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)

The incidence of cancer in agricultural workers is generally low, in part due to the low prevalence of cigarette smoking in this group. However, agricultural workers have elevated risks for several specific cancer types including leukemia, Hodgkin's disease, non-Hodgkin's lymphoma, multiple myeloma, and cancers of the lip, stomach, prostate, brain, and connective tissue. Two major groups of risk factors have been proposed as causes of hematologic malignancies in agricultural workers. The first group includes various agricultural chemicals. In particular, several studies have found increased risks of malignant lymphoma and soft tissue sarcoma in persons exposed to phenoxy herbicides. However, the evidence is inconsistent and there is a wide variation in relative risk estimates. The second group of risk factors includes various animal viruses. There is currently little evidence concerning the zoonotic nature or human carcinogenicity of these viruses. However, leads have been suggested by recent evidence of increased risks of hematologic malignancies in abattoir workers, veterinarians, and meat inspectors. A third hypothesis, for which little evidence is currently available, is that agricultural work may involve prolonged antigenic stimulus leading to lymphoproliferation. The factors responsible for the increased risks for cancers other than hematologic malignancies are not well understood but may also involve exposure to chemicals or viruses.
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PMID:Epidemiologic studies of cancer in agricultural workers. 220 46

A 3-year-old boy was referred to our hospital in September 1985, because of pancytopenia. His bone marrow was normocellular with 18% blasts, which had Auer rod and were positive for peroxidase staining. A diagnosis of refractory anemia with excess blasts in transformation was made according to FAB criteria. Chromosome analysis of bone marrow cells showed normal male karyotype. He attained complete remission with aclarubicin and BH-AC and continued it until August 1987 when pancytopenia and hypoplastic bone marrow developed. Chromosome analysis of bone marrow cells showed normal male karyotype and gene analysis revealed germ-line configuration of breakpoint cluster region (bcr). Overt leukemia developed in May 1988 when his WBC count increased to 60, 600/microliters with 91% blasts, which were negative for peroxidase staining, positive for anti-Ia and CDw 41 by cell surface analysis, and positive for ultrastructurally demonstrable platelet peroxidase. A diagnosis of megakaryocytic leukemia was made. Chromosome analysis of bone marrow cells showed 46, XY, t(9;22) (q34;q11) and gene analysis revealed rearrangement of bcr. He died in November 1988. Our results and review of literature suggest that late appearing ph1 chromosome and rearrangement of bcr may occur in a variety of hematologic malignancies and influence the course of disease.
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PMID:[Myelodysplastic syndrome in a child which developed into megakaryocytic leukemia with late appearing Ph1 chromosome and rearrangement of breakpoint cluster region]. 221 96

We report the clinical presentation and the morphologic, histochemical, and immunophenotypic characteristics of seven patients with acute leukemia who had trisomy/tetrasomy 13 as the sole cytogenetic abnormality in their leukemia. Five patients had trisomy 13 at diagnosis of acute leukemia. All five of these patients had undifferentiated leukemias. The sixth patient, who had French-American-British (FAB) type M2 acute nonlymphocytic leukemia (ANLL), and the seventh patient with biphenotypic acute leukemia developed the trisomic clone as a new abnormality late in the course of their disease. A review of the literature revealed 28 previously reported hematologic malignancies with trisomy 13 or tetrasomy 13q as a solitary cytogenetic abnormality. Trisomy 13 appears to represent another rare but nonrandom cytogenetic abnormality in acute leukemia. In our series trisomy 13 is largely associated with acute leukemia with little myeloid or lymphoid differentiation.
Leukemia 1990 Nov
PMID:Trisomy/tetrasomy 13 in seven cases of acute leukemia. 223 92

