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)

During the National Influenza Immunization Program in 1976, 147 children with neoplastic diseases received Wyeth split-product bivalent influenza vaccine: A/New Jersey/8/76 (HSW1N1), A/Victoria/3/75 (H3N2). Thirteen normal siblings served as controls. Seventy-one patients received two doses of the vaccine four weeks apart. After the second injection of A/NJ/8/76, there was a difference between the response of the patients on chemotherapy and those off therapy greater than or equal to 30 days--38% vs. 76%, P less than 0.01 for four-fold rise and 26% vs. 57%, P less than 0.05 for the attainment of protective (greater than or equal to 32) hemagglutination inhibition (HI) titers. These differences were observed in both leukemia-lymphoma and solid tumor patients. There was a difference in HI titers to A/Vic/75 between patients on and off chemotherapy after a single injection, 34% vs. 71%, P less than 0.001 for a four-fold rise. After the second immunization, only 52% on, and 86% off therapy (P less than 0.05) had a four-fold rise in titers. Thirty-two percent of the patients on treatment who achieved "protective" titers did so only after the second immunization. Immunoglobulin levels and neutropenia did not correlate with the inability to obtain a four-fold rise in titers. Our findings suggest that patients on chemotherapy cannot be effectively vaccinated by a new antigen, and that single yearly boosters may be insufficient for recall of old antigens. Patients off chemotherapy greater than or equal to 30 days respond as normal controls.
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PMID:Influenza immunization of children with neoplastic diseases. 735 92

Patients with B cell chronic lymphocytic leukemia (B-CLL) have decreased capacity to mount relevant antibody responses upon immunization, and development of hypogammaglobulinemia is part of the natural history of the disease. We investigated the influence of histamine type-2 (H2) receptor blockade by ranitidine on the in vivo antibody production in B-CLL patients following vaccination. Anti-polysaccharide antibodies in B-CLL patients, vaccinated with a tetanus-toxoid conjugated vaccine against Haemophilus influenzae type-B (Hib), reached long-term protective levels in more than 90% of B-CLL patients randomized to ranitidine treatment, as compared to 43% of the untreated patients (P = 0.024). No difference in the response to vaccination against influenza virus types A and B protein could be detected between the two groups. Plasma histamine levels were 2-fold to 20-fold higher in 23 out of 31 B-CLL patients, compared to normal controls, and these levels showed a significant positive correlation to disease duration. These findings indicate the possibility of improving in vivo antibody production against a highly relevant pathogen in B-CLL patients by histamine type-2 receptor blockade, and the combined finding of an immune-stimulatory effect of ranitidine and increased plasma histamine levels, strongly suggests the involvement of histamine in the pathogenesis of B-CLL immunodeficiency.
Leukemia 1995 Nov
PMID:Improved vaccination response during ranitidine treatment, and increased plasma histamine concentrations, in patients with B cell chronic lymphocytic leukemia. 747 82

In 1985, Cancer and Leukemia Group B initiated a multi-institutional study to define the role of interferon alpha in therapy of previously untreated active hairy cell leukemia (HCL). This is a long-term follow-up report of the study. Fifty-five evaluable patients were treated with recombinant interferon-2b 2 million units/m2 subcutaneously three times a week for 1 year. Treatment was well tolerated; toxicity mainly consisted of flu-like syndrome and pancytopenia, both of a transient nature. Seventy-three percent of patients had objective beneficial responses with 8.3 months median time to achieve at least a partial response (PR). After 1 year of therapy, the patients have been observed for a median of 5 years. There was a continual trend towards relapse throughout this period but 28% have remained in remission beyond 6 years. Forty-six patients (83%) are alive at 6 years. Among the 40 patients who achieved at least a PR, there were 28 with splenomegaly at the beginning of study: the spleen size was reduced in all with interferon alpha therapy and none required splenectomy. This study confirms the results of other investigators, and demonstrates that recombinant alpha interferon-2b is an effective agent for treatment of hairy cell leukemia.
Leukemia 1995 Jul
PMID:Recombinant alpha-2b-interferon in therapy of previously untreated hairy cell leukemia: long-term follow-up results of study by Cancer and Leukemia Group B. 763 Jan 81

