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)

The hazards and complications of BCG immunotherapy, as well as the potential for enhanced tumor growth, make it imperative that the clinician know the clinical setting in which BCG can offer therapeutic benefit. This would include the intratumor injection of localized intradermal tumor deposits of melanoma and breast cancer, chemoimmunotherapy with BCG to prolong remission in acute myelogenous leukemia, and possibly the use of BCG as an adjuvant to control minimal residual disease. Aside from these situations, it is advisable to treat patients only on clearly defined experimental protocols.
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PMID:Hazards and complications of BCG immunotherapy. 127 90

Native resistance to conventional chemotherapy remains an important cause of treatment failure in the adult acute leukemias. Delineation of cellular mechanisms of drug resistance therefore represents a prerequisite to the development of more effective treatment strategies. The multidrug resistance (MDR) phenotype represents one such mechanism of resistance with direct clinical relevance. This phenotype occurs normally in certain mammalian tissues, and is detectable in tumor cell lines selected for resistance to naturally occurring antineoplastics. The mdr1 gene or its glycoprotein product, P-glycoprotein, is detected with high frequency in secondary acute myeloid leukemia (AML) and poor-risk subsets of acute lymphoblastic leukemia. In prospective studies in AML, MDR overexpression is an independent determinant of response to treatment and overall survival with conventional-dose induction regimens. Investigations of mdr1 regulation in normal hematopoietic elements has shown a pattern which corresponds to its regulation in acute leukemia, explaining the linkage of mdr1 to specific cellular phenotypes. Therapeutic trials are now in progress to test the ability of various MDR-reversal agents to restore chemotherapy sensitivity in high-risk acute leukemias.
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PMID:Multidrug resistance in acute leukemia: a conserved physiologic function. 128 51

A rare case of spinal epidural granulocytic sarcoma (GS) preceding acute myelogenous leukemia is described. A 10-year-old boy presented with lower leg weakness. The initial diagnosis was a histiocytic lymphoma, and he was treated accordingly. No evidence of bone marrow involvement was found at that time. The correct diagnosis of epidural GS was made possible in retrospect by using immunoperoxidase staining for lysozyme fourteen months later when the patient showed the full-blown features of leukemia. This rare tumor should be considered in the differential diagnosis of an epidural mass with cord compression in patients with or even without acute leukemia, because early diagnosis followed by appropriate combined chemotherapy and radiation may obviate surgical intervention and eventually prevent leukemic transformation.
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PMID:Spinal epidural granulocytic sarcoma preceding acute myelogenous leukemia. 128 31

Only in these latest years has been possible to consider Hodgkin disease (HD) as a neoplastic syndrome, thank of immunohistochemistry and cytogenetic techniques which have confirmed the monoclonal origin of typical cellular marker of disease: the Reed-Sternberg cell (R-S cell). Interesting associations have been observed between children suffering from HD and the positivity of EBV antigen above all in the socio-economically developed countries. The histopathologic classification of HD is divided in four sub-types, with different incidence in the pediatric age: the nodular sclerosis and the mixed cellularity are more rap-presented than the lymphocyte predominance and mostly the lymphocyte depletion. Histopathologic classification is essential for the prognosis and a correct therapeutic approach to disease. The management of HD is based on chemotherapy and radiotherapy associated; the results of treatment are more and more encouraging with a global survival over 95%. Sequelae of treatment are reduced in modern therapeutic trials: in particularly injury to somatic growth, cardiopulmonary system, gonadal and thyroid functionality is reduced by using low dose and involved fields for the early stage patients. The most important sequela in children treated for HD is the risk to developed a second malignant neoplasm; in particularly acute nonlymphocytic leukemia and non Hodgkin's lymphoma. In patients treated with radiotherapy alone increase the risk to develop solid tumors like sarcomas and carcinomas, which can appears several years after diagnosis.
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PMID:[Hodgkin's disease in childhood]. 130 82

