Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following in vitro stimulation of murine sarcoma virus Moloney isolate (M-MuSV)-immune spleen cells with syngeneic antigenically related Moloney leukemia cells, highly efficient cytotoxic T-lymphocytes (CTL's) were generated. The cytotoxic effect was directed only against H-2-compatible target cells bearing M-MuSV tumor-associated antigens (TAA). However, in a cold target competition assay a weak but detectable capacity to block CTL activity was also obtained when allogeneic Moloney leukemia cells were added. Moreover, when M-MuSV-immune spleen cells from mice inoculated with virus 14 days previously were stimulated by allogeneic Moloney leukemia cells, a strong cytotoxic effect toward syngeneic and allogeneic tumor cells bearing M-MuSV TAA was elicited.
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PMID:Secondary in vitro generation of cytolytic T-lymphocytes (CTL's) in the murine sarcoma virus system. Virus-specific CTL induction across the H-2 barrier. 8 Apr 57

A rabbit antiserum raised by repeated immunization with BALB/c fetuses obtained at 10-14 days of gestation was used to search for oncofetal antigens (OFA) in murine sarcomas which had previously been characterized for the expression of endogenous murine leukemia virus (MuLV). Iodinated protein A from staphylococcus aureus (IPA) was used to quantitate binding of the antiserum to cultured tumor or fetal cells or to saline extracts of tumors and fetuses. Use of the "antigen" extracts facilitated the assay: the extracts bound to plastic and served as targets for the binding assay, eliminating the need to establish tumors in culture. After absorbtion in vitro and in vivo with adult tissues the rabbit antiserum bound to day 10-14 fetal cells and extract but not to endogenous MuLV (BALB virus 1). The antiserum bound equally well to MuLV-negative and MuLV-positive sublines of MCA-induced sarcomas 1420 and 1414 but not to Moloney sarcoma cells and MCA-induced sarcoma 1386. Thus, the absorbed antiserum detects a class of common cross-reacting antigens which are serologically distinct from MuLV-associated antigens.
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PMID:Expression of oncofetal antigens on murine sarcomas characterized for expression of endogenous MuLV. 8 Nov 87

The expression of immune response-associated (Ia) antigens on the surface of mouse strain GR (H-2dx) ascites leukemia (GRSL) cell lines was studied by cytotoxic tests, immunofluorescence, and immunoprecipitation assays. Ia expression varied among the three GRSL cells lines (GRSL 2, GRSL 14, and GRSL 15) studied by cytotoxic assay. GRSL 14 cells showed the strongest expression of Ia antigens among these three cell lines. A time-course study of tumor growth in mice revealed that Ia antigens on the tumor cells demonstrated the strongest expression 10 days after injection of GRSL cells into GR mice, and that subsequently it decreased until the death of the animal. Cells treated with neuraminidase exhibited more readily detectable Ia antigens, expecially in the late stages of leukemia, which suggested that Ia antigens had been masked by sialic acid. Immunoprecipitation studies revealed that Ia molecules on the leukemia cell had the same molecular weight as those on the normal lymphocytes. Immunofluorescence studies disclosed that Ia antigens were distributed diffusely on the surface of the tumor cells.
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PMID:Immune response-associated antigens on mouse leukemia cells. I. Detection of Ia antigens on GRSL cells. 8 49

Young female AKR mice made leukemic by iv inoculation of 10(3) spontaneous AKR thymoma cells were treated with repeated injections of irradiated cells from the same tumor. Treatment began 1 day after injection of the viable cells. The cytotoxicity of sera and lymphoid cells from healthy mice immunized with lymphoma cells from either treated or nontreated mice with leukemia grafts revealed that the tumor cells could be subdivided into four distinct antigenic types. One type (clone A) accounted for about 97% of the lymphoma cells in each mouse with spontaneous leukemia, whereas the remaining 3% were subdivided into three other distinct antigenic types (clones B, C, and D). Lymphoma cells from treated mice with grafted leukemia were never clone A type but either clone B, C, or D type. Repeated sc injections of 10(7) irradiated cells from spontaneous AKR thymomas induced from 15 to 34% cure in mice with grafts of leukemia cells. Treatment with only clone A induced about 32% cure, whereas treatment with clone B, C, or D had no beneficial effect. Treatment with 10(7) cells each of clone A plus clone B gave 33% cure; clone A plus clone B plus clone C, 45%; and all four clones cured 92% of the mice with leukemia grafts. The efficiency of immunotherapy may be influenced by the natural clonality of the tumor to be treated.
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PMID:Natural polyclonality of spontaneous AKR leukemia and its consequences for so-called specific immunotherapy. 8 93

