Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We undertook a study to determine the specificity of the monoclonal antibody, B-ly-7, for hairy cell leukemia (HCL) by examining the expression in 150 samples from B-cell lymphoproliferative diseases as well as screening for reactivity in a number of other hematologic malignancies. Within the B-cell lineage we found that the expression of B-ly-7 was highly specific for HCL and reacted with all 28 cases examined, as well as with 3 of 9 cases of a variant form of HCL. Cells of other closely related B-cell disorders, prolymphocytic leukemia, and splenic lymphoma with villous lymphocytes were negative. Investigation of the peripheral blood and bone marrow of patients with HCL before and after treatment with alpha-interferon or deoxycoformycin suggests that B-ly-7 may be useful in the assessment of minimal disease after therapy. In addition to HCL, we found that B-ly-7 was positive with cells of three mature, CD4+ T-cell malignancies. In view of the reactivity with malignancies of activated B and T cells, we searched for the expression of B-ly-7 on activated, normal B and T cells and found that B-ly-7 reacted specifically with activated normal peripheral blood CD8+ T cells. B-ly-7 has a number of applications, including the precise classification of mature B-cell neoplasia and the diagnosis HCL and its assessment after treatment. In addition, B-ly-7 recognizes a small subset of T-cell disorders. Its expression on these malignancies and on in vitro activated peripheral blood CD8+ T cells suggests that B-ly-7 detects a lymphocyte activation antigen.
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PMID:B-ly-7, a monoclonal antibody reactive with hairy cell leukemia, also defines an activation antigen on normal CD8+ T cells. 190 45

Hexadecylphosphocholine (HPC) was tested in comparison with the membrane-toxic reference ether lipid ET-18-OCH3 for cytotoxic (trypan blue dye exclusion) and cytostatic/antiproliferative [( 3H]thymidine uptake) activity in six cell lines of human hematologic malignancies, six cell lines of human solid tumors and four drug-resistant sublines and their respective non-resistant parent lines in vitro. HPC showed time- and dose-dependent antiproliferative and cytotoxic activity in almost all cell lines, including drug-resistant sublines over a dose range of 2-120 microM and after incubation times of 24, 48 and 72 h. However, ET-18-OCH3 showed a significantly higher activity than HPC, when both compounds were compared on an equimolar basis. The human tumor clonogenic assay confirmed these results. Furthermore, no cross-resistance for HPC with colchicine or methotrexate and partial cross-resistance for HPC with adriamycin was found in cell lines selected for drug resistance. In conclusion, HPC is cytotoxic for neoplastic cells of different histologies including drug-resistant sublines in vitro. Although its cytotoxicity starts at somewhat higher doses when compared to ET-18-OCH3, further testing as an experimental anticancer drug in vivo and comparative cytotoxicity studies with hematopoietic progenitor cells from bone marrow are recommended.
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PMID:Cytotoxic effects of hexadecylphosphocholine in neoplastic cell lines including drug-resistant sublines in vitro. 213 72

A 15-year-old girl presented with an aggressive giant-cell granuloma (GCG) of the maxilla with local invasiveness and bony destruction. The tumor recurred twice and attained a diameter of 6 cm. Previously, this patient had had two hematologic malignancies for which she had received therapeutic doses of radiation to the site where the GCG occurred. It is therefore possible that this tumor was radiation induced.
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PMID:Recurring giant-cell granuloma at the site of previous radiation therapy. 221 5

The spread of metastatic cancer to the pericardium is the most common cause of cardiac tamponade in medical inpatient settings. Lung cancer, breast cancer, and the hematologic malignancies account for some three quarters of the cases. Occasionally, usually in lung cancer, the pericardial involvement is the first clinical presentation of the neoplastic disease. Differential diagnosis includes radiation pericarditis and cardiac toxicity from chemotherapeutic drugs, as well as any of the causes of pericardial disease in patients without neoplasm. Idiopathic nonneoplastic, noninflammatory pericardial effusion is surprisingly common in cancer patients. The initial cardiac tamponade may be managed with either needle tap or subxiphoid pericardiostomy. Pericardiocentesis, performed with echocardiographic guidance and followed by percutaneous catheter drainage for several days, is safe and effective in neoplastic pericardial effusion. It may be the only local therapy that is needed. Further local treatment, for those patients who develop recurrent cardiac tamponade after an initial drainage procedure, may include tetracycline sclerosis of the pericardial space, instillation of cancer chemotherapeutic agents, radiation therapy, and pericardiectomy. No controlled clinical trials of these methods of treatment are available. The choice of therapy is based on various considerations in individual patients, particularly the patient's general condition and the likelihood of a long-term response to treatment of the systemic neoplastic disease.
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PMID:Neoplastic pericardial disease. 224 21

