Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An autopsy case of a 33 years old doctor with chronic lymphocytic leukemia (CLL) was reported. Two remissions were noted with chemotherapy and irradiation. The special characteristic of this case was the tumor formation in the sellar fossa similating a pituitary tumor which was considered as a type of meningeal leukemia, showing visual disturbance. Leukemic cell infiltration was hardly observed in any other organs. From the analysis of five cases of CLL, the author proposes that CLL may be classified into two types: the one is the severe type showing a short clinical course and the other is a mild one, showing a long clinical course. Details such as histopathological findings, cause of death and clinical findings were discussed.
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PMID:Chronic lymphocytic leukemia showing pituitary tumor with massive leukemic cell infiltration, and special reference to clinicopathological findings of CLL. 73 16

N-Propyl-N-nitrosourea is a strong leukemogen that induces myelogenic leukemia in Donryu rats and thymic lymphoma in F344 rats when administered in drinking water. In the present study, a single or multiple doses of PNU (total 500 mg/kg body weight) was given to young male and female F344 rats via a stomach tube. The results demonstrated that the percentage of tumor-bearing rats was 100% in all PNU-treated male groups, while that of the control group was 46%. Predominant tumors induced by PNU in male rats were lung adenoma/adenocarcinoma followed by peritoneal mesothelioma, and forestomach papilloma. In females, the tumor incidence of PNU-treated groups varied between 58% and 92% while that of the control group was 42%. Although pituitary tumor was the most frequent tumor in PNU-treated female rats, it was thought to be spontaneous since its incidence in each experimental group was not statistically different from that of the control group. Lung tumors and forestomach papillomas were also induced by PNU in female rats. No thymic lymphoma, however, was found in any of the PNU-treated groups of either sex. Lung tumors developed in almost all PNU-treated male rats and in about one-third of PNU-treated female rats. Mesothelioma was induced only in male rats, and its incidence depended on the treatment schedule. Induced mesotheliomas were extensively examined histologically, histochemically, immunohistochemically, and electron microscopically.
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PMID:Induction of lung tumors and peritoneal mesotheliomas in F344 rats given intragastric N-propyl-N-nitrosourea and histochemical, immunohistochemical, and ultrastructural characteristics of induced mesotheliomas. 245 26

Pituitary metastases constitute 1% to 8.3% of all metastatic brain tumors. The most frequent localization is in the posterior lobe and diabetes insipidus may be the only symptom of dysfunction. Cerebral aspergillosis is an unusual disease and it has been described complicating an underlying malignancy or following intracraneal surgery. We describe a case of hypopituitarism and hyperprolactinemia in a patient with pituitary metastases of a colon carcinoma and aspergillosis. Two years before a colon adenocarcinoma (Class C1 of Duke) had been resected. There were no clinical signs of hypopituitarism or galactorrea. The laboratory findings showed deficiency of cortocotropin (ACTH), luteinizing hormone (LH), follicle stimulating hormone (FSH) and slight hyperprolactinemia (PRL). Cerebral magnetic resonance image (MRI) revealed an intra and suprasellar mass which extended to the hypothalamus. Chest X-ray film and computed tomographic scanning (TC) confirmed a macronodular mass at the apical segment of the inferior left lung lobule with mediastinal hypertrophic lymph nodes. A non functional pituitary tumor was diagnosed and transphenoidal surgery was carried out. At microscopic examination a malignant proliferation was found suggesting colonic differentiation. Fragments of tumoral pituitary tissue showed hyphae of aspergillus in the form of abscess. Aspergillosis complicating neoplastic disease is more often present in leukemia and lymphoma than in solid tumors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypopituitarism caused by colonic carcinoma metastasis associated with hypophysial aspergillosis]. 785 93

