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)

A chronic lymphatic leukaemia (CLL) with hepato-splenomegaly was treated in a 76 years old female patient by means of extracorporeal irradiation of blood (ECIB), after which a complete involution of the tumour in the spleen had taken place. Leukocytes initially increased to 35,500/mm3, amounting to 10,700/mm3 later on. The patient died of pneumonia in general cachexia. No signs of CLL could be found macroscopically after autopsy. An involution of the lymphatic infiltration could be identified microscopically in the bone-marrow.
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PMID:[Clinical treatment of chronic lymphatic leukemia by means of extracorporeal blood irradiation]. 8 Mar 60

Integrated viral DNA sequences were detected in tissues from two gibbon apes, a leukemic gibbon (6G-1) from whose leukocytes a distinct strain of gibbon ape leukemia virus (GaLVH) was isolated, and gibbon 6G-4, a contact of 6G-1 from the same colony that had uremia and cachexia of unknown origin. Although 6G-4 had no detectable neoplasia or viral proteins, its serum contained persistent antibody against GaLV antigens. Whereas DNA from most of the tissues of 6G-1 contained GaLV provirus, DNA from only three tissues (kidney, spleen, and liver) from 6G-4 showed detectable viral sequences, and the extent of hybridization in each case was lower than with 6G-1. After cleavage with BamHI, two virus-specific DNA fragments were detected in tissues of 6G-1. Only one of these fragments was detected in the positive tissues of 6G-4. The results indicate that: (i) 6G-4 was exposed to and infected by GaLV; (ii) early target sites for infection of gibbon by GaLV may be limited to a few tissues; and (iii) infection can be contained by integration of only partial provirus in a few tissues.
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PMID:Retrovirus sequences in a leukemic gibbon and its contact: evidence for partial provirus in the nonleukemic gibbon. 28 41

Melanoma-derived lipoprotein lipase inhibitor (MLPLI) is a factor purified from the conditioned medium of a human melanoma cell line, SEKI, which induced severe cachexia in tumor-bearing nude mice. Amino acid sequencing revealed that the amino-terminal portion was identical to that of leukemia-inhibitory factor (LIF). To determine whether MLPLI is actually LIF, the expression of LIF mRNA was examined in the SEKI melanoma cell line. Northern blot analyses revealed that the cell line displayed an intense hybridizable band with a molecular size of 3.8 kilobases, suggesting that MLPLI is identical to LIF. The relationship between the development of the cancer cachexia syndrome and the expression of LIF mRNA was examined in four melanoma xenografts, SEKI, G361, A375 and MEWO, in nude mice. SEKI- and G361-bearing nude mice developed cancer cachexia syndrome, and their body weights decreased by the 25th day after the transplantation to 73.6% and 73.8% of the control, respectively. A375- and MEWO-bearing nude mice, however, did not develop the syndrome. Northern blot analyses revealed that G361 as well as SEKI expressed a large amount of LIF mRNA, but A375 and MEWO did not, suggesting a close relationship between the expression of LIF mRNA and the development of the syndrome. These data support the concept that MLPLI, or LIF, plays an important role in the development of the cancer cachexia syndrome observed in melanoma-bearing nude mice.
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PMID:Cancer cachexia syndrome developed in nude mice bearing melanoma cells producing leukemia-inhibitory factor. 174 40

A case of chronic myelogenous leukemia (CML) of 10-year survival in described. A 44-year old male was admitted to our hospital because of general malaise, abdominal fullness and fever in February, 1977. On physical examination, giant splenomegaly and hepatomegaly were detected. Peripheral blood examination revealed leukocytosis without hiatus leukemia , normochromic macrocytic anemia and thrombocytosis. NAP rate and score were 16% and 22. Cytogenetic analysis of PB without stimulator revealed 46, XY, Ph1. Then he was diagnosed as having a typical type of Ph1-positive CML. He had been successfully treated over 9 years by intermittent administration of busulfan. However, anemia suddenly progressed in February, 1986 followed by leukopenia and thrombocytopenia. Hemorrhage was not detected by the examination. Though he had been received blood transfusion, the anemia progressed rapidly. He was died of cachexia on 4th of August, 1987. The postmortem examination revealed bone marrow aplasia with no signs of blast crisis nor myelofibrosis. Secondary hemochromatosis was seen in the liver, spleen, pancreas and some other organs.
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PMID:[Bone marrow aplasia without blast crisis in a case of CML of 10-year survival]. 279 87

