Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Bcl-2 proto-oncogene was discovered at the t(14;18) breakpoint found in most follicular B-cell lymphomas and some diffuse large-cell lymphomas. Bcl-2 is unique among proto-oncogenes, being localized to mitochondria and extending cell survival by blocking programmed cell death. We examined Bcl-2 protein expression in 82 hematologic malignancies and reactive lymphoid processes. All lymphomas with Bcl-2 rearrangement demonstrated high levels of Bcl-2 protein. However, most follicular and diffuse lymphomas without Bcl-2 rearrangement also displayed intense Bcl-2 staining. In these cases, mechanisms other than classic translocation may be deregulation Bcl-2. The pattern of Bcl-2 staining in follicular lymphoma is the inverse of the pattern in reactive hyperplasia, confirming a role for Bcl-2 immunolocalization in routine diagnosis. Small lymphocytic malignancies, including small lymphocytic lymphoma, mantle zone lymphoma, and chronic lymphocytic leukemia, expressed intermediate levels of Bcl-2. Bcl-2 protein varied in plasma cell dyscrasias. Bcl-2 protein levels in T-cell lymphomas reflected their corresponding stage of development. No substantial Bcl-2 was present in the Reed-Sternberg cells of nodular sclerosing Hodgkin's disease. Chronic myelogenous leukemia was strongly positive for Bcl-2, consistent with the presence of Bcl-2 in normal myeloid progenitors. Immunohistochemistry identified an expanded spectrum of hematopoietic neoplasms in which Bcl-2 may provide a cell survival advantage.
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PMID:Immunolocalization of the Bcl-2 protein within hematopoietic neoplasms. 186 40

Indirect immunofluorescence staining with monoclonal antibody (MoAb) CL203.4 of malignant cells from 269 patients with hematologic malignancies showed a heterogeneous expression of CD54/intercellular adhesion molecule-1 (ICAM-1). This marker was expressed by malignant cells of 57 out of 118 patients with myeloid malignancies and 69 out of 135 with B-lymphoid malignancies. On the other hand, CD54 was not detected on malignant cells of 16 patients with T-lymphoid malignancies. In myeloid malignancies, CD54 is preferentially expressed by "stem cell-derived" malignancies, being detectable on blast cells from almost all patients affected by chronic myelogenous leukemia in blast phase or myelodysplastic syndromes and by only 34% of patients with de novo acute myeloid leukemia (AML). The expression of CD54 did not correlate with any specific myeloid FAB subtype, although three cases of highly undifferentiated AML (FAB MO) displayed maximal levels of the antigen. The expression of CD54 in AML was significantly associated with that of CD34 and HLA-DR antigens. In B-lymphoid malignancies, CD54 expression appears to correlate with the differentiation stage of malignant cells, since B-origin acute lymphoblastic leukemias and conventional B-chronic lymphocytic leukemias (B-CLL; ie, "dim SIg" CLL) expressed lower levels of CD54 than more mature lymphoproliferative disorders ("bright SIg" CLL, prolymphocytic leukemias, and lymphoplasmacytic tumors). "High-grade" B-cell non-Hodgkin's lymphomas (B-NHL) express in general a higher level of CD54 than "low-grade" ones. This finding in conjunction with the expression of CD54 in all 17 patients with "bright SIg" CLL investigated (characterized by marked organomegaly and poor prognosis) suggest that the differential expression of CD54 in lymphoproliferative disorders may also relate to their degree of malignancy.
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PMID:Differential expression of CD54/intercellular adhesion molecule-1 in myeloid leukemias and in lymphoproliferative disorders. 197 71

Spontaneous splenic rupture is an unusual complication of hematologic malignancies with a high mortality rate. We report two cases of non-traumatic splenic rupture: the first one was a patient with myelomonocytic leukaemia and the second one a previously undiagnosed patient with non Hodgkin's lymphoma, both of them survived after splenectomy. Emphasis on the necessity of an early diagnosis and treatment are made.
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PMID:[Non-traumatic rupture of the spleen in malignant hemopathies. 2 new cases]. 208 67

On the basis of data obtained from hospitals and outpatient clinics in Lower Silesia the incidence of haematological malignancies was analysed in the years 1972-1985. Totally 3739 cases were notified, mainly in urban populations. The mean annual index of incidence of leukaemias and lymphoproliferative disorders was in men 4.57/100,000 population, and in women 3.79, while the incidence index of chronic lymphoreticular system malignancies was 6.91 in men and 4.5 in women. With the exception of acute myeloid leukemia an increasing trend of incidence was noted, which was slight for Hodgkin's disease, chronic myeloid leukaemia and polycythaemia vera, and highest for non-Hodgkin lymphoma. About 30% of haematological malignancy cases have not been notified, and perhaps this was due to inadequate terminology of these diseases in the international register.
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PMID:[Incidence of neoplasms of the hematologic and lymphoreticular systems in Lower Silesia 1972-1985. I. Incidence in the entire region]. 213 17

