Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pseudomonas cepacia is a gram negative rod, having no fermentative activity on glucose. This organism was detected in the sputum, throat swab, or throat washing of 22 inpatients treated between January, 1990, and December, 1990, at the First Department of Internal Medicine, Kagawa Medical School. The primary diseases for which these 22 patients were hospitalized were leukemia in 12, malignant lymphoma in 5, lung cancer in 2, myelodysplastic syndrome in 1, and embryonal cell carcinoma in 1. Twelve of the 22 patients had episodes of pneumonia which complied clinically with the diagnostic criteria provided to facilitate the National Nosocomial Infection Study. The complication of pneumonia occurred in 7 patients with leukemia, 2 with malignant lymphoma, 2 with lung cancer, and 1 with myelodysplastic syndrome. In 10 of these 12 patients, the organism was detected before the onset of pneumonia. All 22 patients in whom the organism was demonstrated had received antibiotics. The antibiotics which was most frequently used to treat these patients 1 month before detection of Pseudomonas cepacia were amikacin and ceftizoxime, which were used in 13 patients. Of the antibiotics in which the susceptibility to Pseudomonas cepacia was, evaluated, minocycline was effective in 100% (21/21), ceftazidime in 50% (11/22), and ofloxacin in 27.3% (6/22). Physicians should be especially aware of the possibility of colonization and nosocomial respiratory infection by Pseudomonas cepacia in patients with severe underlying diseases.
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PMID:[Nosocomial respiratory infection caused by Pseudomonas cepacia in immunocompromised hosts]. 138 85

Mutational activation of ras oncogenes is frequently encountered in human tumors. For unexplained reasons, K-ras mutations are predominantly found in pancreatic cancer, colorectal cancer and adeno-carcinoma of the lung, N-ras is predominantly found in a subset of acute leukemias and in myelodysplastic syndromes, while H-ras mutations are rare. In most tumors, ras mutations are not clearly associated with specific clinical or biological features, but in lung cancer, childhood lymphoblastic leukemia and possibly in myelodysplastic syndromes ras mutations may predict a poor prognosis. Accumulating evidence suggests that exposure to chemical carcinogens is responsible for many ras mutations in humans.
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PMID:ras and human tumors. 142 Nov 68

A case of secondary myelodysplastic syndrome (MDS) following chemotherapy for lung cancer is reported. A 78-year-old man, with a smoking history of 20 cigarettes/day for 55 years, was incidentally, diagnosed as having stage IV squamous cell carcinoma of the lung in 1987 during admission for transurethral resection of bladder cancer. He received combination chemotherapy of mitomycin C, vincristin, and cisplatin for his lung cancer between July and September 1988. His clinical course remained almost stable until October 1989, when his blood count showed severe anemia and thrombocytopenia. He was diagnosed as having secondary MDS induced by cytotoxic agents used for the treatment of lung cancer, based on the dysplastic findings of precursor cells in the bone marrow and the chromosome abnormality of 51XY, +8, +9, +21, 3p-, 5q-, +2mar. He died of infection with the progression of MDS in March 1990.
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PMID:[A case of secondary myelodysplastic syndrome following chemotherapy for lung cancer]. 146 83

We studied the association between myelodysplastic syndromes (MDS) and malignancies in a cohort of 155 patients with MDS, 21 of whom presented malignant solid tumors. Myelodysplasia was present after the diagnosis of cancer in eight patients (interval between the diagnosis of both conditions 18 months, median survival 49.5 months), simultaneously with diagnosis in 11 (median survival 8 months), and before malignancy in two patients (interval between the diagnosis of both conditions 47 and 7 months). One patient was given chemotherapy for lung cancer, and three patients received radiotherapy for adenocarcinoma of the kidney and cancer of the prostate. At the time of diagnosis of MDS, nine patients already presented metastatic spread. Fourteen patients died, ten as a result of tumor-related complications and four because of transformation to acute nonlymphocytic leukemia. The analysis of the incidence of malignancy in patients with MDS was statistically significant for males, and the relative risk was significant in both sexes. The results of this study show that MDS patients present a higher incidence of malignant tumors than the general population, that MDS may be of real paraneoplastic significance, and that the occurrence of MDS in cancer patients may be considered to be related to the malignancy rather than an independent phenomenon.
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PMID:Myelodysplastic syndromes and malignant solid tumors: analysis of 21 cases. 150 93

A 77-year-old man was diagnosed as having acute myelomonocytic leukemia (M4) with increased ringed sideroblasts in the bone marrow (BM) in October, 1979. Complete remission was achieved and ringed sideroblasts disappeared after two courses of CMP (cytarabine, 6-mercaptopurine, prednisolone) therapy. Following remission, there was no increase of blasts during the course of the disease, but monocytosis and dysmyelopoiesis persisted for about seven years. The monocytosis was controlled by 6-mercaptopurine. In June, 1986, however, monocytosis in peripheral blood (PB) and BM developed again, and there was severe pancytopenia and reappearance of ringed sideroblasts without increase of blasts. The patient died of pneumonia on September, 1986. Postmortem examination revealed hypercellular marrow with a few blasts, leukemic cell infiltration into spleen, liver and lymph nodes, ad lung cancer. His clinical and hematological features after remission of acute leukemia accorded with those of CMMoL. The dysmyelopoiesis observed in this case in not induced by anti-leukemic agents, but originated from the same clone as the initial AMMoL, and his disease was thought to be CMMoL converted from blastic crisis to chronic phase.
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PMID:[Long survival of a patient presented with blastic crisis of chronic myelomonocytic leukemia]. 231 5

