Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q8NB91 (FAB)
 3,573 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated plasma levels of plasminogen activator inhibitor 2 (PAI-2) in 40 patients with hematological malignancies including acute leukemia, chronic leukemia, hemophagocytic histiocytosis (HH) and histiocytic sarcoma (HS). The plasma PAI-2 levels in the patients with mononuclear phagocyte system (MPS) proliferative disorders (M4, M5, and CMMoL on FAB classification, HH and HS) were all above the cut-off value in healthy subjects. In a patient of reactive HH, there was a close correlation between Plasma PAI-2 and serum ferritin levels during the clinical course. These results indicate that the increase of plasma PAI-2 would be a diagnostic indicator of MPS proliferative disorders.
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PMID:[Plasma concentrations of plasminogen activator inhibitor 2 in patients with hematological malignancies and their clinical significance]. 202 44

A 20-year-old male developed both coccygeal and leg pain and followed by rectocystic disturbance. Disc herniation between L5 and S was suspected and laminectomy was performed. At surgery, an easily curretable tumor occupied the epidural space from L5 to the end of the sacrum. In part, the tumor spread out of the vertebral canal and invaded the surrounding muscle tissue. This muscle tissue and part of the lamina were checked histologically. Initial blood analysis revealed 5% blast-like cells, but failed to confirm them as leukemic cells. Histologically, the tumor cells had round or oval nuclei with large nucleoli and scanty cytoplasm without granulocytic differentiation. Malignant lymphoma or Ewing's sarcoma was initially suspected, but the definite diagnosis was uncertain. Immunohistochemical staining with the PAP method and enzyme histochemistry revealed that the tumor cells were positive for lysozyme and naphthol ASD chloracetate esterase. Thus, granulocytic sarcoma was finally diagnosed. Electron microscopic findings supported this diagnosis. Subsequent karyotyping of bone marrow cells revealed 8; 21 translocation, thus the final diagnosis of this patient was myelodysplastic syndrome, refractory anemia with excess blast cells in transformation or acute myelogenous leukemia, M2, by the FAB classification.
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PMID:A case of epidural granulocytic sarcoma preceding acute leukemia. 209 94

A 36-year-old woman presented with obstructive jaundice, found at laparotomy to be due to a granulocytic sarcoma in the head of the pancreas. Six months later she developed lymphadenopathy in the left supraclavicular fossa. In spite of chemotherapy containing cytarabine and vincristine, she developed acute myeloid leukaemia (French-American-British [FAB] type M4) 16 months after the onset of her illness.
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PMID:Obstructive jaundice. An unusual presentation of granulocytic sarcoma. 243 27

Mitochondria specific dye, rhodamine-123 (Rh-123), has been labeled with radioactive iodine and tissue distribution of the radiolabeled product has been studied in mice. Transplantable KHT sarcoma and a spontaneous adenomammary carcinoma served as tumor models. The FAB mass spectra of iodinated Rh-123 indicated that mono and di-iodo products were formed which, as shown by other in vitro tests, were positively charged, and were heavily taken up by the mitochondria of living cells in culture. In animals, it was observed that, initially the radioactivity was taken up by all major organs from which it cleared rapidly including that from the KHT sarcoma; but not from the spontaneous adenomammary carcinoma. As a result, the spontaneous tumors retained much higher radioactivity than the equal weight of blood (x4.3) or muscle (x9.5), and were unequivocally detectable by external scintigraphy. The mitochondria selectivity and the specificity of the radioiodinated Rh-123 for the tumors of epithelial origin are exciting and warrant further studies of its use in diagnosis and therapy.
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PMID:Radioiodinated rhodamine-123: preparation and preliminary evaluation as an agent for tumor scintigraphy. 325 74