Several immunohistochemical methods are now available for the staining of neoplastic cells in tissue sections. The authors have found that the alkaline phosphatase-anti-alkaline phosphatase (APAAP) method is sensitive and reliable. Murine monoclonal or nonmurine polyclonal antibodies can be used to label a variety of membranous and/or cellular constituents in tissues that have been routinely processed in a histopathology laboratory. The monoclonal antibody against leukocyte common antigen (CD45) can be used to differentiate hematologic from nonhematologic tumors. Monoclonal antibodies (L26, LN1, LN2, LN3, MB1, MB2) label B-cell lymphomas, whereas other monoclonal antibodies (UCHL1, MT1) more characteristically stain T-cell lymphomas. Polyclonal antibodies against CD3 specifically mark neoplastic cells from T-cell lymphomas and leukemias but as yet are not commercially available. Monoclonal antibodies Leu-M1 (CD15), Ber H2 (Ki-1; CD30), and LN2 label Reed-Sternberg cells from most cases of nodular sclerosis, mixed cellularity, and lymphocyte-depleted Hodgkin's disease. Monoclonal antibodies Mac 387, KP1 (CD68), and NP57 (antielastase), as well as polyclonal antibodies against lysozyme, help identify subtypes of acute myeloid leukemia and extramedullary myeloid cell tumors. Although there are now excellent reagents ready for use, there is still a significant need for more lineage-specific (particularly against CD epitopes) monoclonal antibodies capable of labeling neoplastic cells in paraffin-embedded tissue sections from patients with hematologic malignancies.
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PMID:Immunophenotyping of hematologic neoplasms in paraffin-embedded tissue sections. 218 Feb 77

DNA from 161 patients with various forms of hematologic malignancies were investigated for mutations in exons 1 and 2 of the N-RAS, K-RAS and Ha-RAS gene by direct sequencing of DNA amplified in vitro by the polymerase chain reaction. Mutations involving either codons 11, 12, or 13 of the N-RAS gene were identified in 18 of the 161 patients. The relative frequencies of N-RAS gene mutations in these hematologic disorders was as follows: acute myelogenous leukemia (AML), 15%; acute lymphoblastic leukemia (ALL), 14%; myelodysplastic syndromes, 24%; and myeloid and lymphoid blast crisis of chronic myelogenous leukemia (CML), 3%. No correlation was observed between the presence of mutations and cytologic features or immunophenotype of these malignancies. Mutations involving codons 12 or 13 were equally prevalent, with a glycine to aspartic acid substitution being the most frequently encountered change. A single T-ALL case had a codon 11 mutation resulting in substitution of alanine with threonine. We failed to find mutations in exons 1 and 2 of the K-RAS or Ha-RAS genes in any case except a single AML with a mutation in codon 61 of the K-RAS gene. Also, no mutations were identified in chronic phase of CML, chronic lymphocytic leukemia. Ph1 positive ALL, non-Hodgkin's lymphoma, Hodgkin's disease, or multiple myeloma. These results indicate that RAS mutations, especially those involving exon 1 of the N-RAS gene, are frequent only in a subset of hematologic malignancies.
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PMID:The pattern of mutational involvement of RAS genes in human hematologic malignancies determined by DNA amplification and direct sequencing. 218 88

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

Graft-vs-host disease can develop in immunosuppressed individuals who receive blood-product transfusions that contain immunocompetent lymphocytes. We report two cases of fatal transfusion-associated graft-vs-host disease that developed in patients with Hodgkin's disease who were undergoing therapy. We review all cases of this entity in patients with malignancies, represented predominantly by patients with hematologic malignancies. The groups at risk for development of transfusion-associated graft-vs-host disease, the clinical presentation and course, and methods of diagnosis are summarized. Prevention of this highly fatal condition is possible by irradiation of blood products given to patients at risk, but problems remain in determining the groups that warrant such measures. Dermatologists need to have heightened awareness of this entity to facilitate more complete diagnosis and allow establishment of effective standards of care.
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PMID:Transfusion-associated graft-vs-host disease in patients with malignancies. Report of two cases and review of the literature. 222 41

In summary, autologous BMT is emerging as a way to deliver myeloablative therapy to patients with hematologic cancer ineligible for allogeneic BMT. Moreover, there are likely circumstances in which autologous is preferable to allogeneic BMT--most notably in Hodgkin's disease, but likely also in the older adult acute leukemia patient. Work is clearly required to produce upgraded conditioning regimens, and to define the need for and utility of marrow purification procedures. However, these pressing needs should not obscure the benefits of the current use of autologous BMT techniques for selected patients--nor prevent the realization that improved patient selection is the most immediate method to improve current results.
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PMID:Autologous bone marrow transplantation for hematologic cancer. 223 63

The in vivo migration of [111In]oxine-labeled peripheral mononuclear cells (PMNC) was studied in 20 patients with various lymphatic malignancies and palpable enlarged lymph nodes. The maximal labeling dose of 10 microCi (0.37 MBq) [111In]oxine/10(8) PMNC was found not to adversely influence either cell viability or lymphocyte proliferation in vitro. For in vivo studies, 1.5 X 10(9) PMNC were gained by lymphapheresis and reinjected intravenously after radioactive labeling, 150 microCi (5.55 MBq). The labeling of enlarged palpable lymph nodes was achieved in three out of three patients with Hodgkin's disease and in five out of five with high-malignant lymphoma, whereas three out of seven patients with low malignant lymphoma and no patient with chronic lymphatic leukemia had positive lymph node imaging. We thus conclude that PMNC retain their ability to migrate after [111In]oxine labeling and that these cells traffic to involved lymph nodes of some, but not all hematologic malignancies.
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PMID:In vivo tracing of indium-111 oxine-labeled human peripheral blood mononuclear cells in patients with lymphatic malignancies. 250 May 1


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