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)

Conventionally fractionated, extended portal radiotherapy (CFEPRT) has been used to treat two diseases in which there was no marrow infiltration (viz. Hodgkin's disease and medulloblastoma). Blood count indices have been monitored during therapy and in the recovery phase. The lymphocytes were the most sensitive and the monocytes the most refractory leucocytes to change; the monocyte count tended to recover during CFEPRT. The platelet count fell gradually and soon after the neutrophil count. The nadir counts for white cells and platelets occurred early or toward the middle of CFEPRT, after which levels were maintained. The hemoglobin slightly and progressively declined. The patterns of change were similar for the two portals analyzed. Absolute eosinophilia occurred in 9 of the 53 CFEPRT patients, often in the recovery period. All patients who maintained their early nadir levels throughout the rest of the CFEPRT demonstrated fast recovery of all indices following completion of radiotherapy; the lymphocyte count recovered fastest. Recent prior CFEPRT or standard MVPP (nitrogen mustard, vinblastine, procarbazine, prednisolone) chemotherapy rendered the blood count more liable to radiation induced cytopenia. A lapse of more than 3 months between MVPP and CFEPRT allowed greater tolerance to the radiotherapy. Recent MVPP may be less myelosuppressive than recent mantle radiotherapy with respect to subsequent tolerance to CFEPRT.
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PMID:The effects of conventionally fractionated, extended portal radiotherapy on the human peripheral blood count. 640 37

Cerebrospinal fluid eosinophilia is an unusual finding that can be caused by Hodgkin disease with central nervous system involvement. To date, only three cases have been reported; in only one of these was central nervous system involvement demonstrated at autopsy. This is the second autopsy-proven case of eosinophilic meningitis associated with intracerebral involvement in Hodgkin disease.
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PMID:Eosinophilic meningitis in Hodgkin disease. 719 13

Diagnosis of Hodgkin's disease was made in a patient who had been treated with diphenylhydantoin sodium for 4 years. Three different neoplastic diseases of the lymphoid tissue following therapy with hydantoin derivatives have been reported. Pseudolymphoma is characterized by lymph node enlargement, fever, arthralgias, cutaneous rash, hepatosplenomegaly and eosinophilia. The lymph node biopsy reveals a non-malignant histopathologic pattern. Pseudolymphoma develops few weeks after administration of hydantoin and it completely disappears when medication is discontinued. Pseudo-pseudolymphoma has similar clinical and histologic characteristics than those of pseudolymphoma, but patients in this category develop a true lymphoma after an asymptomatic period. Lymphomas (Hodgkin's disease and non-Hodgkin's lymphomas) appear following prolonged treatments with hidantoin derivatives. Risk to develop lymphoma is two to four times higher for patients taking such medication. Carcinogenic mechanism of hydantoin is unknown, but it might be related to the immunosuppressive effect of this drug.
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PMID:[Hodgkin's disease following treatment with hydantoins. Report of a case and review of the literature (author's transl)]. 739 7

Analysis of most hematologic neoplasms indicates the involvement of one or more cell lineages in the bone marrow and/or the blood but rules out the involvement of all lineages in any one neoplasm. It is important to detect lineage involvement in order to clarify which stem cells are involved in leukemia, to predict prognosis, and to select appropriate treatment. Our aim was to study the cell lineage involvement of some of the recurrent chromosomal abnormalities seen in hematological neoplasms. The direct morphology-antibody-chromosomes (MAC) method was used. The deletion 20q in myeloproliferative diseases (MPD), the deletion of 5q and t(1;7) in myelodysplastic syndromes (MDS), and t(3;3) in acute myeloid leukemia subtype M7 (AML-M7) were seen in all or at least in two myeloid lineages. These were interpreted as stem cell abnormalities. Deletion 13q in MPD, t(8;21) in AML-M2 and t(15;17) in AML-M3 were seen in granulocytic lineages only; t(14;18) in non-Hodgkin's lymphoma and trisomy 12 as the sole abnormality in chronic lymphocytic leukemia (B-CLL) were seen only in immunoglobulin light chain clonal B cells; inversion 14 in T-CLL was seen only in T cells, whereas t(15;14) in acute lymphocytic leukemia with eosinophilia (ALL-EO) was seen in lymphoid stem cells but not in mature granulocytes or lymphocytes. Additional abnormalities (in addition to the Philadelphia chromosome) in chronic myeloid leukemia (CML) were seen in all myeloid cell lineages and also in mature granulocytes, B cells, and large granular lymphocytes. Abnormalities in Hodgkin's disease were restricted to CD30-positive Reed-Sternberg cells. Trisomy 8 and monosomy 7 are abnormalities that may be present in either stem cells or any of the single cell lineages.
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PMID:Cell lineage involvement of recurrent chromosomal abnormalities in hematologic neoplasms. 752 Feb 72

