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

The cases are presented of 4 hydantreated epileptic patients developing malignant lymphomas (1 Hodgkin's lymphoma). The duration of the hydantoin therapy ranged from 7 to 23 years. There was no evidence of an allergic drug reaction, with the exception of slight blood eosinophilia. Prior to the lymphoma one patient exhibited leukopenia and a second thrombocytopenia. Hydantoins were discontinued in 3 cases but the lymphomas never disappeared spontaneously and only once did tumor progression came to a stillstand. Two patients were successfully treated with either chemo- or radiotherapy. Possible correlations between the documented immunosuppressive action of hydantoin derivatives and tumor induction are discussed. Malignant lymphomas may be sequelae of long-term hydantoin therapy and are not always preceded by the well-known reversible hydantoin lymphadenopathy.
 ...
PMID:[Malignant lymphoma following years of hydantoin treatment for epilepsy]. 121 68

In this study we examined the P170-expression (mdr-phenotype) in 42 non-Hodgkin's Lymphomas with variant entities immunohistochemically with the mab JSB1. The mdr-phenotype was related to the tumor proliferation as measured by Ki67-expression and AgNOR numbers. Furthermore the mdr-phenotype was related to the tumor associated T-lymphocytes. The mdr-phenotype showed no relation to histological type and the proliferation of the tumor. There was a positive correlation between the mdr-phenotype and CD2-reactive lymphocytes. There was also a significant positive correlation between CD4-reactive lymphocytes and the mean number of AgNOR's. Possibly P170-expression and proliferation of the tumor cells have a lymphotactic effect on T-lymphocytes. The latter could promote tumor progression by means of paracrine mechanisms.
 ...
PMID:[Tumor proliferation, MDR phenotype and tumor associated t-lymphocytes in non-Hodgkin's lymphomas]. 128 69

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.
 ...
PMID:Mediastinal lymphoblastic lymphoma with an immature B-cell immunophenotype. 131 99

These studies were designed to look for a correlation of intrathymic survival of virus-infected thymocytes with lymphomagenesis. Cells from the normal-appearing prelymphoma thymus of SL3-3 virus-treated AKR mice were studied. Also, phenotypic properties of the malignant cells from the virus-induced lymphomas are described. In this model system, 100% of mice inoculated with virus at three days of age develop thymic lymphoma between 60 and 90 days of age. The experiments show that cells with malignant potential do not appear in the thymus until 36 days after virus inoculation. These cells are initially thymus-dependent (TD) in that they produce lymphoma of donor-type in recipients after intrathymic inoculation with long latency. They do not produce lymphoma after subcutaneous inoculation in syngeneic hosts. At 39 days after virus inoculation, the first thymus independent (TI) lymphoma cells appear. These cells, like the cells isolated from thymi with overt tumors, produce lymphoma of donor-type after a short latency when inoculated by the intrathymic or subcutaneous route. Thymocytes from normal-appearing thymi of mice at 42 days after virus inoculation, which could be expected to include TD, TI or no lymphoma cells, were evaluated for their ability to survive in a recipient thymus for three weeks after intrathymic inoculation. They were compared to thymocytes from age-matched control mice. Thymi receiving the virus-infected thymocytes showed 15% to 80% donor cells at three weeks. The highest numbers of donor cells were from thymi which were shown to contain TI lymphoma cells. However, cells from thymi with TD and no lymphoma cells could also be detected in significant numbers at three weeks after intrathymic inoculation. Less than 2% of donor-type thymocytes could be found after inoculation of thymocytes from normal control AKR mice. These data provide evidence that virus infection of thymocytes, even before the appearance of cells with lymphomagenic potential, endows them with a capacity for prolonged intrathymic survival. This appears to be a necessary step for tumor progression in this model. A remarkable phenotypic diversity of the virus-induced lymphomas was shown. The effect of various growth environments, intrathymic, subcutaneous, and in vitro on lymphoma cell phenotypic expression revealed individual differences in each tumor and in each environment.
 ...
PMID:Observations on lymphomagenesis and lymphoma in AKR mice. A description of prelymphoma changes in the thymus and phenotypic diversity of lymphomas induced by SL3-3 virus. 138 66