To study the regulation of expression of the myc protooncogene, cells from normal individuals and patients with acute myelogenous leukemia (AML), and chronic phase and blastic crisis of chronic myeloid leukemia (CML) cells were put in overnight culture in the presence or absence of fetal calf serum. Myc expression in normal marrow cells and chronic phase CML cells fell after culture in vitro. In contrast, myc expression was maintained or increased in a majority of the AML and blastic crisis CML specimens. These data demonstrate that the regulation of myc expression is disordered in many AML and blastic crisis specimens but not in chronic phase CML cells.
Med Oncol Tumor Pharmacother 1992
PMID:Abnormal regulation of the myc gene in myeloid leukemia. 134 25

We have measured the serum levels of soluble CD4, CD8 and IL-2R in 43 patients with AML in complete remission (AML-CR). The sCD8 levels of AML-CR patients (443.9 +/- 224.4 u/ml) were significantly high as compared to that of the normal controls (177.1 +/- 76.3 u/ml), p < 0.01. The sIL-2R levels of AML-CR patients were 715.0 +/- 646.3 u/ml, which significantly differed when compared to 322.1 +/- 65.7 u/ml for the normal controls, p < 0.01. However, the sCD4 levels of AML-CR patients were 9.6 +/- 4.7 u/ml, which did not differ from the 8.3 +/- 2.6 u/ml of the normal controls. The AML-CR patients showed significantly increased sCD8 and sIL-2R levels at all ranges during the remission from one to 188 months. The sCD8 levels and sIL-2R levels of the AML-CR patients showed a close correlation, p < 0.01. Further, the sCD8 levels and lymphokine activated killer cell cytotoxic activity showed a close correlation, p < 0.05. The presence of the activation of anti-tumor immunity may be related to the continuance of the remission in the AML-CR patients.
Med Oncol Tumor Pharmacother 1992
PMID:Serum soluble CD4, CD8 and IL-2R levels in adult acute myeloid leukemia in remission. 134 17

A 72 hours fluorometric microculture cytotoxicity assay (FMCA) was used for the study of chemotherapeutic drug resistance in tumor cell suspensions from patients with acute myelocytic leukemia (AML). A marked heterogeneity with respect to sensitivity was observed for a panel of cytotoxic drugs tested in 76 samples from 60 patients with treated or untreated AML. Primary resistance to vincristine (Vcr) and prednisolone in untreated AML was observed as well as 'acquired' resistance to several other antileukemic drugs. Cross resistance patterns for AML active drugs revealed significant positive relationships between anthracyclines, VP16 and amsacrine (Amsa), whereas mitoxantrone (Mitox) was more weakly correlated. Sensitivity to cytosine arabinoside was unrelated to the anthracyclines, VP16, Amsa and Mitox but showed a significant relationship to 6-thioguanine. Several resistance modifying agents, including the novel non-immunosuppressive cyclosporin A analogue PSC 833, were able to potentiate the effects of doxorubicin and Vcr at concentrations achievable in the clinic. However, the pattern of activity was heterogenous and the frequency of responsive samples was higher in relapse compared to de novo cases. Individual in vitro/in vivo correlations based on quartile distributions of all accumulated drug sensitivity data from AML patients indicated a high specificity with respect to the identification of drug resistance. The results suggest that the FMCA may provide clinically valuable information on chemotherapeutic drug resistance in AML.
Med Oncol Tumor Pharmacother 1992
PMID:In vitro analysis of drug resistance in tumor cells from patients with acute myelocytic leukemia. 134 18