Three new cases of monosomy 7 are described. Two children, before onset of overt leukemia, had a preleukemic state: one with thrombopathy and myelodysplastic syndrome, the other with a moderate splenomegaly and an absolute monocytosis. In these two cases the leukemia was chemoresistant. The last child had a subacute myelomonocytic syndrome (juvenile type of chronic myelogenous leukemia) without high fetal hemoglobin value. She died from cachexia. The poor prognosis of monosomy 7 is underlined and such a chromosome deletion should be searched in myeloproliferative syndrome with monocytosis.
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PMID:[Bone marrow monosomy 7 in children]. 324 43

The toxicity of methotrexate and cyclophosphamide determined by LD50 was depressed in the early period of development of sarcoma Sa-180. In the late period of development of Sa-180 and in mice with leukemia L-1210 the toxicity was higher than in healthy mice. The growth of transplantable neoplasms leads to cachexia, hypoproteinemia and dysproteinemia.
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PMID:Acute toxicity of methotrexate and cyclophosphamide in mice inoculated with malignant neoplasms. 725 81

Because the cells previously designated plasmacytoid T cells share major immunophenotypic features with cells of the mononuclear-phagocyte system, they have been re-named and are now known as plasmacytoid monocytes (PM). We describe a unique case of chronic myelomonocytic leukemia with circulating PM. The patient, a 48-year-old man, presented initially with refractory anemia. Four years later his general condition deteriorated, accompanied by an increase in leukocytes to 200,000/microliters blood. The bone marrow histology was interpreted as compatible with a diagnosis of chronic myelomonocytic leukemia. Two months before he died, the patient developed generalized lymphadenopathy clinically simulating malignant lymphoma. Histologic examination of an axillary lymph node revealed diffuse infiltration by PM. The PM in the lymph node and some circulating cells closely resembling PM expressed L-selectin, a finding that could be interpreted as a morphologic correlate of their marked lymphotropism. The detection of large numbers of CD56/CD33 double-positive circulating blast cells by FACS analysis strongly supported the diagnosis of a leukemia of myelogenous origin. The patient died of tumor cachexia. Autopsy revealed widespread leukemic infiltrates (always containing clusters of PM) in bone marrow, spleen, liver, lymph nodes, and mucosa-associated lymphoid tissue of the oropharynx. The final diagnosis was one of chronic myelomonocytic leukemia with marked lymphotropism and partial differentiation towards PM. We consider that the rare instances of a hematologic tumor with differentiation towards PM should be classified amongst the myelogenous leukemias.
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PMID:Evidence for a lymphotropic nature of circulating plasmacytoid monocytes: findings from a case of CD56+ chronic myelomonocytic leukemia. 754 May 56