Cytogenetic analyses were performed on 12 adult patients with abnormal megakaryoblastic proliferation which was detected by ultrastructural cytochemical study (platelet peroxidase) and platelet-megakaryocytes-specific monoclonal antibodies (TP-80, Plt1, AN51, and KOR-77). The patients consisted of two patients with myelodysplastic syndromes (MDS), three with acute megakaryoblastic leukemia (AMKL), six with megakaryoblastic transformation in Philadelphia-positive chronic myelogenous leukemia (CML-meg-BC), and one case of chronic myeloproliferative disorder (CMPD). Among them, an inversion of the long arm of chromosome 3 [inv(3)(q21q26)] was found in one AMKL patient with a normal platelet count. Chromosome change at band 3q26 was also found in one MDS patient without thrombocythemia. Furthermore, the long arm of chromosome 13, where rearrangements in myelofibrosis are clustered (13q12----q22) was seen in one MDS patient. Trisomoy of chromosome 19 was found in one AMKL patient and three CML-meg-BC patients. These findings indicate that cytogenetic abnormalities involving 3q26, 13q, and trisomy 19 are associated with hematologic neoplasia with megakaryocytic lineage in adult patients, although these abnormalities were not related to the survival of the patients. During the period of this study, two acute myelogenous leukemia patients (AML-M2 and AML-M5b) with chromosome rearrangements at band 3q21 and thrombocythemia were found, indicating that chromosome abnormality at band 3q21 is related to quantitative platelet dysfunction, whereas that at 3q26 is related to hematologic malignancies with a proliferation of megakaryocytic lineage.
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PMID:Cytogenetic findings in adult acute leukemia and myeloproliferative disorders with an involvement of megakaryocyte lineage. 229 63

We report a case of acute promyelocytic leukemia who suffered spontaneous splenic rupture with massive hemoperitoneum while receiving intensive induction chemotherapy. Emergency computed tomography of the abdomen helped in the diagnosis of intra-abdominal bleeding. The patient was successfully treated with immediate splenectomy and made an uneventful postoperative recovery. Ten days after surgery chemotherapy could be resumed and complete remission was achieved. Although spontaneous splenic rupture is a rare complication of hematologic malignancies, this diagnosis should be considered in all patients with leukemia who develop acute abdominal pain with hypotension, even in the absence of splenomegaly.
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PMID:Spontaneous splenic rupture during induction chemotherapy for acute promyelocytic leukemia successfully treated with splenectomy. 233 92

In a study of 7498 American men of Japanese ancestry in Hawaii, 26 incident cases of leukemia or non-Hodgkin's lymphoma were identified after a follow-up period of 19 years. Two of the cases, who were brothers, were diagnosed with adult T-cell leukemia/lymphoma (ATL). Both of these brothers had human T-cell lymphotropic virus type I (HTLV-I) antibodies in their stored serum which were obtained 4 and 18 years before diagnosis. None of the 24 patients with other hematologic malignancies or the 26 matched controls were HTLV-I antibody positive. This finding lends further support for a role of HTLV-I in the etiology of adult T-cell leukemia/lymphoma.
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PMID:Human T-cell lymphotropic virus type I (HTLV-I) antibodies in pre-diagnostic serum of patients with familial adult T-cell leukemia/lymphoma (ATL). 237 93

We have recently demonstrated that interleukin 2 (IL-2), when administered in high doses for several days beginning on the day of allogeneic bone marrow transplantation (BMT), markedly diminishes graft-versus-host disease (GVHD) mortality in lethally irradiated mice. An optimal anti-GVHD effect was attained by coadministering T-cell-depleted (TCD) syngeneic marrow. We demonstrate here that the full graft-versus-leukemia effect of allogeneic T lymphocytes is obtained even when GVHD is markedly diminished by the coadministration of IL-2 and TCD syngeneic marrow. This methodology represents an approach to the treatment of leukemia in which the beneficial effects of allogeneic T cells can be exploited while their major deleterious effect, GVHD, is avoided. These results may thus have an impact on the clinical use of BMT for the treatment of hematologic malignancies.
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PMID:Interleukin 2 prevents graft-versus-host disease while preserving the graft-versus-leukemia effect of allogeneic T cells. 237 1

