, with the prevalence being increased in MM-expressing cyclin D1 (P = .015) and decreased in MM with t(4;14) (P = .055). We conclude that RAS mutations often provide a genetic marker if not a causal event in the evolution of MGUS to MM. Surprisingly, RAS mutations were absent in bone marrow tumor cells from all patients with ExPCT, a result significantly different from intramedullary MM (P = .001). From 3 of 6 patients with paired intramedullary and extramedullary PCs and identical immunoglobulin heavy chain gene (IgH) sequences, RAS mutations were identified only in extramedullary PCs, suggesting a role for RAS mutations in the transition from intramedullary to extramedullary tumor.
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PMID:Possible roles for activating RAS mutations in the MGUS to MM transition and in the intramedullary to extramedullary transition in some plasma cell tumors. 1533 50


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