p53 is a tumor suppressor gene that commonly undergoes mutations in human tumors, including lymphomas. Because p53 mutations are not restricted to a single locus, immunohistochemistry is useful to detect p53 expression and correlate this finding with lymphoma phenotype. Cryostat sections from 125 cases of lymphoma were analyzed for p53 expression using three different monoclonal antibodies (pAb 421, 1801, 240) which react with human cellular p53 and a common conformational epitope on mutant p53. A control antibody (pAb 246) reacts only with wild type p53 of murine origin and was negative in all cases. Tissue from 29 cases of lymphoid hyperplasia, including six from human immunodeficiency virus-positive (HIV+) patients, were negative for p53. p53 was predominantly localized in nuclei of high-grade lymphomas, including 14 of 46 cases of B cell immunoblastic lymphomas and two of five T cell immunoblastic lymphomas. p53 expression was relatively common in lymphomas from HIV+ patients, and unusual in intermediate and low-grade lymphomas of follicular center cell type. Low-grade lymphoma of small lymphocytic type disclosed p53+ large cells (paraimmunoblasts) that may play a role in tumor progression in this lymphoma subtype. p53 was also strongly expressed in the nuclei of Reed Sternberg cells from 19 of 37 cases of Hodgkin's disease, including six cases of mixed cellularity, and 13 cases of nodular sclerosing type. Immunohistochemical staining is a rapid method to identify p53 expression in lymphomas.
 ...
PMID:Immunohistochemical analysis of p53 expression in malignant lymphomas. 146 98

Fifteen previously untreated dogs with histologically confirmed, high-grade multicentric lymphoma were entered into a phase I study to evaluate combined doxorubicin and whole-body hyperthermia (DOX/WBH). Groups of three, four, and eight dogs were treated with whole-body hyperthermia and concurrent doxorubicin at 12 mg/m2, 24 mg/m2 and 30 mg/m2, respectively, after one doxorubicin induction dose at 30 mg/m2. Plateau temperature (42 +/- 0.1 degree C) was maintained for 90 minutes using a radiant heating device. A total of five DOX/WBH treatments per dog were planned, and these were given every 21 days. Treatment-related toxicity was not seen in the 12-mg/m2 doxorubicin dose group. Tumor progression prohibited administration of more than three DOX/WBH treatments to any dog in the 12-mg/m2 group. Premature ventricular contractions developed after the fifth treatment in one of the four dogs treated with 24 mg/m2 of doxorubicin. Two dogs (25%) in the 30-mg/m2 dose group had treatment-related toxicity. One dog experienced acute serious myelosuppression 1 week after the third treatment. This dog received all planned DOX/WBH treatments. Asymptomatic cardiac toxicosis consisting of decreased ejection fraction and fractional shortening developed in the second dog. This dog received only two DOX/WBH treatments. The three dogs treated at 12 mg/m2 had partial responses of short duration (60-83 days). Four dogs treated at 24 mg/m2 had complete responses for 150, 164, 186, and 200 days. Eight dogs treated at 30 mg/m2 had complete responses with a mean and median duration of 241 and 190 days, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Phase I evaluation of doxorubicin and whole-body hyperthermia in dogs with lymphoma. 152 56

The treatment of metastatic growth still constitutes a challenge for cancer research. Tumor progression is often accompanied by a loss in sensitivity to previously efficient drugs. Decreased intracellular accumulation of cytotoxic agents is probably the major reason for drug resistance, although other mechanisms have also been described. Properties of the cell membrane have been shown to determine the metastatic phenotype. This cellular organelle is also responsible for the multiple drug resistance phenomenon. Membrane-active agents may increase cell permeability to drugs, counteracting thereby drug resistance. In the present study the effect of the nonionic detergent Tween 80 on sensitivity to adriamycin (ADR) of cells derived from Lewis lung carcinoma 'primary tumors' (PT)-the local growth following subcutaneous inoculation - and 'metastatic tumors' (MT) - lung tumors which develop following intravenous injection - was compared. Flow cytometry analysis demonstrated several differences between cells derived from the PT and the MT: (1) single ADR treatment showed that MT cells possessed a lower percentage of a high ADR permeability subpopulation than PT cells; (2) a dose-dependent shift to a higher ADR accumulating population was seen in the presence of Tween 80 for both cell types. However, the increase in percentage of high ADR permeability cells was more pronounced in MT (up to x4.7) than in PT (up to x1.3) cells. This differential effect of the membrane-acting agent was evident at various ADR (10-50 micrograms) and Tween 80 (0.1-0.4%) concentrations. The present results corroborate previous data obtained in our group in another tumor progression model, AKR lymphoma.
 ...
PMID:Effect of a membrane-active agent on uptake of adriamycin in Lewis lung carcinoma cells derived from 'primary' and 'metastatic' growths. 161 5