It has been suggested that abnormalities of chromosome 3 at bands q21 and q26 are associated with the presence of increased numbers of abnormal megakaryocytes in patients with hematologic malignancies. The pretreatment bone marrows of 287 patients with leukemia (acute myeloid leukemia (AML), 225 patients; acute lymphocytic leukemia (ALL), 36 patients; or chronic myelogenous leukemia in blast crisis (CML-B), 26 patients) were reviewed to identify those with normal or increased numbers of megakaryocytes. Thirty-two patients with AML, one with ALL, and 10 with CML-B had normal or increased numbers of megakaryocytes. Of the 32 patients with AML, 19 patients had significant numbers of mononuclear or binuclear small megakaryocytes as well as megakaryocytes with separated nuclei ("micromegakaryocytes"). Cytogenetic analyses were obtained in 29 of 32 patients with AML and showed inv(3)(q21q26) (one patient); Ph1 (two patients); -5 and/or -7 (seven patients); normal karyotypes (10 patients). No patient with micromegakaryocytes had a chromosomal abnormality associated with a favorable prognosis. Overall, among 225 patients with AML, four had inv(3)(q21q26) or t(3;3)(q21;q26). Only one of these four patients had normal or increased numbers of megakaryocytes, although all four had micromegakaryocytes. One patient with CML-B had inv(3)(q21q26) but had decreased numbers of megakaryocytes and a platelet count of 24 x 10(3)/microliters. All five patients with abnormal chromosome 3 at bands q21 and q26 had additional cytogenetic abnormalities (Ph1 in two patients; -7 in three patients). Mean and median platelet counts were greater than 100,000/microliters for patients with marrow megakaryocytosis regardless of morphology, as well as for the patients with abnormalities involving 3q21 and 3q26. Abnormalities of megakaryocyte morphology, increases in the numbers of megakaryocytes, and normal to increased platelet counts are not uncommon in patients with acute leukemia and CML-B, and are not uniquely associated with changes involving chromosome 3.
Leukemia 1990 May
PMID:Clinical and cytogenetic correlations of abnormal megakaryocytopoiesis in patients with acute leukemia and chronic myelogenous leukemia in blast crisis. 238 80

Within the adolescent survivor sample, the psychosocial response of having been diagnosed and successfully treated for cancer is not universal as evidenced by the variability in psychosocial adjustment. Data from the MHI suggests that adolescent cancer survivors do experience more global psychological distress than a comparison group of healthy adolescents. In addition, the majority of these patients reported persistent, intrusive thoughts about their illness and its treatment. Conversely, the adolescent cancer survivors did not differ from a normative sample on social competence, manifestation of problems behaviors, or school achievement. Thus, our data suggest that adjustment in this population is multi-dimensional with variability. While they are functioning quite adequately at school and in social situation, they continue to experience heightened and persistent distress of both a global and illness-specific quality. A number of factors that are conducive to psychosocial intervention appear to be related to adjustment. Family communication and family cohesion were significantly related to the mental health of the adolescent survivors, suggesting a need to further explore the family context of adolescent adjustment. The present work also represents the first attempt to directly examine the psychosocial functioning of young adult, acute leukemia survivors. When compared with normative samples of nonpatients, these survivors (taken as a whole group), reported heightened levels on several indicators of psychological distress. While not entirely consistent across different psychological measures, these young people were generally one standard deviation above the mean for psychological distress. But when compared to normative samples of psychiatric outpatients, our survivors reported significantly less psychological distress. For instance, leukemia survivors reported less intrusive and avoidant cognitions associated with the stressor of being diagnosed and treated for cancer than those associated with patients experiencing traumatic stress disorders. In aggregate, these findings again suggest that the psychosocial adjustment of leukemia survivors is quite variable. Finally, while group comparisons shed light on the psychosocial functioning of leukemia survivors, in general, wide variability in psychosocial adjustment may mask identification of a cohort of cancer survivors most at-risk for psychosocial dysfunction. Sociodemographic, disease/treatment and psychological distress variables only partially explain this variability. The findings from our data suggest several clinical recommendations. First, the prevalence of persistent, psychiatric comorbidity is quite low among long-term survivors of hematologic malignancies survivors. Second, if survivors do experience some psychological distress, usually, it is of non-psychopathological proportions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Surviving hematological malignancies: stress responses and predicting psychological adjustment. 240 18

In tumor cells from virtually all patients with chronic myelogenous leukemia, the Philadelphia chromosome, a fusion of chromosomes 9 and 22, directs the synthesis of the P210bcr/abl protein. The protein-tyrosine kinase activity and hybrid structure of P210bcr/abl are similar to the oncogene product of the Abelson murine leukemia virus, P160gag/v-abl, which induces acute lymphomas. To determine whether P210bcr/abl can induce chronic myelogenous leukemia, murine bone marrow was infected with a retrovirus encoding P210bcr/abl and transplanted into irradiated syngeneic recipients. Transplant recipients developed several hematologic malignancies; prominent among them was a myeloproliferative syndrome closely resembling the chronic phase of human chronic myelogenous leukemia. Tumor tissue from diseased mice harbored the provirus encoding P210bcr/abl. These results demonstrate that P210bcr/abl expression can induce chronic myelogenous leukemia. Retrovirus-mediated expression of the protein provides a murine model system for further analysis of the disease.
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PMID:Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. 240 2


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