Amount and type of fat and energy density of diets may influence tumor incidences. The purpose of this report is to summarize the influence of corn oil gavage and different nonpurified diets on spontaneous tumor incidences in 64 diet and 59 corn oil gavage control groups in two-year studies involving approximately 6,100 control Fischer 344 rats of each sex. The maximum mean body weight attained during the course of the study, survival at 106 weeks of age, and spontaneous tumor incidences of groups fed different nonpurified diets with or without corn oil gavage were summarized and evaluated for differences. Male rats fed NIH-07 open-formula diet with or without corn oil gavage had significantly higher body weight, lower survival, and higher incidence of pancreatic acinar cell tumors than rats fed commercial proprietary diets with or without corn oil gavage. Female rats fed NIH-07 diet with or without corn oil gavage had significantly higher body weights and pancreatic tumor incidences than groups fed commercial diets. Time-related trends could account for other apparent differences in tumor incidences between the groups fed commercial and NIH-07 diets. Corn oil gavage significantly increased the body weight and pancreatic tumor incidences but decreased the incidence of leukemia, a lethal tumor, which resulted in higher survival in male rats. Corn oil gavage significantly lowered the body weight and anterior pituitary tumor incidence in female rats. The pancreatic acinar cell tumor incidence appears to be due to a combination of fat intake and body weight.
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PMID:Influence of corn oil and diet on body weight, survival, and tumor incidences in F344/N rats. 844 12

The inhibition of adenylyl cyclase (AC) by a 12-lipoxygenase metabolite of arachidonic acid, 12(S)-hydroxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12-HETE), was investigated using three different kinds of cells: NRK-49F (normal rat kidney fibroblasts), AtT-20 (mouse pituitary tumor cell line) and HL-60 (human leukemia cells) cells. The inhibition was very obvious in NRK-49F and AtT-20 cells, but it was almost negligible in HL-60 cells. There was no difference in terms of the binding of 12-HETE to NRK-49F and HL-60 cells. Pretreatment of NRK-49F cells with pertussis toxin almost completely ADP-ribosylated Gi proteins, but it did not affect the inhibition of 12-HETE on AC in this cell. This result excludes the involvement of Gi proteins in 12-HETE-mediated inhibition of AC. It was revealed that the characteristics of ACs in these cells were quite different in response to agonists and forskolin, suggesting that these cells do have different isoform of AC. We conclude that 12-HETE inhibits the activity of AC depending upon the isoform.
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PMID:Inhibition of adenylyl cyclases by 12(S)-hydroxyeicosatetraenoic acid. 891 39

Reliable data on familial risks are important for clinical counseling and cancer genetics. We wanted to study incidence trends and familial risks for pituitary adenomas and associated tumors through parental and sibling probands, using the nation-wide Swedish Family-Cancer Database on 10.5 million individuals, containing families with parents and offspring. Cancer data were retrieved from the Swedish Cancer Registry from years 1958 to 2002, including 3239 pituitary tumor patients. Familial risk for offspring was defined through standardized incidence ratio (SIR), adjusted for many variables. The incidence of pituitary adenoma has increased moderately from 1958 to the 1990s and declined thereafter. There were only three offspring-parent pairs with a concordant pituitary tumor, the SIR was not significant. Parental skin cancer (SIR 1.60) and leukemia (1.90, chronic lymphatic leukemia 2.59) were associated with offspring pituitary adenoma diagnosed at any age up to 70 years. There was a strong association of pituitary adenomas with nervous system hemangiopericytomas, SIR 182. The only significant association among siblings was between pituitary tumors and breast cancer (1.46). The risk of pituitary adenoma was marginally increased in individuals whose siblings were diagnosed with colorectal cancer. The results suggest an association of pituitary adenomas with nervous system hemangiopericytomas and breast and colorectal cancers, in addition to some other tumor types. Whether these associations can be explained by the recently identified pituitary adenoma predisposing gene, AIP, remains to be established.
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PMID:Incidence and familial risks in pituitary adenoma and associated tumors. 1739 79

Aneuploidy is frequent in cancers. Recently it was found that pituitary tumor transforming gene (PTTG; also called Pds1p or securin) is overexpressed in many different tumors. Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that primarily infects CD4+ T lymphocytes and causes adult T-cell leukemia. Here, we report that overexpression of human PTTG cooperated with the HTLV-I Tax oncoprotein in cellular transformation. Coexpression of Tax and PTTG enhanced chromosomal instability and neoplastic changes to levels greater than overexpression of either factor singularly. Cells that overexpressed both PTTG and Tax induced tumors more robustly in nude mice than cells that expressed either PTTG alone or Tax alone.
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PMID:Evidence for cooperative transforming activity of the human pituitary tumor transforming gene and human T-cell leukemia virus type 1 Tax. 1750 65

