Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surgical resection is the option for sternal metastasis from breast cancer. But surgical treatment is the subject of controversy for sternal metastasis except from breast cancer. Four cases of secondary malignant tumors of the sternum except from breast cancer were reported. Primary lesions included thyroid cancer, gastric cancer, malignant fibrous histiocytoma of the chest wall and multiple myeloma. In 3 cases, operation were done and they survived 11 months, 13 months and 3 years respectively. In case of secondary malignant tumor of the sternum except from breast cancer, surgical treatment should be considered.
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PMID:[Cases of sternal metastasis except from breast cancer]. 1047 56

In this paper the use of arsenic compounds as anticancer agents in clinical trials and in in vitro investigations is reviewed, including the experience at our institute. Treatment of newly diagnosed and relapsed patients with acute promyelocytic leukemia (APL) with arsenic trioxide (As2O3) has been found to result in complete remission (CR) rates of 85-93% when given by intravenous infusion for 2-3 h at a dose of 10 mg/day diluted in 5% glucose saline solution. Patients exhibit a response in 28-42 days. CR rates after administration of Composite Indigo Naturalis tablets containing arsenic sulfide and of pure tetraarsenic tetrasulfide reached 98% and 84.9%, respectively. At higher concentrations (1-2 microM), arsenic induced apoptosis, while at lower concentrations (0.1-0.5 microM), it triggered cell differentiation in vitro. As2O3-induced apoptosis has been observed in many cancer cell lines, including esophageal carcinoma, gastric cancer, neuroblastoma, lymphoid malignancies, and multiple myeloma. Its effectiveness was confirmed in the treatment of multiple myeloma. Arsenic compounds are effective agents in the treatment of APL and their activity against other types of cancer requires further investigation.
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PMID:Arsenic compounds as anticancer agents. 1158 71

AIM:To clone mouse anti-human gastric cancer mAb(3H11) variable genes and to construct 3H11 human-mouse chimeric antibody.METHODS: The entire VH and VL genes of anti-gastric cancer mAb 3H11 were cloned by RT-PCR method from 3H11 hybridoma cells, using 5' primers for leader sequences. The 3H11 VL gene was then inserted into human-mouse chimeric light chain expression vector and transfected into murine Sp2/0 myeloma cells.RESULTS: DNA sequence analysis indicated that the cloned genes included the whole leader sequences and the mature Ig variable region encoding sequences. After gene transfection, transient expression of chimeric light chain protein was detected.CONCLUSION: DNA sequences and transient expression indicated that the cloned gene was functional. This work laid basis for constructing 3H11 human mouse chimeric antibody in the future.
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PMID:Cloning of 3H11 mAb variable region gene and expression of 3H11 human-mouse chimeric light Chain. 1181 28

Dysregulation of the human transforming acidic coiled coil (TACC) genes is thought to be important in the development of multiple myeloma, breast and gastric cancer. However, even though these proteins have been implicated in the control of cell growth and differentiation, the mechanism by which they function still remains to be clarified. Using the yeast two-hybrid assay, we have now identified the histone acetyltransferase (HAT) hGCN5L2 as a TACC2-binding protein. GST pull-down analysis subsequently confirmed that all human TACC family members can bind in vitro to hGCN5L2. The authenticity of these interactions was validated by coimmunoprecipitation assays within the human embryonic kidney cell line HEK293, which identified the TACC2s isoform as a component consistently bound to several different members of HAT family. This raises the possibility that aberrant expression of one or more TACC proteins may affect gene regulation through their interaction with components of chromatin remodeling complexes, thus contributing to tumorigenesis.
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PMID:The transforming acidic coiled coil proteins interact with nuclear histone acetyltransferases. 1476 76

