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)

Carcinoembryonic antigen (CEA), a oncofetal glicoprotein, has been regarded as specific marker for colorectal cancer initially and restricted to the significance of tumor-associated antigen afterwards. Circulating CEA levels were determined in 47 patients with hematologic malignancies, resulting elevated in 10 (21%). The highest values had been discovered in a chronic lymphocitic leukemia complicated by primary hepatoma, causing the problem of the role played by the second tumor, likewise to another CEA-positive patient with the association "Hodgkin's disease-pancreatic carcinoma". The CEA employment had not been particularly satisfactory in the therapeutic monitoring and in the early detection of the relapses, in opposition to the results referred in the colorectal, mammary and bronchogenic carcinoma.
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PMID:[Evaluation of carcinoembryonic antigen (CEA) in patients with neoplasms and hematologic diseases]. 734 Jul 29

Thirty patients with histologically proven malignant disease were selected for reticuloendothelial scans and bone scans because of suspected bone or bone marrow involvement. Reticuloendothelial scans were abnormal in 83% of the patients and bone scans were abnormal in 47%. Focal defects on the reticuloendothelial marrow scan correlated better with tumor infiltration of the marrow than did diffusely abnormal scans. Focal defects were found in nine patients (30% of total), four of whom had negative or equivocal bone scans. In multiple myeloma, reticuloendothelial marrow scans were more sensitive than bone scans, but were not clearly better than bone scans in patients with solid tumors. In the interpretation of reticuloendothelial scans, consideration must be given to the effects of radiation, chemotherapy, and uremia, all of which may cause decreased reticuloendothelial uptake and falsely positive reticuloendothelial scans. Reticuloendothelial scans seem most useful for hematologic malignancies that have not been previously treated. The advantages and disadvantages of reticuloendothelial scans are discussed.
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PMID:Comparison of reticuloendothelial scans with bone scans in malignant disease. 746 Apr 51

We studied samples containing deletions of the long arm of chromosome 11 (11q) from patients with hematologic malignancies by using cytogenetic and fluorescence in situ hybridization (FISH) techniques. Cytogenetic analysis of 28 patients and of a cell line showed that all deletions included band 11q23. FISH analysis demonstrated that the proximal part of 11q23, including NCAM, was deleted in 13 of 15 patients and the cell line. Recurring chromosomal losses in human tumors have been regarded as evidence that the affected regions contain tumor-suppressor genes. These results suggest that the putative tumor-suppressor gene is proximal to the MLL gene which is also located in 11q23.
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PMID:Analysis of deletions of the long arm of chromosome 11 in hematologic malignancies with fluorescence in situ hybridization. 751 68

Deletions of chromosomal band 9p21 have been detected in various tumor types as well as in more than 20% of acute lymphoblastic leukemia (ALL). These deletions frequently include the entire interferon (IFN) gene cluster as well as the methylthioadenosine phosphorylase (MTAP) gene. Recently, the CDKN2 gene (p16INK4A, MTS I, CDK41) was proposed as a candidate tumor-suppressor gene on 9p21 because it is frequently deleted in cell lines derived from multiple tumor types. To determine if CDKN2 or another closely related gene on 9p is the target of 9p deletions in ALL and other hematologic malignancies, we analyzed 20 primary patient samples (13 ALL, 2 acute myeloid leukemias [AML], and 5 non-Hodgkin's lymphomas [NHL]) with 9p rearrangements using Southern blot analysis, fluorescence in situ hybridization (FISH), and single-strand conformation polymorphism (SSCP) for alterations of CDKN2. Homozygous deletions of the CDKN2/CDKN2B (p15) region were detected in 10 cases (50%; 6 ALL, 2 AML, and 2 NHL). In 1 additional case, the intensity of the Southern blot band was significantly reduced, suggesting a CDKN2 deletion in a subpopulation of the malignant cells. No CDKN2 or CDKN2B rearrangements were seen. The IFN gene cluster was homozygously deleted in 2 of 15 (13%) analyzed cases, whereas the MTAP gene was deleted in 6 of 15 cases (40%). In addition, hemizygous deletions of the CDKN2 region were identified in 6 ALL cases using interphase FISH. No point mutation of the coding region of CDKN2 was detected by SSCP in these cases. We conclude that CDKN2 is the most frequently homozygously deleted marker on 9p. The absence of point mutations in the coding region of CDKN2 in cases with hemizygous 9p deletions and the frequent codeletion of MTAP, CDKN2B, and other yet unidentified neighboring genes suggest that the simultaneous deletion of these genes may be necessary for the selective growth advantage of malignant cells.
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PMID:Refined mapping of genomic rearrangements involving the short arm of chromosome 9 in acute lymphoblastic leukemias and other hematologic malignancies. 754 47

