Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the late 1970s, 18 clinical studies have been conducted in Japan with various types of human interferon (IFN) for their possible anti-tumor efficacy under the control of the Special Committee for Clinical Application of IFN of the Ministry of Health and Welfare. Objective antitumor effects have been observed in renal cell carcinoma, brain tumor, multiple myeloma, malignant lymphoma, adult T cell leukemia, chronic lymphocytic leukemia, chronic myelogenous leukemia, and by local injections in skin cancer such as malignant melanoma and cutaneous lymphoma. In this paper, updated results of clinical studies of the 3 types of IFNson various malignant tumors in Japan was reviewed, and the potential usefulness of IFNs as the first cytokine introduced into a clinical trial of the treatment of cancer was discussed.
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PMID:[Clinical studies on interferon in cancer therapy in Japan]. 243 62

Fifty-eight patients with malignant pericardial effusion were seen from 1979 to 1986. A Kifa catheter was inserted into the pericardial sac and allowed to drain for 12 to 24 hours during electrocardiographic monitoring. Lidocaine hydrochloride, 100 mg, was instilled intrapericardially, followed by tetracycline hydrochloride, 500 to 1,000 mg, in 20 ml of normal saline solution. The catheter was clamped for 1 to 2 hours and then reopened. This procedure was repeated daily until the net drainage was less than 25 ml/24 hours. There were 22 male and 36 female patients (median age 58 years). The primary malignancy included lung (27 patients), breast (16 patients), stomach (3 patients), adenocarcinoma of unknown primary (7 patients), mesothelioma (2 patients) and chronic granulocytic leukemia, ovary and lymphoma (1 patient each). Fifty-six patients received 1 to 5 tetracycline instillations. In 1 patient, the catheter could not be inserted and in another, clotting occurred within the catheter before injection of tetracycline. Complications included transient atrial arrhythmias (5 patients), pain after injection (9 patients) and temperature higher than 37.5 degrees C (5 patients). One patient had a cardiac arrest during pericardiocentesis. Forty-three patients (74%) had control of their effusions for longer than 30 days (median survival 168 days, range 30 to 1,149+), and 5 patients (9%) died before 30 days without effusion. Eight patients (14%) did not achieve control. One declined further therapy after 1 instillation, and 3 died within 6 days with progressive malignancy. One patient had persistent drainage after 3 instillations, and 3 had reaccumulation of fluid 2, 6 and 27 days after catheter removal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Medical management of malignant pericardial effusion by tetracycline sclerosis. 244 87

In order to better understand the patho-physiologic role of granulocyte colony-stimulating factor (G-CSF), we estimated its serum levels in healthy persons and patients with various disorders, using a newly developed enzyme immunoassay (Motojima et al). In 49 of 56 normal healthy persons (88%), the levels were beneath the sensitivity of the assay (less than 30 pg/mL), while in the remaining seven healthy persons, the levels ranged from 33 to 163 pg/mL. On the other hand, nine of 11 patients (82%) with idiopathic aplastic anemia (AA), one patient with Fanconi's anemia, six of 12 patients (50%) with myelodysplastic syndrome (MDS), five of 12 patients (42%) with acute leukemia without any blast cells in the blood (M4: one, M5: one, L1: one, and L2: two), six of 18 patients (33%) with chronic myeloid leukemia (CML), one of two patients with chronic lymphoid leukemia (CLL), two of four patients with lung cancer, one patient with cyclic neutropenia, two of seven patients with malignant lymphoma, and four patients with acute infection had G-CSF levels ranging from 46 pg/mL to greater than 2,000 pg/mL. Interestingly, a reverse correlation between blood neutrophil count and serum G-CSF level was clearly demonstrated for aplastic anemia (r = -.8169, P less than .01). Moreover, it was found that the G-CSF level rose during the neutropenic phase of cyclic neutropenia and after chemotherapy or bone marrow transplantation (BMT) in three patients with leukemia; also high G-CSF levels were positively correlated to blood neutrophil counts in some cases of infectious disorders and lung cancer. The cellular sources and the mechanisms for production and secretion of circulating G-CSF were not investigated in this study, but the data presented here strongly indicate that G-CSF plays an important role as a circulating neutrophilopoietin.
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PMID:Serum granulocyte colony-stimulating factor levels in healthy volunteers and patients with various disorders as estimated by enzyme immunoassay. 246 34