The interleukin-mediated Janus kinase (JAK)/STAT pathway plays a crucial role in carcinogenesis. Recently, increased STAT3 activity was found in hepatocellular carcinoma and multiple myeloma in which there was silencing of SOCS-1 (suppressor of cytokine signalling-1) by gene promoter hypermethylation. We investigated the expression level of interleukin-6 (IL-6) and SOCS-1 in gastric cancer cell lines. Expression of SOCS-1 correlated with IL-6 level in most of the cell lines, except for AGS cells in which SOCS-1 was absent despite a high level of IL-6 production. Methylation analysis by methylation-specific polymerase chain reaction and bisulphite sequencing revealed that CpG island of SOCS-1 was densely methylated in AGS cells. Demethylation treatment by 5'aza-deoxycytidine restored SOCS-1 expression and also suppressed constitutive STAT3 phosphorylation in AGS cells. Moreover, methylation of SOCS-1 was detected in 27.5% (11 of 40) of primary gastric tumours samples, 10% (one of 10) of adjacent noncancer tissues but not in any (zero of nine) normal gastric mucosa. Methylation of SOCS-1 also correlated with the loss of mRNA expression in some primary gastric cancers. In conclusion, this is the first report to demonstrate that hypermethylation of SOCS-1 led to gene silencing in gastric cancer cell line and primary tumour samples. Downregulation of SOCS-1 cooperates with IL-6 in the activation of JAK/STAT pathway in gastric cancer.
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PMID:Constitutional activation of IL-6-mediated JAK/STAT pathway through hypermethylation of SOCS-1 in human gastric cancer cell line. 1535 12

The objective of this study was to analyse incidence and mortality cancer trends in the Italian Network of Cancer Registries (about 8,000,000 inhabitants) during the period 1986-1997. Included were 525,645 newly diagnosed cancers and 269,902 cancer deaths (subjects > 14 years). Joinpoints (points in time where trend significantly changes from linearity) were found and estimated annual percentage changes (EAPC) used to summarize tendencies. Overall cancer incidence increased in both sexes and cancer mortality significantly decreased (since 1991 among men). Lung cancer showed significantly decreasing incidence (EAPC = -1.4%) and mortality (EAPC = -1.6%) among men and increasing trends among women. In women, breast cancer incidence significantly increased (EAPC= +1.7%) and mortality decreased since 1989 (EAPC= -2.0%). Stomach cancer incidence and mortality decreased in both sexes. Prostate incidence sharply increased since 1991 and mortality decreased. Colon cancer incidence increased and rectum mortality decreased significantly in both sexes. Significant increases in incidence were also found for kidney (up to 1991 among men), urinary bladder, skin epithelioma, melanoma, liver (up to 1993 among men), pancreas, mesothelioma, Kaposi's sarcoma (up to 1995 among men), testis, thyroid, non-Hodgkin's lymphomas and multiple myeloma. Mortality significantly decreased for cancers of the oral cavity and pharynx, oesophagus, liver (women), larynx (men), bone, cervix (since 1990), central nervous system, urinary bladder, thyroid, Hodgkin's lymphomas and leukaemias (men). Non-Hodgkin's lymphoma mortality increased in both sexes. In conclusion, most of the changes seen can be explained as the effect of changes in smoking habits and of the extension of secondary prevention activities. The Italian health care system will also have to cope with growing cancer diagnostic and therapeutic needs due to population ageing.
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PMID:Population-based incidence and mortality cancer trends (1986-1997) from the network of Italian cancer registries. 1555 57

We report on two female patients who presented with painful recurrent palpable purpura, ulcers and necroses on the extremities. The results of all examinations and laboratory tests considered together suggested a diagnosis of necrotizing leukocytoclastic vasculitis. Leukocytoclastic vasculitis is an inflammatory necrotizing condition of the superficial dermal vessels, presenting with variable clinical symptoms. In most cases it becomes manifest as palpable purpura, but hemorrhagic-necrotizing, bullous, nodular and urticarial presentations also occur. Common etiological factors include bacterial, viral or drug antigens, chronic infections (hepatitis B and C), non-Hodgkin lymphomas (monoclonal gammopathy, multiple myeloma), leukemia (hairy cell leukemia), and tumors (bronchial, breast, and gastric cancer) and also connective tissue disorders. In the course of the work-up, a plasmocytoma was discovered as the cause of the leukocytoclastic vasculitis, presenting in a similar way to livedo reticularis in one case and to pyoderma gangraenosum in the other.
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PMID:[Rare types of vasculitis as markers of plasmocytoma]. 1565 29