Table 6 is a summary of the organisms discussed with a listing of the environmental source, the endogenous source, the predisposing factors including neoplasms, and the postulated mechanisms by which the organism can gain access to the circulation. The evidence considered indicates that the entrance of one of these microorganisms into the bloodstream of a human being depends on the presence of multiplicity of predisposing factors. In the majority of cases of bacteremia due to one of these unusual organisms, two or more predisposing factors are present. Certain predisposing factors, such as cancer chemotherapy or intravenous catheterization, often provide a barrier break, while others, such as liver disease, may render the host immune system less capable of clearing organisms from the circulation. For organisms such as Campy-lobacter, Listeria, and Salmonella spp., attributes that allow the invasion of a healthy host are present and seem to be enhanced by the simultaneous presence of a predisposing condition, such as liver disease, in the host. Although somewhat fragmentary, a number of individual case reports describe bacteremia due to one of these organisms occurring weeks to years after surgery and after other therapeutic measures had effected a supposed cure of a cancer. It may be speculated that cancer patients, even after a cure, are still susceptible to bloodstream invasion by one of the aforementioned organisms by virtue of the presence of one or more predisposing metabolic, physiologic, or immunologic factors, even though these factors may be cryptic. The predominance of hematologic malignancies among cases of bacteremia due to these unusual organisms is also apparent. Although, as pointed out by Keusch (169), the reduction in the performance of immune function in hematologic malignancies compared with solid tumors is likely to be responsible, other associations of certain organisms with specific neoplasms warrant further examination. The frequency of bloodstream infections of Salmonella typhimurium and Capno-cytophaga canimorsus in Hodgkin's disease patients seems likely due to a particular mechanism which infection by these species is favored. The specific nature of these mechanisms remains to be determined. The recovery of any unusual bacterium from blood should warrant a careful consideration of the possibility of underlying disease, especially cancer. Microbiologists should advise clinicians of the unusual nature of the identified organism and provide the counsel that certain neoplastic processes, often accompanied by neutropenia, render the human host susceptible to invasion by almost any bacterium. The recovery of such organisms as C. septicum or S. bovis should prompt the clinician to aggressively seek to identify an occult neoplasm if one has not yet been diagnosed.
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PMID:Recovery of uncommon bacteria from blood: association with neoplastic disease. 755 69

This paper describes a case of squamous cell carcinoma (SCC) of the ureter which showed marked leukocytosis without any evidence of infection and hematologic malignancies. The level of serum granulocyte colony-stimulating factor (G-CSF) assayed by enzyme immunoassay increased and the immunohistochemical staining of the ureter tumor showed the presence of G-CSF in tumor cells. These findings indicate that SCC of the ureter produced G-CSF which stimulated leukocyte production in bone marrow and resulted in leukocytosis. To our knowledge, this is the first report of ureter tumor with leukocytosis producing G-CSF.
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PMID:Squamous cell carcinoma of the ureter with marked leukocytosis producing granulocyte colony-stimulating factor. 757 Nov 81

The diagnosis of primitive hematologic malignancies in extramedullary sites (lymphoblastic lymphoma of T- or B-cell type and myeloid sarcoma) on paraffin-embedded tissue sections is difficult and often impossible because of the primitive morphology of the neoplastic cells. The authors studied 21 extramedullary tumors of lymphoid or myeloid blasts. They used a panel of 22 antibodies on frozen sections and 9 antibodies on paraffin sections to determine the spectrum of immunophenotypes and to develop a practical panel for diagnosis. All but two of the cases could be classified as lymphoid or myeloid using immunohistologic analysis. Thirteen cases were classified as lymphoblastic lymphoma/acute lymphoblastic leukemia (LBL/ALL); 10 were classified as precursor T (CD7+, CD3+/-, CD45+) and 3 as precursor B-cell (CD19+/-CD10+CD45-) type. Five cases were classified as myeloid sarcoma (CD13+ myeloperoxidase+, lysozyme+). Two LBL/ALL coexpressed either CD33 (1 case) or CD15 (1 case), and one myeloid sarcoma coexpressed TdT and CD7. One case appeared to be truly mixed lineage, coexpressing CD3 with myeloperoxidase and lysozyme, and two cases expressed no lineage-specific antigens. There were clinical differences between the three major tumor types, and within the category of T-precursor LBL/ALL, classification according to stage of thymocyte differentiation was associated with distinctive clinical features. In conclusion, the spectrum of immunophenotypes detected on frozen section was similar to that reported by flow cytometry on peripheral blood and bone marrow specimens. The most useful antigens on frozen sections were CD7 and CD3 (T cell), CD10 and CD19 (B cell), and CD13 (myeloid). TdT was coexpressed by one myeloid sarcoma and was undetectable in 40% of LBL/ALL. On paraffin sections, myeloperoxidase and lysozyme were reliable markers of myeloid lineage, but none of the markers used on paraffin sections distinguished between LBL/ALL of T- and B-precursor types. Both B-LBL/ALL and myeloid sarcomas were often CD45- on paraffin sections, which may be a obstacle in determining the diagnosis. These distinctions appear to have clinical relevance.
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PMID:Extramedullary tumors of lymphoid or myeloid blasts. The role of immunohistology in diagnosis and classification. 757 94

