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)

In both animal models and human studies in leukemia, residual disease on day 8 following myelosuppressive therapy is in a proliferative phase and therefore may be sensitive to the S-phase specific drug cytarabine. Based on this concept, 17 patients with refractory or relapsed leukemia or lymphoma undergoing either autologous or allogeneic bone marrow transplantation (BMT) were treated on a Phase I protocol using high doses of busulfan (16 mg/kg, days -10, -9, -8, -7) and cyclophosphamide (120 mg/kg, days -6, -5) followed by escalating doses of a 48-h continuous infusion of cytarabine (starting dose 1000 mg/m2/48 h, days -3, -2). Ten patients received autologous transplants (two with Hodgkin's disease, seven with non-Hodgkin's lymphoma, one with chronic myelogenous leukemia (CML) in blast phase). Seven received allogeneic BMT (two with refractory acute myelocytic leukemia (AML), one with refractory acute lymphoblastic leukemia (ALL) undergoing a second BMT, one with Burkitt's-type leukemia, one with ALL in fifth relapse and two with CML in accelerated/blast phase). Two of these patients received a T cell-depleted haploidentical transplant. The maximum tolerated dose of cytarabine was 1500 mg/m2/48 h; a pulmonary syndrome including dyspnea, hypoxemia, and interstitial infiltrates which responded to aggressive diuresis was the dose limiting toxicity. Of the 10 patients who received cytarabine doses of 2000 or 2500 mg/m2/48 h, five patients developed adult respiratory distress syndrome (ARDS) with three patients requiring intubation; two recovered. Of the nine patients with lymphoma, seven responded with complete tumor clearance (CTC) with two patients tumor-free 13 and 15 months post-BMT, one remained refractory and one died too early to evaluate (TETE).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I study of busulfan, cyclophosphamide, and timed sequential escalating doses of cytarabine followed by bone marrow transplantation. 154 48

In order to study the long-term immunogenicity of interferon-alpha 2c (Berofor) in cancer patients, serum was collected starting in 1983 from study patients with various proliferative diseases who received interferon-alpha 2c at different doses, according to different schedules, and via different routes. A total of 1992 samples were tested for the presence of anti-interferon-alpha 2c antibodies. Due to long-term interferon-alpha 2c treatment, 346 patients were eligible for induction of neutralizing anti-interferon antibodies over a treatment period of 2-52 months. Most patients were treated for longer than 6 months. Of the 346 patients, three patients (0.87%) exhibited measurable titers of neutralizing antibodies following therapy with interferon-alpha 2c. One hundred and sixty-three patients suffered from non-Hodgkin lymphomas, leukemias, and preleukemias. One patient with chronic myeloid leukemia experienced antibody induction under therapy. The other 183 patients had solid tumors. Two of them reacted with antibody production. All titers were very low (1:12, 1:8, and 1:64). Compared with figures reported for other interferon-alpha preparations, the propensity of interferon-alpha 2c to induce neutralizing antibodies seems to be very low. This property might be related to arginines occurring as critical residues in positions 23 and 34 of the interferon-alpha 2c molecule.
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PMID:Low incidence of antibody formation due to long-term interferon-alpha 2c treatment of cancer patients. 160 Mar 38

A 52 year old male presenting chronic myeloid leukemia (CML) Philadelphia chromosome positive (Ph) four years after the diagnosis of a non Hodgkin's lymphoma is described. The patient had received high total doses of alkylating drugs (cyclophosphamide and chlorambucil) as part of chemotherapy treatment for a diffuse mixed lymphoma. At four years of diagnosis of the lymphoma the appearance of hepatosplenomegaly, leukocytosis with myeloma and basophilia and thrombocytosis were observed. These alterations augmented progressively until a cytogenetic study of the bone marrow two years late established the diagnosis of CML upon demonstrating the presence of the Ph chromosome with no other karyotypic anomalies being observed. The explorations carried out at that time confirmed that the lymphoma continued to be in remission. The CML initially responded to treatment with busulphan. However, following a year and a half the disease evolved to a phase of acceleration and the patient died a few weeks later due to pneumonia with no signs indicative of lymphoma activity having been detected since the diagnosis of the CML.
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PMID:[Chronic myeloid leukemia after chemotherapy treatment for non-Hodgkin's lymphoma]. 163 10

Thirty-nine Tropical Splenomegaly Syndrome (TSS) patients. 19 males and 20 females, aged 13 to 69 years, with a mean age of 44.4 years, seen over a two-year period, January 1987 to December, 1988, at the consultant Medical Out-patient Clinics of the University of Nigeria Teaching Hospital, Enugu, Nigeria, were retrospectively studied. The aetiopathogenetic basis of the syndrome was briefly reviewed. The implications of the probable extent of this medical problem TSS in the tropics was emphasized. The spectrum of clinical presentation, haematological picture and results of other investigations were reviewed. An attempt was made to possibly distinguish TSS from such other similarly presenting conditions as Hodgkin's Lymphoma, Chronic granulocytic leukaemia and Chronic lymphocytic leukaemia, on clinical grounds and simple laboratory data that can be easily available to the tropical physician. The probable complications of TSS, the ease of treatment and the impressive results of therapy were highlighted. The place of the different antimalarial chemoprophylactic agents in the treatment of TSS was reviewed. Finally, the question of the appropriate duration of therapy for TSS was entertained.
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PMID:Tropical splenomegaly syndrome in Nigerian adults. 163 45