Alterations in lipid metabolism characterized in major part by a decrease in lipoprotein lipase (LPL) activity in adipose tissue are a central feature of cachexia from chronic infection or malignancy. These metabolic derangements may be mediated in large part through endogenous host proteins produced in response to various pathological stimuli. Differentiation factor/leukaemia inhibitory factor (D-factor) is a cytokine whose functions overlap those of tumour necrosis factor-alpha (TNF), IL-6 and IL-1. Recombinant murine D-factor produced a dose- and time-dependent inhibition of heparin-releasable LPL activity in differentiated 3T3-L1 adipocytes. Although 2-10 fold less potent than recombinant murine TNF, D-factor inhibited LPL activity at concentrations of 1-10 ng/ml. When added together, D-factor and TNF produced a synergistic inhibition of LPL activity. Interleukin 6 (IL-6) was 100-fold less potent than D-factor; 0.1 ng/ml of D-factor or 10 ng/ml of IL-6 caused a 50% inhibition of LPL activity. D-factor and TNF increased IL-6 production in 3T3-L1 cells. Ten ng/ml of D-factor or 1.0 ng/ml of TNF stimulated the release of < 1 ng/ml of IL-6 and inhibited LPL activity to 11 +/- 3% and 3 +/- 2% of control, respectively, whereas 50 ng/ml of recombinant IL-6 was required to decrease LPL activity to 24 +/- 19% of control. TNF produced a marked decrease in LPL mRNA, whereas D-factor had minimal or no effect at doses which inhibited LPL activity almost completely. Western blot analysis of cell extracts showed that TNF caused a greater decrease in LPL protein production than D-factor.2+ with TNF, may contribute to the manifestations of cachexia.
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PMID:Characterization of differentiation factor/leukaemia inhibitory factor effect on lipoprotein lipase activity and mRNA in 3T3-L1 adipocytes. 794 51

A variant of gelatinous transformation of marrow was described in leukemic patients post-chemotherapy. This lesion was found in 8 out of 1833 post-chemotherapy bone marrows from 429 patients with leukemia. Histologically, this variant form was identical to the classical gelatinous transformation except for the absence of fat atrophy. In marrow smears, mucoid strands were seen between marrow particles and oriented along the direction of spread. In clot and trephine sections, an eosinophilic ground substance was widespread, filling out spaces around the fat cells, which occupied the normal proportion of marrow space. At high magnification, this ground substance appeared granular and fibrillary, a non-specific feature which could also be seen in fibrin clot commonly found in marrow sections. This eosinophilic ground substance, however, can be distinguished from fibrin clots by positive staining with Alcian Blue (pH 2.3) and inhibition of the staining after treatment with hyaluronidase. Clinically, in contrast to the classical form, this variant form of gelatinous transformation was acute in onset, transient, and associated with chemotherapy but not with cachexia.
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PMID:A variant of gelatinous transformation of marrow in leukemic patients post-chemotherapy. 826 50

The polyunsaturated omega-6 fatty acid, arachidonic acid ([AA] 20:4n-6), is both the key of the immunoregulatory substances, prostaglandins, and leukotrienes, and an essential component of immune cell membrane phospholipids, providing stability and flexibility to ensure cellular function. To explore possible effects of the physiological burden of viral replication in chronic viral infections on AA availability, plasma total esterified fatty acid (FA) proportions were measured in the feline leukemia (FeLV) model. Plasma FA profiles of 12 specific-pathogen-free cats with chronic infections with Rickard strain feline leukemia virus (FeLV-R) were compared with 12 age- and sex-matched uninfected specific-pathogen-free cats at 4 months after infection. A significant decrease from normal of average AA proportion was found in FeLV-R-infected cat plasma, while other major FA (palmitic, stearic, and oleic and omega-3 FA normally remained present until near death. Since plasma FA content rapidly affects circulating immune cell membrane composition and since FeLV infection also targets immune cells, we compared FA profiles of feline T4-thymic lymphoma 3201 cell membranes that were infected with virulent FeLV-R or less virulent FeLV-A, at 20 days after viral inoculation with sham-inoculated uninfected 3201 cells. Significantly altered FA proportions and ratios of saturated to unsaturated FA found in infected cell membranes were similar to plasma FA changes and paralleled the virulence of the FeLV inoculum. Altered postinfection FA proportions may impart serious functional defects to the immune cells of chronic FeLV-infected cats, contributing to the inability of their immune systems to eliminate FeLV by depleted plasma AA stores and modified cell membrane composition. Decreased AA availability may be an important factor in the cachexia and fatal outcome of FeLV infection.
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PMID:Chronic feline leukemia virus infection alters arachidonic acid proportions in vivo and in vitro. 838 Sep 29


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