Abnormalities of the short arm of chromosome 12 are relatively common in hematologic malignancies and deletions of the region. 12p12-13 are found in approximately 5% of the patients with acute lymphoblastic leukemia (ALL). As a potent inhibitor of cyclin-dependent kinases, p27KIP1 prevents the progression of the cell cycle and the gene encoding p27KIP1 represents a potential tumor-suppressor gene. Its recent assignment to the chromosomal region (12p12.3) prompted us to study the p27KIP1 gene in a series of 61 children with ALL. Microsatellite polymorphic markers flanking the p27KIP1 gene were analyzed to detect losses of heterozygosity (LOH). Eleven patients displayed LOH for at least one of the markers. The deleted are encompassed the p27KIP1 gene locus in 10 cases, but inactivation of the remaining allele by deletion, translocation, or mutation was never observed. In addition, in 1 patient, the p27KIP1 gene was situated outside of the region of LOH. Thus, p27KIP1 does not seem to be the target gene of 12p12-13 alterations. However, this study indicates that 12p12-13 alterations at the molecular level, which are present in about 27% of the children with B-lineage ALL, are much more common than had previously been reported by usual chromosome analysis. Moreover, LOH mapping allowed us to better define the location of a putative tumor-suppressor gene implicated in these malignancies and should therefore help in identifying this gene.
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PMID:Loss of heterozygosity in the chromosomal region 12p12-13 is very common in childhood acute lymphoblastic leukemia and permits the precise localization of a tumor-suppressor gene distinct from p27KIP1. 757 55

Although combination chemotherapy has had a significant impact on survival for malignancies such as Hodgkin's disease, testicular cancer, and childhood acute leukemias, the majority of cancers are either initially resistant to chemotherapy (renal, colon, etc.) or are initially chemosensitive but acquire resistance during treatment, such as lymphoma and breast cancer. Resistance to chemotherapy remains an obstacle to the successful treatment of human cancer and has been the subject of numerous investigations aimed at identifying the molecular mechanisms of resistance in cancer cells. An improved understanding of the mechanisms by which tumor cells develop resistance to chemotherapy may not only enhance the activity of cytotoxic therapy in advanced malignancies but may ultimately improve the impact of adjuvant therapy, potentially resulting in prolonging disease-free intervals and survival. In this review, therefore, we discuss our current understanding of the MDR1 gene, encoding P-glycoprotein, which is responsible for one mechanism of multidrug resistance (MDR). We also review the evidence supporting the clinical relevance of the MDR1 gene and clinical trials aimed at reversing MDR-mediated resistance. Although MDR-mediated drug resistance has been well characterized in preclinical models, its role in clinical drug resistance is not as well characterized and requires further investigation. Prospective studies are necessary to establish the role of MDR1 gene expression in the clinical resistance. The ability to identify tumors with increased MDR1 gene expression has several potential applications (for example, the prediction of response to chemotherapy and the design of studies aimed at reversal of resistance with agents that inhibit MDR-mediated drug efflux). The initial goal of such trials is to demonstrate the ability to reverse MDR1-mediated drug resistance in the appropriate advanced refractory malignancies. Ultimately, it will be important to incorporate these reversal strategies in the treatment of early-stage disease, at which time the tumor burden is smaller and fewer mechanisms of resistance may be present. Prospective phase I, II, and III clinical trials using reversing agents in conjunction with chemotherapy in malignancies that express the MDR1 gene, such as the hematologic malignancies and breast cancer, are necessary before routine use of agents such as verapamil, quinidine, and cyclosporine, which carry innate toxicities. MDR is a mechanism of drug resistance that provides the potential for an alteration in drug efflux, which may have a significant impact on response and possibly result in improved survival for some cancer patients.
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PMID:Clinical reversal of drug resistance. 760 Aug 45

Comparative genomic hybridization (CGH) represents a new technique for global analysis of a whole genome for net loss or gain of chromosome regions. It offers several advantages over alternative techniques. It permits analysis of a whole genome in a single hybridization reaction, it does not require the generation of metaphases from tumor cells, and it only requires very small numbers of tumor cells. Most previous studies have concentrated on the application of CGH to the analysis of chromosome defects associated with solid tumors. In this paper we report the use of CGH to study bone marrow samples from a patient with acute myeloid leukemia and complex karyotypic abnormalities. The results obtained using CGH were compared with G-banding analysis. Both G-banding and CGH detected a 5q deletion, a 7q deletion, additional material derived from 8q, and an HSR on 11q. However, several apparently discrepant results were also obtained. Paints for chromosomes 3, 5, 7, 8, 11, 12, 14, 17, 22, and X were therefore used to resolve these differences. Our results demonstrate that CGH detected chromosome abnormalities associated with acute myeloid leukemia and that CGH provided information that was not obtained by G-banding analysis alone. These data suggest that CGH may prove a useful adjunct to conventional cytogenetic and molecular analysis of hematologic malignancies.
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PMID:Comparative genomic hybridization in acute myeloid leukemia. A comparison with G-banding and chromosome painting. 762 45


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