Tumor necrosis factor-alpha (TNF-alpha) production by unstimulated and lipopolysaccharide (LPS)-stimulated peripheral monocytes has been studied in 17 acute myeloid leukemia (AML) patients, 54 AML patients in complete remission (AML-CR), 9 acute lymphoblastic leukemia (ALL) patients and 13 ALL patients in complete remission (ALL-CR). TNF-alpha production by the unstimulated monocytes in ALL patients (n = 6, mean: 6.6 +/- 4.9 u/ml) was higher than that of normal controls (n = 13, 0.9 +/- 0.7 u/ml), AML patients (n = 14, 2.0 +/- 2.1 u/ml) and AML-CR patients (n = 21, 1.4 +/- 1.2 u/ml). TNF-alpha production by the LPS-stimulated monocytes of the AML-CR patients (n = 54, 12.4 +/- 13.4 u/ml) was significantly higher than that of the normal controls (n = 21, 3.5 +/- 2.5 u/ml) and the AML patients (n = 17, 2.6 +/- 2.4 u/ml), p < 0.01, but there were not any significant differences among the AML-CR patients and the ALL patients or the ALL-CR patients. We separated the AML-CR patients into 3 groups, depending on the length of their remission, and found that AML-CR patients with longer than 6 months (M) but less than 60 M (n = 21, 15.7 +/- 16.9 u/ml) and the patients with a remission longer than 60 M (n = 11, 18.2 +/- 15.9 u/ml) had significantly higher TNF-alpha production than that of the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Med Oncol Tumor Pharmacother 1992
PMID:The monocyte tumor necrosis factor-alpha production in patients with acute leukemia in complete remission. 134 64

A microemulsion of lipid composition resembling low-density lipoprotein (LDL), but devoid of apolipoproteins and labeled with [14C]-cholesteryl oleate was injected into 16 healthy subjects and into 15 patients with acute myeloid leukemia (AML). Removal from plasma of the lipid label was higher in the leukemic group compared to healthy subjects in terms of fractional clearance rate (0.185 +/- 0.205 and 0.080 +/- 0.030 h-1, respectively, P < 0.03). When the emulsion was again injected into 10 of the AML patients after complete hematological remission, the fractional clearance rate of cholesteryl ester was reduced to one third of the value observed prior to treatment (0.061 +/- 0.038 h-1) and was not different from that obtained for the healthy subjects. Also, in untreated AML patients, serum LDL-cholesterol levels inversely correlated with the values of fractional clearance rate of the microemulsion. This correlation was no longer observed after treatment. These data suggest that the LDL-like microemulsion was selectively taken up by the neoplastic cells presumably by interaction with LDL receptors. Therefore, microemulsions may function as potential carriers for anticancer drugs that are targeted to tumor cells for patients with acute myeloid leukemia. Unlike native LDL, microemulsions are suitable for utilization in routine clinical practice.
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PMID:Increased plasma removal of microemulsions resembling the lipid phase of low-density lipoproteins (LDL) in patients with acute myeloid leukemia: a possible new strategy for the treatment of the disease. 134 20

We have examined a population of patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) for loss of heterozygosity of polymorphic markers on chromosomes 5 and 7. The rationale for this study was the observation that the majority of patients with therapy-related leukemia (t-AML or t-MDS), resulting from cytotoxic treatment for prior malignancies, have loss of chromosome 5 and/or 7 or deletions involving the long arms of one or both of these chromosomes. This cytogenetic finding suggested that tumor-suppressor genes, important in the development of AML, may be located in these chromosomal regions. We analyzed a total of 60 patients, 43 with primary MDS/AML de novo and 17 with t-MDS/t-AML. Leukemia cells were evaluated for restriction fragment length polymorphisms (RFLPs). Leukemia cell genotypes were compared with lymphoblastoid cell genotypes from the same patients. Two cases of loss of heterozygosity were identified from chromosomes lacking visible deletions: one involving chromosome 5 in a patient with AML de novo who had a visible deletion of 5q at a later stage of the disease, and one involving chromosome 7 in a patient with t-AML. We conclude that allele loss from loci on chromosomes 5 and 7 in MDS/AML, when it occurs, usually results from major deletion or simple chromosome loss, rather than from mitotic recombination or chromosome loss with duplication of the remaining homologue.
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PMID:Chromosomal loss and deletion are the most common mechanisms for loss of heterozygosity from chromosomes 5 and 7 in malignant myeloid disorders. 134 9


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