T-cell non-Hodgkin's lymphomas can be considered the neoplastic equivalents of immunologically functional, site-restricted T lymphocytes. Little is known about the occurrence and clinical behavior of T-cell lymphomas that are the neoplastic equivalents of different functional T-cell subsets. Here, we investigated the prevalence, preferential site, immunophenotype, and clinical behavior of the neoplastic equivalents of activated cytotoxic T cells (CTLs) in a group of 140 nodal and extranodal T-cell lymphomas. Activated CTLs were shown immunohistochemically with a monoclonal antibody against granzyme B, a major constituent of the cytotoxic granules of activated T cells. Granzyme B-positive T-cell lymphomas were mainly found in mucosa-associated lymphoid tissue (MALT; nose, 63% of the cases; gastrointestinal tract, 46%; and lung, 33%). Granzyme B-positive cases with primary localization in MALT were more often associated with angioinvasion (P = .005), necrosis (P = .002), and histologic characteristics of celiac disease in adjacent mucosa not involved with lymphoma. Eosinophilia was more often observed in granzyme B-negative cases (P = .03). Most cases belonged to the pleomorphic medium- and large-cell group of the Kiel classification. CD30 expression was more often found in granzyme B-positive lymphomas of MALT (P = .04), whereas CD56 expression was exclusively found in nasal granzyme B-positive lymphomas. Immunophenotypically, most of the cases should be considered as neoplastic equivalents of activated CTLs based on the presence of T-cell markers on tumor cells. In two cases of nasal lymphoma, tumor cells probably were the neoplastic counterparts of natural killer cells. The prognosis of the granzyme B-positive gastrointestinal T-cell lymphomas was poor but did not differ from granzyme B-negative gastrointestinal T-cell lymphomas. This indicates that, in peripheral T-cell lymphomas, site of origin is more important as a prognostic parameter than derivation of activated CTLs.
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PMID:Granzyme B-expressing peripheral T-cell lymphomas: neoplastic equivalents of activated cytotoxic T cells with preference for mucosa-associated lymphoid tissue localization. 752 49

A 15-year-old girl developed massive, fatal eosinophilic disease following autologous bone marrow transplantation (BMT) for Hodgkin's disease (HD). Prior to autologous BMT, the erythrocyte sedimentation rate (ESR) was elevated, with active HD, but eosinophilia was absent. Post-autologous BMT, ESR and peripheral eosinophilia were observed to correlate with respiratory symptoms. Initial evaluation revealed no recurrent tumor, infection or other identifiable etiology. A diagnosis of chronic eosinophilic pneumonia was made following lung biopsy. A complete response was initially achieved with steroid therapy; however, when steroid therapy was tapered, the eosinophilia and elevated ESR recurred with worsening respiratory symptoms. Terminally, severe pulmonary disease developed and recurrent HD was found in lung, lymph nodes and bone marrow. During episodes of eosinophilia, the patient's serum stimulated her bone marrow as well as control marrow to produce predominantly eosinophilic colonies. Eosinophilic colony production was not observed with patient's sera obtained prior to or during autologous BMT or with control sera. This patient died of eosinophilic inflammatory disease following autologous BMT. The etiology of this disease was not definitely identified but appeared to be due to an eosinophilic-stimulating factor which developed after autologous BMT.
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PMID:Fatal eosinophilic disease following autologous bone marrow transplantation. 799 53

Eosinophil leukaemia is a rare and poorly defined entity characterized by neoplastic proliferation of eosinophil cell line. This form of the hypereosinophilic state is considered to be a variant form of CML, although as a diseases entity is not generally accepted. A history of a patients is reported, whose clinical course is thought to fulfill the requirements of eosinophil leukaemia. On the basis of the initial results (pathological lymphogram, eosinophilia, Ph-negativity) lymphogranulomatosis was suspected and explorative laparotomy was performed. However, only marked eosinophilic infiltration of the spleen was detected. After splenectomy his disease was stable without treatment for six months when his leukocytosis and eosinophilia increased. Despite the administration of hydroxyurea the leukocyte count exceeded 100 x 10(9)/l (eosinophil cells 70%), and the bone marrow revealed massive (80%) eosinophilic infiltration. Neither Ph-chromosome, nor cabl and bcr gen rearrangement were demonstrated, but the expression and amplification of c-myc oncogene indicated disease progression. Interferon therapy produced long-term clinical and haematological improvement, but blastic transformation was developed in the second year of his disease. Autopsy showed multiple organ involvement characteristic of CML, but no marked eosinophilic infiltration was found. The feature of this case suggest that eosinophil leukaemia might represent an uncommon form of Ph-negative CML.
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PMID:[Eosinophilic leukemia: a rare form of Philadelphia chromosome negative chronic myeloid leukemia?]. 805 96