The experience of 13 bone marrow processings is reported: 7 patients were affected by Acute Leukemias, 4 by Non Hodgkin's Lymphomas, 1 by Chronic Myelogenous Leukemia in complete remission after induction chemotherapy, 1 by Ewing's Sarcoma. Gravity sedimentation technique with 6% hydroxyethyl starch was used in all cases. A mean value of 0.754 x 10(8)/kg body weight mononuclear cells was harvested after sedimentation, with a mean recovery of 74.554%. Mean CFU-GM value was 0.543 x 10(4)/kg body weight. Only one evaluable patient, affected by ANLL, underwent Autologous Bone Marrow Transplantation and a full engraftment was noted on day +14. Results are discussed and further studies are proposed to clarify the relationship between the in vitro CFU-GM growth and the bone marrow engraftment.
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PMID:Bone marrow processing with a gravity sedimentation technique: experience of 13 cases. 169 88

High percentage of neoplastic cells in S, G2 and M phases of cell cycle is unfavourable prognostic sign in human haematological malignancies. In chronic leukaemias (CML and CLL) it is true for peripheral blood leukaemic cells, in non-Hodgkin lymphomas--for lymph node cells, in multiple myeloma--for bone marrow plasma cells. In acute leukaemia results are controversial: some authors found a correlation between proliferation parameters of bone marrow blast cells while others did not. These parameters correlate positively with the rate of complete remission and negatively with its duration. It is concluded that proliferation parameters of neoplastic cells may be used for individual prognosis in patients with haematological tumours especially in combination with other biological and clinical prognostic markers.
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PMID:Prognostic significance of neoplastic cell proliferation parameters in human haematological malignancies. 170 8

To evaluate the potential teratogenicity of modern cancer treatment, 43 children born to mothers with hematological malignancies (18 with non-Hodgkin lymphoma, 14 Hodgkin disease, seven acute leukemia, and four with chronic granulocytic leukemia) who received chemotherapy during some portion of their pregnancy, including 19 of these 43 who received chemotherapy during the first trimester, were examined for physical health, growth, and development. Immunological, hematological, and cytogenetic status also were evaluated. The children's ages ranged from 3 to 19 years. The children had a careful history and physical examination to detect any abnormal symptoms or signs and the mother's previous chemotherapy was carefully documented. In all of the children studied, physical, neurological, psychological, hematological, immune function, and cytogenetics were normal. These results suggest that chemotherapy can be administered during pregnancy, even during the first trimester, because it is not hazardous to the fetus; nevertheless, this study is inadequate in size to exclude the possibility of teratogenesis, and more reports are necessary to define the best treatment from cancer during pregnancy.
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PMID:Growth and development of children of mothers treated with chemotherapy during pregnancy: current status of 43 children. 170 27

Among 262 inpatients with hematologic diseases who were referred for chemotherapy or immunosuppressive therapy between January, 1985, and December, 1989, nine (3.4%) patients, including two with Hodgkin's disease (HD), three with acute myeloblastic leukemia, one with chronic myelogenous leukemia, two with multiple myeloma and one with aplastic anemia, were found to be hepatitis B virus (HBV) carriers before their chemotherapy began. All six HBV carriers who received chemotherapy containing glucocorticoid showed mild-to-moderate elevations in serum transaminase levels after the chemotherapy. Five showed a rise in titer of the hepatitis B surface antigen, HBsAg. In contrast, three HBV carriers not receiving glucocorticoid showed no change in serum transaminase after chemotherapy. One HBV carrier with HD suffered from severe icteric hepatitis after the withdrawal of multiagent chemotherapy containing glucocorticoid. The HBV-DNA polymerase rose markedly and was accompanied by a marked rise in titer of HBsAg. The results warn us to keep in mind the possibility of glucocorticoid inducing an activation of HBV infection, which may result in severe hepatitis in some HBV carriers. Although further investigation is required, it is recommended that HBsAg-positive patients with hematologic malignancies should, if possible, be treated without glucocorticoid.
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PMID:Activation of hepatitis B virus infection by chemotherapy containing glucocorticoid in hepatitis B virus carriers with hematologic malignancies. 175 16

Activity of 8 glycosidases (6 acid lysosomal and 2 neutral cytosolic enzymes) was estimated in lymphoid cells of 28 patients with different forms of lymphoproliferative disorders: B- and T-chronic lymphocytic leukemia (CLL), non-Hodgkins lymphoma (NHL), Sezary syndrome, hairy cell leukemia (HCL) and B- and T-acute lymphoblastic leukemia (ALL). Activity of these glycosidases was also studied in mononuclear cells and granulocytes of healthy volunteers and in immature myeloid cells of 16 patients with chronic myeloid leukemia (CML). In lymphoid cells of all the patients studied (except of ALL) the glycosidases activity was decreased as compared with that of normal mononuclear cells and immature myeloid cells. Activity of the majority enzymes studied was higher in T-lymphoid cells of patients with lymphoproliferative disorders as compared with B-cells. The highest glycosidases activity was found in ALL cells and the lowest--in CLL cells of the patients with B-lymphoid cells forms of the disease. Activities of N-acetyl-beta-D-hexosaminidase, alpha-D-mannosidase and beta-D-glucuronidase were distinctly dissimilar in cells of the patients with B-CLL, B-NHL and HCL. Estimation of these glycosidases activity in lymphoid cells may be of importance in differential diagnosis of lymphoproliferative disorders.
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PMID:[Lymphoid cell glycosidases in various forms of lymphoproliferative disorders]. 181 21

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


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