Burkitt's lymphoma was first reported by Burkitt in 1958 as a sarcoma involving the jaw in African children with characteristic symptoms. Forty three Japanese cases have been reported since the first description by Oboshi et al. in 1969. We report a case of Burkitt's lymphoma with left total ophthalmoplegia. A 73-year-old Japanese female was admitted in Sadamoto Hospital on July 11, 1983 with a two-week history of headache, ptosis and double vision. The patient was exposed to the atomic bomb in Hiroshima and had ten-year history of hypertension. On admission, physical examination showed hypertension and neurological examination revealed only left total ophthalmoplegia (such as left ptosis, external ophthalmoplegia, mydriasis and deficit of light reflex). Plain X-ray film and enhanced CT scan showed no remarkable abnormalities. Laboratory examinations revealed high serum levels of GOT(51 K.U.) and LDH (1300 U.). Left carotid and right retrograde branchial angiograms showed no remarkable abnormal findings. While the patient was treated only conservatively, left abducent and trochleal nerve palsy appeared on August 5, 1983. On plain and enhanced CT scans at the time, abnormal density mass with bone destruction of the left sphenoidal sinus was demonstrated. Biopsy specimen from the left sphenoidal sinus showed lymphosarcomatous cells. Peripheral blood and bone marrow smears showed lymphoma cells which are compatible with L3-Burkitt's type according to FAB leukemia classification. The patient was diagnosed as leukemic transformation of Burkitt's lymphoma and treated with CHOP; Cyclophosphamide (C), Hydroxydaunorubicin(H), Vincristine (O), and Prednisolone (P).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Burkitt's lymphoma with total ophthalmoplegia]. 408 40

A 3-year-old boy presented with a marked right exophthalmos of a few days duration. This was due to a retrobulbar granulocytic sarcoma that was subtotally removed at a lateral orbitotomy. Subsequent studies revealed acute myelogenous leukemia (AML) of FAB-type M2. The orbital tumor disappeared totally after local irradiation and cytostatic treatment. Another granulocytic sarcoma developed 3 months later in the left orbit. It disappeared also during repeated cytostatic induction therapy although only transient hematologic remission was achieved. After 1 month a recurrence of the tumor in the left orbit was noted. The disease progressed without response to treatment and the patient died 11 months after diagnosis.
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PMID:Orbital granulocytic sarcoma as a presenting sign in acute myelogenous leukemia. 659 57

We describe a 68-year-old patient who developed granulocytic sarcoma of the prostate 9 years after complete remission following successful treatment of acute myelogenous leukemia (FAB, M2). PCR analysis of bone marrow samples in first remission and at the time of relapse detected an AML1/ETO rearrangement typical for AMLs with t (8;21). The CD56 antigen was not expressed on the leukemic cells. Systemic chemotherapy led to a short-lasting regression of the tumor, but the patient subsequently developed overt bone marrow relapse and died during chemotherapy. While granulocytic sarcoma as a primary manifestation of AML is well known, as the first manifestation of relapse it appears to be very uncommon.
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PMID:Granulocytic sarcoma of the prostate as the first manifestation of a late relapse of acute myelogenous leukemia. 814 23

Granulocytic sarcomas are localized deposits of myeloid leukemia cells that may precede or occur concurrently with disseminated disease. In either event, the origins of the cells comprising the malignancy are the same. Published reports of granulocytic sarcomas have described, in the majority of cases, a morphology typical of AML-M2 and the presence of the t(8;21)(q22;q21) typical of that FAB type. In a smaller number of cases, the inv(16)(p13q22) characteristic of AML-M4 has been recorded in cells with a myelomonocytic appearance. We report two patients with granulocytic sarcomas showing monocytic morphology in which the malignant cells showed t(9;11)(p22;q23) typical of AML-M5. This abnormality is seen in up to 7% of childhood AML, but has not previously been reported in granulocytic sarcoma. The detection of this cytogenetic abnormality facilitated the precise characterization of the malignant cells and selection of the most appropriate therapy, emphasizing the value of cytogenetic analysis in cases of granulocytic sarcoma.
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PMID:Granulocytic sarcoma with translocation (9;11)(p22;q23): two cases. 921 17