A 28-year-old man with recurrent swelling of both upper eyelids was found to have increased values in several liver function tests (GOT 162 U/l, GPT 356 U/l, gamma-GT 643 U/l, bilirubin 3.0 mg/dl, alkaline phosphatase 925 U/l). Abdominal ultrasonography demonstrated lymph node enlargements up to 3 cm, dilated intra- and extrahepatic bile ducts, as well as a cyst of 3 cm size in the pancreatic tail. Endoscopic retrograde cholangiopancreatography and punch biopsy of the liver revealed sclerosing cholangitis. In addition to the eyelid swellings the patient also had protrusion of the left eyeball, blood eosinophilia (800/microliter) and marked increase in polyclonal IgG (6930 mg/dl) with lymphadenopathy suggesting the diagnosis of angioimmunoblastic lymphadenopathy with dysproteinaemia (AILD, lymphogranulomatosis X), confirmed by lymphocyte surface marker analysis. However, histological examination of a lymph node was more suggestive of a T-zone lymphoma. Treatment with ursodeoxycholic acid (250 mg three times daily) and prednisolone (initially 2 mg/kg daily) quickly led to normal biochemical values and regression of the eye changes. In addition, treatment with interferon alpha-2b (initially 3 mill. U daily for 10 days) was begun. The abnormalities in the bile ducts disappeared 6 months later. The patient has been in full remission for 25 months (prednisolone dosage reduced to 12.5/7.5 mg alternating daily and interferon alpha-2b 3 mill. U three times weekly). This response makes AILD with secondary involvement of the bile ducts the most likely diagnosis.
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PMID:[Angioimmunoblastic lymphadenopathy with dysproteinemia and sclerosing cholangitis]. 812 36

Tissue eosinophilia is commonly seen in Hodgkin's disease and non-Hodgkin's lymphomas of T-cell lineage. In contrast, eosinophilia is infrequent in non-Hodgkin's lymphomas of B-cell origin. We describe five-B-cell lymphomas with exuberant tissue eosinophils. According to the Working Formulation, three were classified as large-cell immunoblastic, one as small lymphocytic lymphoma/chronic lymphocytic leukemia, and one as low-grade, not further subclassified, with features of monocytoid B-cell lymphoma. Immunophenotypic studies in each case revealed B-cell lineage; neoplastic cells expressed monotypic immunoglobulin light chain (four of five cases) or pan-B-cell antigens (five of five cases) and were negative for T-cell antigens. Southern blot hybridization in one case revealed immunoglobulin gene rearrangements, further confirming B-cell lineage. Eosinophilopoiesis is stimulated by interleukin 5 (IL-5), and Epstein-Barr virus (EBV) has been shown to upregulate IL-5 production. Therefore, both EBV infection and IL-5 expression were investigated as possibly pathogenetic mechanisms for the eosinophilia. However, both in situ hybridization studies for EBV mRNA and IL-5 mRNA were negative in the neoplastic cells. In one tumor, IL-5 was abundant in the cytoplasm of the eosinophils, a pattern similar to that seen in five cases of Hodgkin's disease studied with the same technique. Although rare, marked tissue eosinophilia may be associated with B-cell non-Hodgkin's lymphomas. Immunophenotypic or molecular genetic analyses are needed to make the correct diagnosis.
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PMID:Malignant lymphomas of B-cell lineage with marked tissue eosinophilia. A report of five cases. 814 29

A case of non-Hodgkin's T cell lymphoma (diffuse lymphoma, large cell type) associated with marked eosinophilia and pleurisy in a 57-year-old male is reported. The leukocyte count was 12.5 x 10(3)/microliters and eosinophil count was 53% and the absolute count of 6.6 x 10(3)/microliters. The patient's serum and pleural effusion fluid, containing abundant lymphoma cells, showed eosinophil colony stimulating factor (Eo-CSF) activity. Conditioned medium (CM) prepared from patient's T cells (T-CM) produced Eo-CSF and this was enhanced by interleukin-2 (IL-2) stimulation. We demonstrated that the patient's serum contained a significant amount of interleukin-5 (IL-5) and the patient's T-CM, particularly after IL-2 stimulation contained a significant amount of granulocyte-macrophage colony-stimulating factor (GM-CSF). These findings suggest that Eo-CSF produced by neoplastic T cells or normal T cells activated by tumor antigen stimulated the production of eosinophils in this patient and that both IL-5 and GM-CSF might play a role in Eo-CSF activity.
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PMID:[Non-Hodgkin's T cell lymphoma associated with marked eosinophilia]. 823 Jul 43


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