We report on the characterization of four monoclonal antibodies which were prepared against membrane markers of human myeloid lineage. Fusion, isolation of hybridoma cells and their cloning and testing of the monoclonal antibodies by indirect immunofluorescence and FACS 440 analysis were performed by means of standard procedures. The results indicate that the monoclonal antibodies have a specificity against membrane markers of human myeloid lineage (exactly promyelo-granulocytes). These monoclonal antibodies do not react with human T and B lymphocytes, monocytes, erythrocytes and thrombocytes of peripheral blood. In normal bone marrow reactivity to matured myeloid cells was found to occur in promyelocytes and expressed on all granulocytes. These monoclonal antibodies also react with cells of myeloid cell lines and with other precursor cell lines represented by NALM-1, NALM-16, HEL, K-562, REH no reactivity was detected. The produced antibodies react with some leukaemic cells from patients with more mature myeloid cells (AML with promyelocytes, myelocytes and CML) they do not react with pathological cells from patients with CLL, AML (with myeloblasts), ALL, hairy cell leukaemia, erythroleukaemia and several types lymphoma. All antibodies have a IgM class and express granulocytotoxic and granuloagglutination activity. Using flow cytometry comparative analysis with other monoclonal antibodies was performed to detect the membrane structure (X-haptene) included in standard International classification as CD 15 group.
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PMID:Human leukocyte markers defined by monoclonal antibodies. I. Expression of X-hapten structure on cells of myeloid lineage. 246 63

Expression levels of terminal deoxynucleotidyl transferase (TdT) mRNA in fresh leukemia and lymphoma cells were measured by northern blotting analysis. Bands of 2.1 kb mRNA were detected in all of eight cases of TdT activity-positive leukemias: two cases of null-cell acute lymphoblastic leukemia (null-ALL), two of common ALL, one of pre-B ALL, one of T-ALL, and two of chronic myelogenous leukemia in blastic crisis. One of the null-ALL and one of the common ALL cases also showed large TdT mRNA (3.3 kb). Since all TdT activity-positive samples exhibited TdT mRNA, the TdT gene might be mainly regulated at the transcription level in leukemic cells. An elevated level of 2.1 kb TdT mRNA was also detected in one lymphoma case, where neither TdT activity nor immunoreactive TdT was detected. The extensive chromosomal abnormality demonstrated in this case might be associated with the translational anomaly of TdT.
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PMID:Gene expression of terminal deoxynucleotidyl transferase in neoplastic cells of leukemia and lymphoma. 250 Dec 50

A monoclonal antibody, MRK20, in F(ab')2 form [MRK20-F(ab')2], which reacts with 85-kDa membrane protein in a doxorubicin (ADM)-resistant subline (K562/ADM) of human myelogenous leukemia cell line, K562, was examined for reactivity with 41 cultured human leukemia and lymphoma cell lines. None of these cell lines had ever been exposed to any anticancer agent in vitro except K562/ADM. The relative resistance index to various drugs was calculated by dividing the 50% growth-inhibitory concentration (IC50) of the test cell line by IC50 of K562 (the negative control in the antibody experiment). MRK20-F(ab')2 reacted with seven cell lines, KYO-1 derived from chronic myelogenous leukemia in blastic crisis (CMLbc), CMK from acute megakaryoblastic leukemia, HEL from erythroleukemia, P31/FUJ from acute monocytic leukemia, KOPM-28 from CMLbc, PL-21 from acute promyelocytic leukemia and K562/ADM. MRK20-F(ab')2 did not react with 34 other cell lines. All seven MRK20-F(ab')2-positive cell lines had relative resistance index values of 2 or more to anthracyclines (ADM, pyrarubicin, daunorubicin), mitoxantrone, etoposide, bleomycin, and pepleomycin. There was no distinct correlation between the reactivity to MRK20-F(ab')2 and a higher relative resistance index than 2 to vinca alkaloids, actinomycin-D, cisplatin, 4-hydroperoxycyclophosphamide, nimustine hydrochloride, methotrexate or cytarabine. These results indicate that MRK20-F(ab')2 detects a novel multidrug resistance to anthracyclines, mitoxantrone, etoposide, bleomycin and pepleomycin in cultured human leukemia and lymphoma cells.
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PMID:A novel multidrug resistance in cultured leukemia and lymphoma cells detected by a monoclonal antibody to 85-kDa protein, MRK20. 251 73