The identification of a subpopulation of brain tumor cells with potent tumorigenic capacity strengthens the cancer stem cell hypothesis of the origin of the tumors that has recently attracted the attention of many researchers. Reports have been published on the identification of tumor cells with stem cells characteristics in different types of tumors (acute myelogenic leukemia, breast cancer, prostate cancer, bone sarcomas, liver cancer, and melanomas). We and other groups have previously reported the isolation of cancer stem cells from adult glioblastoma multiforme. These cells express stem cell markers, and when differentiated they express glial and neuronal markers. In vivo they give a tumor that recapitulates the characteristics of the tumor in the patient. More recently we have isolated tumor stem-like cells also from benign tumors like pituitary adenomas. Cells derived from pituitary adenomas are able to grow as floating aggregates resembling the neurospheres (typical of normal stem cells) in a medium supplemented by growth factors (EGF and bFGF). The immunocytochemical analysis revealed that pituitary tumor stem-like cells are positives for nestin and, when grown for ten days in differentiation medium they express GFAP, BIII tubulin, and S-100. In vitro tumor stem-like cells derived from a patient with a somatotroph adenoma showed high production of growth hormone and prolactin, while cells derived from the same patient but grown in presence of fetal bovine serum showed no production of hormones.
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PMID:Pituitary adenoma stem cells. 1958 28

15-hydroxyprostaglandin dehydrogenase (15-PGDH) may function as a tumor suppressor that antagonizes the action of the cyclooxygenase-2 (COX-2) oncogene in several types of tumors. However, it is unknown if it has a role in the pituitary. Recently, our group found that 15-PGDH expression was low in prolactin (PRL) secreting adenomas (prolactinomas) and growth hormone (GH) secreting adenomas (GHomas) using fiber-optic BeadArray technology. In this study, we examined the relative expression of 15-PGDH and COX-2 mRNA in clinical specimens and examined the effects of 15-PGDH on GH3 rat pituitary tumor cell proliferation, apoptosis and hormone secretion. 15-PGDH expression was lower and COX-2 expression was higher in prolactinomas and GHomas compared with normal controls. Overexpressed 15-PGDH inhibited tumor cell proliferation and induced apoptosis. It had a significant suppressive effect on mRNA levels and on the secretion of PRL and GH in GH3 cells. The inhibition of cell proliferation was accompanied by the decreased expression of cox-2, matrix metalloproteinase-9 (MMP-9) and B cell leukemia/lymphoma-2 (Bcl-2). These data are suggestive of a previously unrecognized pathway in pituitary tumorigenesis, and this novel observation may shed light on therapeutic strategies for pituitary tumors.
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PMID:Loss of 15-hydroxyprostaglandin dehydrogenase indicates a tumor suppressor role in pituitary adenomas. 2258 Sep 84

The aberrant expression of proto-oncogenes is involved in processes that are responsible for cellular proliferation and the inhibition of myeloid differentiation in acute myeloid leukemia (AML). Pituitary Tumor-Transforming gene 1 (PTTG1), an oncogenic transcription factor, is abundantly expressed in various human cancers and hematopoietic malignancies. However, its expression in normal leukocytes and most normal tissues is very low or undetectable. The mechanism by which PTTG1 overexpression modifies myeloid cell development and promotes leukemogenesis remain unclear. To investigate the mechanistic links between PTTG1 overexpression and leukemia cell differentiation, we utilized phorbol 12-myristate 13-acetate (PMA), a well-known agent that triggers monocyte/macrophage differentiation, to analyze the expression patterns of PTTG1 in PMA-induced myeloid differentiation. We found that PTTG1 is down-regulated at the transcriptional level in PMA-treated HL-60 and THP1 cells. In addition, we identified a binding site for a tumor suppressor protein, Kruppel-like factor 6 (KLF6), in the PTTG1 promoter. We found that KLF6 could directly bind and repress PTTG1 expression. In HL-60 and THP1 cells, KLF6 mRNA and protein levels are up-regulated with a concordant reduction of PTTG1 expression upon treatment with PMA. Furthermore, KLF6 knockdown by shRNA abolished the suppression of PTTG1 and reduced the activation of the differentiation marker CD11b in PMA-primed cells. The protein kinase C (PKC) inhibitor and the MAPK/ERK kinase (MEK) inhibitor significantly blocked the potentiation of PMA-mediated KLF6 induction and the down-regulation of PTTG1, indicating that PTTG1 is suppressed via the activation of PKC/ERK/KLF6 pathway. Our findings suggest that drugs that increase the KLF6 inhibition of PTTG1 may have a therapeutic application in AML treatment strategies.
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PMID:Down-regulation of the oncogene PTTG1 via the KLF6 tumor suppressor during induction of myeloid differentiation. 2397 8


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