Influenza infection is a significant cause of morbidity and mortality in immunocompromised hosts, but its importance in adult cancer patients is largely undescribed. We therefore conducted a prospective study of the incidence and clinical features of influenza infection in patients with acute or chronic leukemia. The cohort, which consisted of all adult leukemia patients undergoing remission-induction chemotherapy during the 1991-1992 influenza epidemic, was followed prospectively for development of signs and symptoms of acute infection of the upper or lower respiratory tract. Of these 294 patients, 111 received chemotherapy as inpatients and 183 as outpatients. Throat swabs and nasal washes for viral culture were obtained from all symptomatic patients, who were then followed until all signs and symptoms resolved. Symptoms of respiratory tract infection developed in 37 leukemia patients (13%). Among these, influenza (A/Beijing/ H3N2) caused 3 (21%) of the 14 infections that developed during hospitalization but only 1 (4%) of the 23 that developed in the community (P = 0.14). Influenza patients presented with fever, rhinorrhea, nasal congestion, headache, and myalgia; those with other infections presented with signs and symptoms of lower respiratory tract infection (productive cough, rales, or rhonchi). Development of pneumonia was common in influenza patients, 1 of whom died from secondary fungal and gram-negative pneumonia. Influenza A virus infections accounted for a substantial portion of acute respiratory infections among adult leukemia patients during a community epidemic. Most infections appeared to be nosocomial and the most likely sources were visitors or hospital personnel. Immunization of household contacts and hospital staff may reduce the risk of influenza infection and its pulmonary complications in leukemia patients.
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PMID:Epidemiology of influenza A virus infection in patients with acute or chronic leukemia. 765 81

For pathogenic viruses such as human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), human influenza A virus, and human T-cell leukemia virus type I (HTLV-I), the evolutionary features were briefly reviewed with special reference to the rates of synonymous and nonsynonymous substitutions. In particular, these rates were discussed in connection with the neutral theory of molecular evolution. It was common to all the five pathogenic viruses that the rate of synonymous substitution was higher than that of nonsynonymous substitution particularly when the entire gene regions were compared between different isolates. This suggests that the viral proteins are quite conservative to functional and structural changes even though most of these viral genomes are evolving at a speed extraordinarily higher than their host genomes. Thus, this feature is consistent with the neutral theory. However, it is also pointed out that positive selection may be operating on some specific sites such as antigenic sites in order for the pathogenic viruses to escape from the host immune system.
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PMID:Evolution of pathogenic viruses with special reference to the rates of synonymous and nonsynonymous substitutions. 799 69

The infection and function of lymph node dendritic cells (DC) were analyzed at different time points of Rauscher leukemia virus infection in mice (3, 7, 14, and 21 days). Infection of DC was apparent after 3 days and significant infection (1-10% of the DC population) was documented after 7 days. DC from infected mice as early as 3 days postinfection had a reduced ability to stimulate allogeneic normal T cells in the mixed lymphocyte reaction. T cells did become infected during the coculture but block of cross-infection of T cells by zidovudine did not abolish the inhibitory effect. Other DC-dependent responses were also reduced on infection including DC-stimulated responses to influenza virus. ConA and PMA induced an increase in [Ca2+]i level in DC from control mice. A low baseline level of [Ca2+]i in DC from infected mice and reduced calcium mobilization upon ConA stimulation was found at all periods of infection. Ultraviolet-inactivated Rauscher leukemia virus failed to provoke significant changes in DC function in vivo. Six or 7 days after RLV infection DC expressed lower levels of Iad but not H2Dd molecules in parallel with lower expression of some adhesion molecules (CD18, CD54, CD44). No differences in expression of B7 surface antigen between control and infected mice were obtained. We did not find any evidence for the induction of apoptosis of naive syngeneic or allogeneic T cells by infected dendritic cells. The changes in DC function may have implications for the pathogenesis of retroviral infections including HIV infection.
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PMID:Murine retrovirus induces defects in the function of dendritic cells at early stages of infection. 808 63