The antigen pattern pertaining to the ABO (A, B, AB, O (H)), Rh (D, C, c, E, e), Duffy (Fya and b), Kell (K, k) and MNS (M, N) systems were determined in 144 patients between 1 and 74 years of age who had leukemia, lymphoma or myeloma. An association of phenotype Fy (a-b+) with acute lymphatic leukemia and phenotype NN with chronic myeloid leukemia was demonstrated (p less than 0.05, chi sq). Other associations were statistically not significant. Thus, a susceptibility of the aforementioned phenotype patterns to the type of leukemia described is suggested by these findings.
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PMID:[Relationship between various erythrocyte antigens and hematologic disorders]. 251 95

A 60-year-old woman presented with diffuse lymphadenopathy. Diagnostic and staging work-up showed that the patient had diffuse small cleaved cell lymphoma (diffuse poorly differentiated lymphocytic lymphoma) with associated histiocytes (lymphoepithelioid cell lymphoma) by the Kiel classification system. Immunohistologic staining showed a T suppressor cell tumour phenotype. Cytogenetic studies revealed the Philadelphia chromosome (Ph1). On DNA studies, the breakpoint cluster region (BCR) gene was not rearranged suggesting that the Ph1 involvement was not identical to that seen in chronic myelogenous leukemia (CML). This case is presented because of the rarity of Ph1 in lymphoid malignancies, particularly in those of T-cell origin, and because of its potentially adverse implications.
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PMID:Philadelphia chromosome without breakpoint cluster region rearrangement in a case of Lennert's lymphoma of suppressor phenotype. 252 33

Developments of oral mucosal ulcers induced by herpes simplex virus (HSV) were studied in patients with hematologic malignancy. Herpes simplex virus type-1 (HSV-1) was identified by immunological staining using virus-specific monoclonal antibodies in the epithelial cells of such ulcers from two patients with malignant lymphoma (ML), three with acute myeloblastic leukemia (AML), one with refractomy anemia with excess blasts, two with chronic myelocytic leukemia (CML), one with acute lymphoblastic leukemia (ALL) and one with aplastic anemia (AA). Herpes simplex virus type-2 (HSV-2) was also identified in an ulcer from a patient with AML. Isolation of HSV-1 was successful in the two patients with ML, one with CML, one with AML, the one with ALL and the one with AA. The ulcers developed on the tongue (four cases), buccal membrane (five cases), hard palate (one case), soft palate (one case), soft palate (one case) and gingiva (two cases). Only one patient with CML and one with AML had accompanying labial vesicular lesions. All patients except the one with AA had previously been given combination chemotherapy with anti-neoplastic agents. The results indicate that HSV may have an important role to play in the development of chemotherapy-related oral mucosal ulcers in patients with hematological malignancy.
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PMID:Herpes simplex virus in oral mucosal ulcers in patients with hematological malignancy. 255 41

Many cancers have been cured by chemotherapeutic agents. However, other cancers are intrinsically drug resistant, and some acquire resistance following chemotherapy. Cloning of the cDNA for the human MDR1 gene (also known as PGY1), which encodes the multidrug efflux protein P-glycoprotein, has made it possible to measure levels of MDR1 RNA in human cancers. We report the levels of MDR1 RNA in greater than 400 human cancers. MDR1 RNA levels were usually elevated in untreated, intrinsically drug-resistant tumors, including those derived from the colon, kidney, adrenal gland, liver, and pancreas, as well as in carcinoid tumors, chronic myelogenous leukemia in blast crisis, and cell lines of non-small cell carcinoma of the lung (NSCLC) with neuroendocrine properties. MDR1 RNA levels were occasionally elevated in other untreated cancers, including neuroblastoma, acute lymphocytic leukemia (ALL) in adults, acute nonlymphocytic leukemia (ANLL) in adults, and indolent non-Hodgkin's lymphoma. MDR1 RNA levels were also increased in some cancers at relapse after chemotherapy, including ALL, ANLL, breast cancer, neuroblastoma, pheochromocytoma, and nodular, poorly differentiated lymphoma. Many types of drug-sensitive and drug-resistant tumors, including NSCLC and melanoma, contained undetectable or low levels of MDR1 RNA. The consistent association of MDR1 expression with several intrinsically resistant cancers and the increased expression of the MDR1 gene in certain cancers with acquired drug resistance indicate that the MDR1 gene contributes to multidrug resistance in many human cancers. Thus, evaluation of MDR1 gene expression may prove to be a valuable tool in the identification of individuals whose cancers are resistant to specific agents. The information may be useful in designing or altering chemotherapeutic protocols in these patients.
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PMID:Expression of a multidrug resistance gene in human cancers. 256 56


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