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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The genetics of late appearing MSV tumors showing a progressive growth pattern in AKR mice was investigated. The late MSV tumor response in F1 hybrids depended on the genetic background of the non-AKR parent. Within the 4-month observation period following virus injection, (CBA X AKR) F1, (DBA/2 X AKR)F1, and (NIH X AKR)F1 developed progressing MSV tumors, which exhibited latency and growth behavior comparable to that seen in AKR mice, (BALB X AKR)F1, (B6 X AKR)F1, and (B10br x akr)f1 mice did not show any late MSV tumors. In contrast to early regressing M-MSV tumors, whose development is independent of Fv-1 genotype, late MSV tumor progression is largely a function of this gene, since all late tumors which appeared in (B10BR x AKR) x AKR were observed in Fv-1n homozygous mice, H-2k halotype is a further factor in the occurrence of late MSV tumors, at least in (B6 x AKR) x AKR mice. In crosses of AKR with Fv-1 compatible mice, tumor appearance was strongly associated with inheritance of AKR-Mulv, and MSV recovered from late tumors of first back-cross animals appeared to be a new pseudotype with the endogenous AKR-MuLV. It is suggested that the host genetic control in both early and late MSV tumors is exerted mainly on the helper component of the leukemia-sarcoma complex.
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PMID:Genetics of murine sarcoma virus (MSV)--induced tumors in AKR mice: Evidence that late progressing and early regressing tumors are controlled by different gents. 6 12

Feline leukemia is an infectious disease caused by a horizontally transmitted virus. Infection of animals or cultured cells with feline oncornaviruses results in the expression of a specific cell membrane antigen, feline oncornavirus-associated cell membrane antigen (FOCMA). The humoral antibody response to FOCMA is directly correlated with tumor progression. The measurement of this antibody is a useful tool for determining virus exposure. Using this procedure it was determined that cats living in leukemia "cluster" households as well as cats used as contact controls in virus injection experiments have a risk of infection of 90% or higher.
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PMID:Immune response of healthy and leukemic cats to the feline oncornavirus-associated cell membrane antigen. 16 20

An experimental system was developed that permitted nonrandom chromosome changes that occur in radiation leukemia virus (RadLV)-induced lymphomas to be followed during tumor progression. RadLV variant-induced preleukemia and leukemia cells originating from female inbred C57BL/6 mice were injected into male animals of the same strain. Since all donors were females and all recipients were males, the sex chromosome complements (XX and XY) were used to distinguish the preleukemia and leukemia cells from those of host origin. The G-banding analysis revealed that more than 50% of animals that were inoculated with preleukemia cells and that developed leukemia possessed tumor stem-lines of 41 chromosomes with a tristomy of chromosome #15. In animals inoculated with overt leukemia cells and in which tumor progression occurred, the G-banding an additional trisomy of chromosome #17. The cytogenic data strongly suggested that the trisomy of chromosome #15 was the first specific tumor-associated chromosome change that occurred in the process of conversion of RadLV-induced preleukemia cells to fully autonomous tumor cells.
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PMID:Chromosome changes (trisomies #15 and 17) associated with tumor progression in leukemias induced by radiation leukemia virus. 20 3

There is abundant evidence that leukemia arise through somatically acquired genetic changes. Familial or congenital predisposition is rarely involved. These genetic changes are often visible as chromosomal aberrations. Molecular analyses of the DNA sequences rearranged in leukemia has demonstrated the presence of cellular oncogenes which are modified (fused, mutated, truncated) by the specific translocations. This results in a disturbance of the delicate balance between proliferation and differentiation and constitute a major step towards cell transformation. Some of these genetic rearrangements have been analyzed in depth, but the exact defect that causes leukemia is often not yet understood. Meanwhile these studies have increased our knowledge of normal cell proliferation and differentiation and provided us with new tools for diagnosis and for developing more specifically targeted treatment. An example would be the production of antibodies that recognize specifically the new chimeric proteins. Oncogenesis is a complex and multiple step process that proceeds by acquisition of successive genetic insults. The different steps do not necessarily occurs following a predetermined order, although some secondary changes are preferentially induced by a given first mutation. In leukemia, sequential changes in karyotype are well documented but molecular makers for tumor progression have not yet been systematically investigated. This is one of our many challenges for the future.
Leukemia 1992 Nov
PMID:Cytogenetics and oncogenes. 143 20

Sixty-day bioassays of iodinated glycerol, trichlorfon, and acetaminophen were conducted using a leukemia transplant model in 6- to 8-week-old F344 rats to investigate the potential of these chemicals to affect tumor progression. The chemicals were administered in the drinking water at doses that approximated those used in previously conducted 2-year carcinogenesis studies. Simultaneous with dose administration, half of a group of young, healthy, syngeneic rats were given subcutaneous transplants of mononuclear cells derived from spleens of leukemic donors. Variables used to quantitate tumor progression included body weight, spleen weight, white blood cell (WBC) and red blood cell (RBC) counts, packed cell volume, hemoglobin concentration, and platelet counts. Iodinated glycerol at 1.25 or 2.5 mg/ml caused a greater increase in leukocytosis in dosed transplant recipients in comparison to that experienced by undosed recipients: trichlorfon at 2.5 or 5.0 mg/ml enhanced splenomegaly and induced greater reductions in RBC parameters in dosed recipients in comparison to that experienced by undosed recipients. Acetaminophen at 3.0 and 6.0 mg/ml resulted in insignificant but dose-related increases in spleen weight and leukocytosis only in the female rat transplant recipients, as was observed in 2-year studies. Based on results from the short-term leukemia transplant model, data from 2-year carcinogenicity studies, and structure-activity considerations, exposure to iodinated glycerol and trichlorfon was more strongly associated with the expression of leukemia than exposure to acetaminophen. The potential carcinogenicity of each of these chemicals should be taken into consideration when calculating estimates of risk and decisions for their use.
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PMID:The effects of iodinated glycerol, trichlorfon, and acetaminophen on tumor progression in a Fischer rat leukemia transplant model. 145 7