The comprehension of tumour progression has advanced due to the use of various models, the most rewarding being probably the study of malignancy variants derived from the same tumour. In the present study the biological behaviours of three AKR lymphoma variants were compared. The three variants, TAU-33, TAU-38 and TAU-39, differed markedly in biological behaviour. The TAU-39 variant formed very large 'primary tumours', TAU-33 produced local growths of intermediate size, and TAU-38 formed small s.c. tumours. However, the metastatic potentials of the variants were inversely related to their ability to produce local tumours. According to various parameters (spread to organs, cachexia and mice mortality rate), the variant of highest metastatic potential was TAU-38, the one of intermediate ability TAU-33 and the TAU-39 had the least aggressive behaviour. A lack of difference in invasive capacity as well as a similar ranking of malignancy by both s.c. and i.v. inoculation indicate a differential behaviour in late metastasis phase. Tumour progression models may contribute to a better understanding of this threatening process and to testing of new treatment modalities suitable for cancer at different stages.
 ...
PMID:Differential metastatic capacity of three AKR lymphoma variants. 162 41

Lymphoma denotes a heterogeneous group of neoplasms derived from lymphoreticular tissues. It can cause neurologic symptoms by infiltrating into the meninges or brain parenchyma. Alternatively, lymphomas may metastasize to bone or infiltrate into the epidural space via intervertebral foramina to cause neurologic dysfunction by compressing adjacent CNS structures. These direct effects can occur at any time during the disease process; most distressingly, meningeal infiltration may be the initial site of relapse after a complete remission. Diffuse and more undifferentiated lymphomas are much more likely to be responsible for producing either meningeal infiltration or intraparenchymal lesions. Direct CNS invasion by lymphoma is associated with significant patient morbidity and short survival despite intensive therapy; whether this manifestation of lymphoma can be prevented by prophylactic CNS treatment remains uncertain. CNS complications may also occur as a result of indirect effects of lymphoma. Therefore, CNS dysfunction may develop as a result of infections that occur secondary to immunosuppression, as a result of antineoplastic therapies, or as a result of true paraneoplastic syndromes. It is important to distinguish between these indirect effects and tumor progression because their recognition permits frequently available appropriate treatment modalities to be administered.
 ...
PMID:Neurologic complications of systemic lymphoma. 175 25

We report a lymphocytic lymphoma showing a combination of two characteristic neoplasia-associated chromosomal changes: trisomy 12, commonly observed in chronic lymphocytic leukemia and lymphocytic lymphoma, and t(18;22)(q21;q11), a variant form of the t(14;18)(q32;q21) found in most follicular lymphomas. Southern blot analysis was performed using probes for the 5' end of the BCL2 gene (18q21) and for the J lambda as well as C lambda immunoglobulin genes (22q11). With these two probes, a unique rearranged fragment was detected. Thus the t(18;22)(q21;q11) can be considered as a variant translocation of t(14;18)(q32;q21). The karyotypic analysis supports the assumption that in our case trisomy 12 occurred first, and t(18;22) appeared during tumor progression as part of the clonal evolution. This is at variance with the typical t(14;18), which has never been found to occur as a secondary change.
 ...
PMID:t(18;22)(q21;q11) with rearrangement of BCL2 as a possible secondary change in a lymphocytic lymphoma. 186 35


1 2 3 4 5 6 7 8 9 10 Next >>