The major hematopoietic growth factors have been produced through recombinant DNA technology and have entered initial clinical trials; results of these trials will be reviewed here. Granulocyte colony-stimulating factor (G-CSF) has been tested in patients with bladder cancer and small-cell carcinoma of the lung. In these studies, G-CSF ameliorated the leukopenia associated with combination chemotherapy, reduced the incidence of mucositis in the bladder cancer patients, and nearly eliminated the occurrence of serious infections in the lung cancer patients. Trials involving another factor, granulocyte macrophage colony-stimulating factor (GM-CSF), have resulted in a marked increase in white blood cell (WBC) counts in patients with myelodysplastic syndromes, and has accelerated the appearance of leukocytes and platelets after autologous bone marrow transplants. GM-CSF can also increase the WBC counts in acquired immunodeficiency syndrome patients treated with zidovudine. Both G-CSF and GM-CSF may produce multilineage effects in certain clinical settings and dose ranges. Finally, interleukin-1 (IL-1) and IL-3, which commit very early stem cells to a myeloid pathway, may be used in combination with G-CSF or GM-CSF to produce a synergistic response to various clinical situations.
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PMID:Status of colony-stimulating factors in cancer and AIDS. 240 93

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 administered recombinant human granulocyte colony-stimulating factor (rhG-CSF) to four patients with myelodysplastic syndrome (MDS) and three patients with non-MDS (two malignant lymphoma and one lung cancer) as a part of a phase II trial and analyzed the effects of rhG-CSF on the neoplastic cells of MDS by performing sequential chromosome analyses on the bone marrow cells. A greater than 3-fold increase in neutrophil count was observed in the MDS patients after rhG-CSF infusions, whereas the number of blasts in the bone marrow did not increase and none of them progressed into the leukemic phase. After rhG-CSF treatment, the bone marrow cells obtained from patients without MDS did not show any particular chromosome abnormalities such as chromosomal breakage. On the contrary, two of the four MDS patients with acquired chromosome abnormalities showed a change in the frequency of marrow cells with clonal abnormalities after rhG-CSF treatment; the proportion of metaphase cells with additional numerical chromosome abnormalities decreased in these two MDS patients. After discontinuation of the treatment, the constitution of marrow cells with chromosome changes reverted to that before treatment. The remaining two MDS patients did not show any particular chromosome changes after the rhG-CSF treatment, indicating that rhG-CSF may not promote the characteristics of dyshematopoiesis in MDS, and act on cells derived from an MDS clone.
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PMID:Hematologic and cytogenetic findings in myelodysplastic syndromes treated with recombinant human granulocyte colony-stimulating factor. 248 Sep 43

The risk of second cancers (SCs) was assessed in 744 patients with Hodgkin's disease (HD) admitted to The Netherlands Cancer Institute from 1966 to 1983. Sixty-nine SCs were observed one month or more after start of first treatment. These included 14 cases of lung cancer, nine cases of non-Hodgkin's lymphoma (NHL), 16 cases of leukemia, and six cases of the myelodysplastic syndrome (MDS). The median interval between the diagnosis of HD and that of second lung cancer, NHL, and leukemia was 8.1, 13.3, and 5.7 years, respectively. The overall relative risks (RR) (observed/expected [O/E] ratios) of developing lung cancer, NHL, and leukemia were 4.9 (95% confidence limit [CL], 2.7 to 8.2), 31.0 (95% CL, 14.2 to 58.9) and 45.7 (95% CL, 26.1 to 74.2), respectively. At 15 years the cumulative risk of developing an SC amounted to 20.6% +/- 2.9%. The 15-year estimates of lung cancer, NHL, and leukemia were 6.2% +/- 1.9%, 5.9% +/- 2.1% and 6.3% +/- 1.7%, respectively. Increased lung cancer risk following HD has not frequently been clearly demonstrated before; that we were able to demonstrate such risk may be due to the completeness of follow-up over long periods that could be achieved in this study. Excess lung cancer risk was only noted in treatment regimens with radiotherapy (RT); also, all lung cancers arose in irradiation fields. Excess risk of leukemia was only found in treatment regimens involving chemotherapy (CT). For NHL, combined modality treatment was shown to be the most important risk factor. Risk of lung cancer and NHL increased with time since diagnosis. A time-dependent covariate analysis (Cox model) performed on leukemia and MDS showed an increasing risk with intensity of CT, age (greater than 40 years), and a splenectomy.
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PMID:Increased risk of lung cancer, non-Hodgkin's lymphoma, and leukemia following Hodgkin's disease. 275 47

It is not yet clear whether some polymorphic variants of the Ha-ras-1 gene confer genetic predisposition to cancer. However, recent data on myelodysplasia and lung cancer are controversial. To clarify this point, 62 colorectal adenocarcinoma patients were examined for the Ha-ras-1 gene restriction fragment length polymorphism and results were compared with those of 108 healthy blood donors. No Ha-ras-1 polymorphic variants specifically associated with the cancer patients were detected. However, a specific genotype was significantly more frequent in the healthy donors than in the cancer patients (16% versus 5%), suggesting an interaction between the two alleles of the gene.
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PMID:Ha-ras-1 restriction fragment length polymorphism and susceptibility to colon adenocarcinoma. 288 94


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