A spontaneous T cell lymphoma of DBA/2 (H-2-d) mice, SL2, was found to react with anti H-2 typing sera raised against certain foreign haplotypes as well as with anti H-2d sera. The cytotoxic anti-SL2 activity of the anti-foreign H-2 sera was detected in a newly developed microradioassay, not however, in a conventional 51Cr release test. Upon culture in vitro the reactivity of the tumor cells with the anti H-2 sera decreased. The anomalous cytotoxic anti-tumor activity of the anti-foreign H-2 sera appeared to be distinct from anti-murine leukemia virus activity, since it was not removed by absorption with either Friend of AKR leukemia virus. Partial absorption was observed with normal lymphoid cells carrying the respective foreign H-2 antigens, but not with cells of unrelated H-2 haplotypes. In each serum tested, the anti-tumor activity could also be absorbed with syngeneic H-2d lymphoid cells. These results show that the anomalous anti-tumor reactivity of certain anti H-2 typing sera, in particular of sera raised in recipients differing in H-2 from the tumor host strains, is not due to the presence of foreign (derepressed) H-2 molecules on the tumor cells. The differences observed between the tumor cells and normal cells seem to be due to unexpected antibodies in the sera reacting with public H-2 specificities which are better exposed on the tumor cells than on normal cells.
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PMID:Characterization of antigens on murine tumor cells reacting with alloantisera against foreign H-2 specificities: analysis by absorption with purified murine leukemia virus and normal lymphoid cells of different H-2 haplotypes. 8 74

A proportion of cancers in endocrine target tissues can show the presence of specific receptors for either steroid or polypetide hormones. Manipulation of the controlling hormones does not guarantee regression. A third of cancers in endocrine target organs (breast, uterine endometrium, and prostate) show a 50% reduction in size of lesions after hormonal therapy. If regression resulting from an aggressive form of therapy lasts a short while and the tumor reactivates by the time the unpleasant effects of the therapy wear off, the treatment is not palliative. Endocrine therapy in prostatic cancer is palliative but there is no evidence that is increases survival. 11 different progestational agents in endometrial cancer therapy in the past 25 years resulted in a 30-35% response. Response must be maintained by continual treatment and may last from 12 months to 7-8 years. In breast cancer, tumors with a significant level of estrogen receptor (ER+) have about a 60% chance of regression vs. tumors without estrogen receptors (ER-), 10%. Advanced cancers of the thyroid of the papillary or follicular type regress when the patient is treated by thyroxine, .3 mg daily. Leukemia and lymphoma are frequently treated, with varying degrees of success with corticosteroid therapy, which may also predispose the patient to intercurrent infection. Renal cancer has been often treated by medroxyprogesterone acetate or testosterone propionate, with little success.
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PMID:Endocrine therapy in cancer. 8 86

Immunochemical studies have shown that labeled, detergent-solubilized extracts of SL2 (H-2d) lymphoma cells contain components reactive with several anti-H-2 alloantisera of restricted specificity. Anti-H-2k and anti-H-2ja as well as anti-H-2d sera precipitated labeled polypeptides of a molecular weight similar to that of H-2 heavy chains. In addition, all antisera tested precipitated a component of 70000 daltons molecular weight, which is antigenically related to gp 69/71 of Friend murine leukemia virus. Reactions with antisera directed against haplotypes other than H-2d could be blocked by addition of unlabeled, detergent-solubilized extracts of H-2d lymphocytes, or by H-2 antigens against which the antiserum was directed. Sequential immunoprecipitations initially using antisera against the K, D, or L region gene products to remove individual known H-2d antigens have made possible the identification of some molecules responsible for these reactions. The results show that antisera against haplotypes other than H-2d which react with SL2 cells, cross-react with normal H-2d antigens. Quantitative absortion of these antisera with intact or solubilized cells has shown that lymphocytes and tumor cells differ in their expression of some H-2 determinants. The antibodies bind only weakly to intact H-2d lymphocytes, but strongly to the corresponding detergent-solubilized antigens. These results do not, therefore, support the derepression hypothesis put forward earlier.
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PMID:Differences in the expression of histocompatibility antigens on mouse lymphocytes and tumor cells: immunochemical studies. 8 49