A young male patient progressed rapidly from localized abdominal lymph node enlargement to overt acute lymphoblastic leukemia. Despite aggressive treatment, he died of progressive CNS leukemia 5 months after initial presentation. At diagnosis, karyotypic analysis of an abdominal lymph node revealed the coexistence of t(14;18) (q32;q21), specific for follicular lymphoma, and t(8;22) (q24;q11), a variant Burkitt translocation. Such cases might be considered as a model for a general mechanism of tumor progression with cascade-like involvement of oncogenes.
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PMID:Simultaneous occurrence of t(14;18) and t(8;22) common acute lymphoblastic leukemia. 155 91

The effects of acute and chronic ethanol administration on tumor progression and metastasis were studied in rat models of leukemia and breast cancer, respectively. Acute administration of 1.5-3.5 g of ethanol/kg body weight significantly reduced survival of rats injected with CRNK-16 leukemia cells in a dose-related manner. Acute administration of 2.5-3.5 g of ethanol/kg body weight, one hour before tumor inoculation, or chronic consumption of liquid diet containing ethanol for two weeks before and three weeks after tumor inoculation, significantly increased the number of lung metastases of MADB106 mammary adenocarcinoma. The ethanol-induced increase in the number of metastases was not correlated with plasma levels of corticosterone and was not altered by the opiate antagonist naltrexone. Incubation of spleen cells in vitro in the presence of ethanol, at concentrations comparable to those measured in the blood of ethanol-treated rats, significantly suppressed natural killer (NK) cell activity against MADB106 cells in a standard chromium-release assay and decreased the binding of effector to MADB106 tumor cells. However, neither acute nor chronic ethanol administration in vivo altered splenic NK activity against this tumor in the same in vitro assay, in which the ethanol would have been washed away. These results suggest that, in the presence of ethanol, tumor progression is facilitated. The possibility that this facilitation is related to ethanol-induced impairment of the normal tumoricidal interaction between NK and tumor cells is discussed.
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PMID:Ethanol increases tumor progression in rats: possible involvement of natural killer cells. 157 4

A human multiple myeloma (MM) cell line, U-266, has developed the ability to grow independently of exogenous interleukin 6 (IL-6) during long-term cultivation in vitro. The early passage, feeder-cell dependent U-266 cell line (U-266-1970) was compared with the late passage U-266-1984 cell line with respect to response to IL-6, IL-1 beta and tumour necrosis factor alpha and expression of IL-6 and IL-6 receptor (IL-6R) mRNA and protein. The results showed that; (a) only the U-266-1970 cell line was stimulated to growth by IL-6, (b) IL-6 and IL-6R mRNA were expressed in both cell lines, (c) the level of IL-6 mRNA was increased in the U-266-1984 cell line and only this line produced IL-6 and, (d) the level of IL-6R mRNA was highest in the U-266-1984 cell line and the number of IL-6R about ten times higher than in U-266-1970. The growth of the IL-6-producing U-266-1984 cell line was inhibited by 30% by anti-IL-6R antibodies suggesting the possibility that an autocrine IL-6 loop might have developed during the long-term cultivation. In addition to many other phenotypic alterations of the U-266 cell line, having developed as a consequence of tumor progression in vitro, its growth factor requirement seems to have evolved from a dependence on IL-6 as a paracrine growth factor to a capacity for autonomous growth, dependent on autocrine IL-6 stimulation. Whether such a development also may take place in MM clones in vivo remains to be established.
Leukemia 1992 Apr
PMID:Increase in interleukin 6 (IL-6) and IL-6 receptor expression in a human multiple myeloma cell line, U-266, during long-term in vitro culture and the development of a possible autocrine IL-6 loop. 158 93

The in vivo role of LFA-1 molecule in the immune reaction to a murine retrovirus-induced tumor was investigated. Local and systemic treatment with high doses of anti-LFA-1 monoclonal antibody led to tumor progression by blocking CTL interaction with tumor cells without interfering with CTL generation and localization in the tumor mass.
Leukemia 1992
PMID:The in vivo role of leukocyte function-associated antigen-1 in cytotoxic cell activity against tumors induced by Moloney-murine sarcoma/leukemia retroviral complex. 160 16

Seven tumors independently derived from a v-Ha-ras-expressing pre-B cell line were examined to determine the oncogene activations cooperating with v-Ha-ras in in vivo tumor progression. The pre-B cell line was generated by infection with Moloney murine leukemia virus (MoMuLV) and a MoMuLV-derived recombinant expressing v-Ha-ras. Two of seven tumors possessed a MoMuLV integration immediately upstream and in reverse transcriptional orientation to c-myc. This correlated with a 3-fold increased level of c-myc mRNA. Two other tumors displayed elevated c-myc mRNA levels, although the mechanism of enhanced expression was unclear. Thus the tumor progression of a v-Ha-ras-expressing murine pre-B cell line selects for the activation of c-myc.
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PMID:Tumorigenesis of a v-Ha-ras-expressing pre-B cell line selects for c-myc activation. 171 20


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