We describe an extremely rare case of granulocytic sarcoma of the porta hepatis causing obstructive jaundice. The patient was an 84-year-old man admitted because of obstructive jaundice. Ultrasonography (US) and computed tomography (CT) scanning of the abdomen disclosed a mass about 2.5 cm in diameter near the neck of the gallbladder, and thickening of the gallbladder wall. Based on these findings, gallbladder carcinoma was suspected. After endoscopic retrograde biliary drainage (ERBD) was performed, the jaundice resolved. However, blast cells were detected in the peripheral blood 51 days after admission, and laboratory studies disclosed acute myelocytic leukemia (AML: French-American-British [FAB] type M0). We treated him conservatively, with antibiotics and ERBD but he died of disseminated intravascular coagulation. Autopsy showed that the suspected gallbladder carcinoma was actually a granulocytic sarcoma arising in association with AML and causing obstructive jaundice. The largest tumor involved the porta hepatis. It should be kept in mind that granuloctyic sarcoma is a possible cause of obstructive jaundice, even in patients with no evidence of AML.
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PMID:An autopsy case of granulocytic sarcoma of the porta hepatis causing obstructive jaundice. 965 26

HOX genes have shown a lineage-specific expression in hematopoiesis and are suggested as being involved in the expression of certain adhesion molecules. Recently, we have demonstrated that HOXC4 and HOXC6, but not HOXC5, are expressed during lymphoid differentiation. Reports on the expression of these genes in myeloid leukemias and normal myeloid cells are still scarce. Therefore, we have investigated the expression of HOXC4, HOXC5 and HOXC6 in purified subpopulations of bone marrow in addition to 36 specimens of acute myeloid leukemias (AMLs), eight chronic myeloid leukemias (CMLs), several myeloid cell lines and cutaneous localizations of three myelomonocytic leukemias and one granulocytic sarcoma by RT-PCR and partly by RNA in situ hybridization (RISH). HOXC4 and HOXC6 transcripts were both detected by RT-PCR in 22/36 and 24/36 AMLs, respectively. The distribution of HOXC4 and HOXC6 gene expression over the different types of AML was largely similar and covered all types of AML. In contrast, HOXC5 gene expression was found in only 6/32 AMLs. Expression of HOXC5 was restricted to AMLs of the granulocytic (FAB M1-M3), early monocytic (FAB M4) and early erythroid (FAB M6) lineage. In general, except in one FAB M5b case, no expression of HOXC5 was found in AMLs derived from late stages of monocytic (FAB M5) and megakaryocytic (FAB M7) lineages. As for HOXC4 and HOXC6, expression of HOXC5 was absent in CMLs. Using RISH significant HOXC4, HOXC5 and HOXC6 expression was found in a number of additionally studied AML samples of different FAB classification (M2, M4, M5b and M5b), (M2 and M5b) (M2, M4, M5b), respectively. In tissue localizations of leukemias a different expression pattern of HOXC4, HOXC5 and HOXC6 was found. In contrast to mature leukemic stages of myeloid differentiation, these skin localizations of leukemias expressed HOXC5 and HOXC6. HOXC4 expression was found both in leukemic cells derived from peripheral blood and from cutaneous localizations. Besides HOXC4 expression in monocytes no expression of HOXC4, HOXC5 and HOXC6 was found in granulocytes and monocytes, colonies of growth factor-induced CD34+ bone marrow cells. In earliest CD34+/CD38low and high cell fractions of bone marrow only HOXC4 and in megakaryocytic cells both HOXC4 and HOXC6 were found. Thus, the expression patterns of these HOXC genes found in the limited number of cell fractions of normal bone marrow suggest that the expression patterns found in AMLs and CMLs might reflect the normal situation. Furthermore, the presence of HOXC5 and HOXC6 expression specifically in skin infiltrates of late differentiation stages of myeloid leukemias, suggests an additional role for these genes in the positioning of these myeloid cells in skin tissue.
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PMID:Differentiation and cell-type-restricted expression of HOXC4, HOXC5 and HOXC6 in myeloid leukemias and normal myeloid cells. 982 47


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