Using radioiodinated Staphylococcus aureus protein A [125I]SPA to measure syngeneic, allogeneic and heterogeneic IgG bound to murine tumor cells, we performed a serological analysis of surface antigens of 8 solid tumors and 2 leukemias of BALB/c mice (3 chemically-induced colon carcinomas, 3 chemically-induced sarcomas, 1 murine leukemia virus (MuLV) induced leukemia, 1 irradiation induced leukemia, 1 spontaneous melanoma and 1 spontaneous sarcoma). We were able to detect and distinguish between at least five separate antigenic specificities on these tumors. Unique tumor-associated antigens were found on 3 of the tumors, MuLV related antigens on 8 tumors, fetal antigens on 7 tumors and two distinct common antigens on 7 tumors (common antigen 1 (CA-1) on 5 tumors and common antigen 2 (CA-2) on 2 tumors). Neither of the common antigens was found to be sarcoma, carcinoma or tissue-tupe specific. A number of tumors which did not originally express either MuLV or fetal antigens in primary cultures expressed these antigens after several serial passages in vitro.
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PMID:Tumor-associated antigens of chemically-induced murine tumors; the emergence of MuLV and fetal antigens after serial passage in culture. 8 20

Leukemic blasts from a patient with acute myelogenous leukemia (AML) and peripheral blood T- and B-lymphocyte subpopulations from his genetically identical normal twin were analyzed with the use of the simian antiserum-defining AML antigens and a rabbit antiserum to immune response-associated (la)-like antigens. Blast cells from the patient consistently reacted with both reagents, whereas the B-lymphocyte populations from the patient's normal identical twin reacted only with the rabbit anti-la serum and in no instances reacted with the antiserum to AML cell antigens. Blast cells from the AML patient significantly stimulated the lymphocytes of his normal twin and his own remission leukocytes, whereas the cells from the normal twin failed to stimulate the cells of the patient. These results suggested the existence on AML cells of tumor-associated antigens that are distinct from various other well-characterized normal human alloantigens and differentiation antigens including B-cell antigens. Changes were reported in the expression of leukemia-associated antigens and Ia-like antigens on the cells of an AML patient undergoing chemotherapy as well as in the ability of the simian antisera to distinguish antigens specific for myeloid leukemias from lymphocytic types of leukemias.
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PMID:Human acute myelogenous leukemia antigens defined by simian antisera: evidence for leukemia-associated antigens distinct from immune response-associated alloantigens. 8 33

Samples of three nonmalignant and seven leukemic human cells were examined for DNA polymerase activity that could be identified as RNA tumor virus reverse transcriptase. Experiments on virus-infected model animal cells provided the basis for cell fractionation procedures, and reconstituted systems of known virus, added to human cells, established a threshold of virus detection by enzyme assay at 1 to 10 particles/cell. DNA polymerase activity with some properties similar to a reverse transcriptase was detected in some of the human leukemic cells. However, parallel analyses of nonmalignant cells showed sufficient similarities to raise serious questions about the specificity of the criteria. Reverse transcriptase activity has been reported to be present in white blood cells from a proportion of cases of leukemia; however, it is concluded from the present study that the usual enzymatic criteria using synthetic template primers, which were used in most of the studies reported, are not sufficient to identify a DNA polymerase activity as viral reverse transcriptase.
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PMID:Detection of reverse transcriptase activity in human cells. 8 60


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