Many Koreans were forced to move to Japan while Korea was occupied by Japan. Consequently, when the atomic bombs were dropped on Hiroshima and Nagasaki an estimated 40,000 Koreans died and 30,000 survived. In 2004, 2,235 Koreans were registered as A-bomb survivors in South Korea. A mail questionnaire survey to evaluate the present status and self-reported diseases of the Korean survivors was conducted. In total, 1,256 questionnaires were returned and analysed. The most frequent chronic diseases reported by Korean survivors were hypertension (40.1 per cent), peptic ulcer disease (25.7 per cent), anaemia (23.3 per cent) and cataracts (23.1 per cent). The most frequent malignant diseases were stomach cancer (1.9 per cent), colon cancer (0.5 per cent) and leukaemia/multiple myeloma (0.4 per cent). This study suggests that further investigations are needed into the health concerns of the survivors and into health protection measures.
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PMID:Present status and self-reported diseases of the Korean atomic bomb survivors: a mail questionnaire survey. 1618 Jul 35

AREG (Amphiregulin), BTC (beta-cellulin), EGF, EPGN (Epigen), EREG (Epiregulin), HBEGF, NRG1, NRG2, NRG3, NRG4 and TGFA (TGFalpha) constitute EGF family ligands for ERBB family receptors. Cetuximab (Erbitux), Pertuzumab (Omnitarg) and Trastuzumab (Herceptin) are anti-cancer drugs targeted to EGF family ligands, while Gefitinib (Iressa), Erlotinib (Tarceva) and Lapatinib (GW572016) are anti-cancer drugs targeted to ERBB family receptors. AREG and TGFA are biomarkers for Gefitinib non-responders. The TCF/LEF binding sites within the promoter region of human EGF family members were searched for by using bioinformatics and human intelligence (Humint). Because three TCF/LEF-binding sites were identified within the 5'-promoter region of human AREG gene, comparative genomics analyses on AREG orthologs were further performed. The EPGN-EREG-AREG-BTC cluster at human chromosome 4q13.3 was linked to the PPBP-CXCL segmental duplicons. AREG was the paralog of HBEGF at human chromosome 5q31.2. Chimpanzee AREG gene, consisting of six exons, was located within NW_105918.1 genome sequence. Chimpanzee AREG was a type I transmembrane protein showing 98.0% and 71.4% total amino-acid identity with human AREG and mouse Areg, respectively. Three TCF/LEF-binding sites within human AREG promoter were conserved in chimpanzee AREG promoter, but not in rodent Areg promoters. Primate AREG promoters were significantly divergent from rodent Areg promoters. AREG mRNA was expressed in a variety of human tumors, such as colorectal cancer, liver cancer, gastric cancer, breast cancer, prostate cancer, esophageal cancer and myeloma. Because human AREG was characterized as potent target gene of WNT/beta-catenin signaling pathway, WNT signaling activation could lead to Gefitinib resistance through AREG upregulation. AREG is a target of systems medicine in the field of oncology.
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PMID:Canonical WNT signaling pathway and human AREG. 1668 31

Anti-calcyclin binding protein (CacyBP) monoclonal antibodies (MAb) were produced using an in vitro immunization method. BALB/c mouse splenocytes were immunized with purified 6 x His-CacyBP fusion protein and fused with myeloma cells using polyethylene glycol (PEG) 4000. By selection using enzyme-linked immunosorbent assay (ELISA), three anti-CacyBP MAbs were obtained. The MAb BD1, whose isotype was IgG1, interacted with the fusion protein. Western blot and immunofluorescence microscopy showed that the MAb BD1 against CacyBP could recognize CacyBP protein derived from human gastric cancer cell lines in both native and denatured forms. This MAb would act as a useful tool for the detection of CacyBP protein in future studies.
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PMID:Establishment and characterization of calcyclin binding protein (CacyBP) monoclonal antibody. 1670 10


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