A quantal assay, based on syncytium formation in the human T cell leukaemia-derived C8166 cell line, was used to determine the kinetics of human immuno-deficiency virus type 1 (HIV-1) strain IIIB neutralization. Three rat monoclonal antibodies (MAbs) were used, under physiological conditions of temperature and antibody concentration. MAb ICR39.3b (IgG2b) neutralized virus with no lag period while the other two MAbs, ICR39.13g (IgG2b) and ICR41.1i (IgG2a), neutralized with lag periods of 5 min and 15 min respectively. It was calculated that the latter two MAbs mediated neutralization by about two and three molecules of IgG per virion respectively. The highest neutralization rate constant (for MAb ICR 41.1i) was over 300-fold less than that of MAbs specific for the haemagglutinin of the enveloped influenza virus type A and for poliovirus type 1.
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PMID:Single- and multi-hit kinetics of immunoglobulin G neutralization of human immunodeficiency virus type 1 by monoclonal antibodies. 820 10

Simple methods are presented to estimate rates of spontaneous mutation from mutant frequencies and population parameters in RNA viruses. Published mutant frequencies yield a wide range of mutation rates per genome per replication, mainly because mutational targets have usually been small and, thus, poor samples of the mutability of the average base. Nevertheless, there is a clear central tendency for lytic RNA viruses (bacteriophage Q beta, poliomyelitis, vesicular stomatitis, and influenza A) to display rates of spontaneous mutation of approximately 1 per genome per replication. This rate is some 300-fold higher than previously reported for DNA-based microbes. Lytic RNA viruses thus mutate at a rate close to the maximum value compatible with viability. Retroviruses (spleen necrosis, murine leukemia, Rous sarcoma), however, mutate at an average rate about an order of magnitude lower than lytic RNA viruses.
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PMID:Rates of spontaneous mutation among RNA viruses. 838 12

The murine antigen-processing-defective mutant cell line RMA-S is leaky in the presentation of certain endogenously synthesized minor histocompatibility and viral antigens to major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTL). The viral antigens include influenza virus nucleoprotein, vesicular stomatitis virus (VSV) nucleocapsid and Rauscher murine leukemia virus (MuLV) antigen. Here we demonstrate Sendai virus antigen presentation by the HAM2 (murine TAP2, transporter associated with antigen presentation type 2)-defective RMA-S cell line and compare antigen presentation after restoration of the defect by murine TAP1/2 gene transfection. Kinetic studies revealed that RMA-S cells required 2-3 h longer incubation and approximately 10 times higher doses of Sendai virus to reach the same level of killing as the RMA parental line. After transfection of RMA-S cells with the murine TAP1/2 gene, Sendai virus antigen presentation was restored to levels of the RMA wild-type line with regard to time of virus infection and dose of virus needed for sensitizing target cells. The presentation of Sendai virus antigen in RMA-S cells was sensitive to brefeldin A (BFA), suggesting that the presentation was mediated via the endogenous pathway. Our findings confirmed leakiness of antigen presentation in RMA-S cells and extended it to Sendai virus. The results underscored the role for intact expression of the TAP 1/2 molecules for efficient MHC class I-mediated antigen presentation.
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PMID:TAP2-defective RMA-S cells present Sendai virus antigen to cytotoxic T lymphocytes. 839 98

Three protein isoforms are encoded by the human T-cell leukemia/lymphotropic virus type I pX region open reading frames (ORF) I and II through alternative splicing. Both the singly and doubly spliced mRNAs from ORF I encode a single 12-kDa protein (p12I), whereas two distinct proteins of 13 kDa (p13II) and 30 kDa (p30II) are encoded from the ORF II alternatively spliced mRNA. Because the p12I protein is very hydrophobic and poorly immunogenic, we genetically engineered its cDNA by adding a short stretch of amino acids from the highly immunogenic epitope HA1 of influenza virus or the AU1 epitope of bovine papillomavirus. The HA1 epitope was also added to the p13II and p30II proteins, albeit rabbit immune sera raised against synthetic peptides were also available. To determine in which cellular compartments these proteins reside, we transfected the tagged and wild-type cDNAs in HeLa/Tat cells and studied their localization by indirect immunofluorescence. The p12I protein was identified in the cellular endomembranes and, particularly, in the perinuclear area. p13II and p30II were found in the nuclei and nucleoli of the transfected cells, respectively. The presence of the HA1 epitope at the carboxy terminus of p13II and p30II did not interfere with their cellular localization, since the rabbit immune sera demonstrated their presence in the same cellular compartments when the untagged proteins were expressed. The defined localization of these proteins in specific cellular compartments warrants further study of their function.
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PMID:The p12I, p13II, and p30II proteins encoded by human T-cell leukemia/lymphotropic virus type I open reading frames I and II are localized in three different cellular compartments. 844 34


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