Alterations of ras, c-myc and bcl-1 have been described in hematologic malignancies of lymphoid origin. We investigated the structure of these genes and evaluated the frequency of point mutations involving H-, K- or N-ras in bone marrow samples from patients with multiple myeloma. No abnormalities were detected in the c-myc and bcl-1 genes, but two of 17 patients were found to have N-ras mutations by differential oligonucleotide hybridization and dideoxynucleotide sequencing following amplification by polymerase chain reaction. Bone marrow DNA from both patients had identical missense mutations of N-ras codon 61 changing CAA to AAA, resulting in a substitution of lysine for glutamine in the encoded protein. Multiple myeloma is the first mature B cell neoplasm found to harbor ras mutations.
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PMID:Oncogenes in multiple myeloma: point mutation of N-ras. 226 33

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

The gene predisposing to retinoblastoma, RB1, has been mapped to 13q14 and a cDNA clone has been isolated. Alterations of this chromosomal region are found not only in retinoblastoma, but in other tumor types including bone and soft tissue sarcomas, gastric tumors, small cell lung cancer, hematologic malignancies, rhabdomyosarcoma, and breast cancer. Genetic alterations implicating RB1 in some of these cancers have been observed. A long-range, overlapping restriction map around RB1 has been derived to provide a basis for study of rearrangements in tumors. Putative CpG islands closely linked to RB1 were identified, the effect of methylation was investigated, and RB1 transcriptional direction was determined. Using data in the literature, the map was oriented with respect to the centromere and it was determined that the distance between esterase D, a nearby gene, and RB1 was greater than 200 kb.
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PMID:A physical map around the retinoblastoma gene. 230 71

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

Hairy cell leukemia (HCL) is a rare chronic lymphoproliferative disorder which has been extensively studied over the past decade. Much has been learned regarding the diagnosis, natural history, biology, and treatment of this unique neoplasm. The disease most commonly affects middle aged men and characteristic clinical features include splenomegaly, cytopenias, and usually the presence in the peripheral blood of distinctive 'hairy cells' with irregular cytoplasmic projections. Diagnosis can usually be confirmed by bone marrow biopsy. Although the natural history can be extremely variable among patients, complications are usually referable to the cytopenias, with anemia and infection being most frequent. In addition to pyogenic infections, patients are susceptible to unusual organisms including atypical mycobacterium, legionella, and fungi. The requirement of red blood cell transfusion, severe granulocytopenia or thrombocytopenia, frequent infections, or painful splenomegaly are all indications for treatment. Splenectomy is the standard initial treatment of choice. However, in the past few years there have been exciting major advances in the therapeutic modalities for HCL. Recombinant alpha-interferon is highly effective, with beneficial responses occurring in close to 90% of patients. The Food and Drug Administration has recently approved the use of interferon for HCL. This represents the first time a biological response modifier has been approved for the treatment of human disease. In addition, preliminary results with the adenosine deaminase inhibitor, 2'deoxycoformycin (dcf), have been encouraging. Further clinical trials are required in order to determine the optimal sequential treatment strategy for HCL. The exact mechanisms of action of both interferon and dcf in HCL remain to be elucidated. A better understanding of the unusual features of the hairy cell and the underlying biological effect of these two agents in HCL may have important applications in other hematologic and non-hematologic malignancies.
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PMID:Hairy cell leukemia: clinical features and therapeutic advances. 244 91

Aspects and Results of Interferon Therapy Interferons are effector molecules with pleiotropic biologic functions. Significant clinical activities have been seen in viral diseases and hematologic malignancies, such as hairy cell leukemia, low-grade nodular non-Hodgkin's lymphoma, cutaneous T-cell lymphoma, and chronic myelogenous leukemia. In contrast, the efficacy in solid tumors has been less impressive. In these disorders, higher doses are necessary to induce remission. Responses to interferons are typically slow with improvement often taking several weeks to months. A wide range of both acute and chronic toxicities have been defined. Since these side effects are dose-related and are rarely tolerable for long-term treatment, optimal doses and schedules should be defined in future clinical trials. A better understanding of the mode of anticancer action is an important area of interferon research. Clinical areas might preferably include situations with minimal tumor load, especially in combination with other cytokines, different cytostatic drugs or local therapeutic modalities.
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PMID:[Various aspects and results of therapy with interferon]. 245 71


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