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

Cancer incidence rates among blacks average 10-20 percent higher than among non-minorities, with a much greater excess for several cancers, namely, esophagus, multiple myeloma, cervix, stomach, pancreas, larynx and prostate. Cancer mortality rates for blacks are 20-40 percent higher than for non-minority men, with the greatest excess evident for esophageal cancer, followed by cervix, multiple myeloma and prostate. Blacks have a five-year relative survival rate 30 percent lower than that for whites primarily because blacks seek treatment at a more advanced stage of disease than whites. Preventive health messages and programs need to be expanded to serve disadvantaged communities.
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PMID:The epidemiology of cancer in black Americans. 206 57

Monoclonal antibody (A9-84) against a hepatocellular carcinoma cell line (PLC/PRF-5) was produced by somatic cell fusion. The hybridoma clones were screened by a rapid solid-phase enzyme-linked binding assay. The target cells were cultured in 96-well Linbro plate and fixed by methanol for screening. The specificity of the antibody was studied by enzyme-linked binding assay and immunofluorescence methods. It shows that A9-84 do not respond to 8 different human cancer cell lines (4 liver cancer, 1 esophageal cancer, 1 stomach cancer, 1 multiple myeloma and 1 lymphoblast cell line) and the peripheral mononuclear cells of 91 normal subjects. A9-84 is the subtype of IgG3. It is capable of inhibiting the growth of cultured PLC/PRF/5 cells with or without complement.
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PMID:[Action of monoclonal antibody against a hepatocellular carcinoma cell line (PLC/PRF/5)]. 301 21

This study evaluated the mortality experience of 1,352 white and 438 nonwhite men who worked in the rubber-reclaiming division of a large rubber manufacturing company. In comparisons of mortality of white reclaim workers with that of nonreclaim workers rate ratios were 2.7 for esophageal cancer (six observed deaths among reclaim workers), 2.1 for bladder cancer (seven observed deaths), and 4.5 for multiple myeloma (six observed deaths). The excess of bladder cancer among white reclaim workers may be associated with their employment in other high-risk areas of the plant, whereas no such explanation was found for the excesses of esophageal cancer and multiple myeloma. Overall, the lung cancer mortality rate of white reclaim workers was similar to the rate of US white males and other white rubber workers. There was a 50% excess of lung cancer deaths among nonwhite reclaim workers compared with other nonwhite rubber workers. However, this observation is based on small numbers, and no firm conclusions can be reached about the risk of lung cancer associated with reclaim operations in this group of rubber workers.
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PMID:Mortality among rubber workers: X. Reclaim workers. 399 47

This report describes mortality occurring between 1940 and mid-1978 among 29,087 men and women employed in a rubber plant for at least two years. Mortality patterns for the period July 1, 1974, to July 1, 1978, were compared to previously published findings for January 1, 1940, through June 30, 1974. Expected numbers of deaths were based on U.S. general population mortality data. There were excess deaths from bladder cancer and leukemia among white male union members during both follow-up periods. During recent follow-up of white male union members employed for at least five years, there were excesses in deaths from three additional cancers: esophageal cancer (11 observed/4.8 expected), biliary and liver cancer (6 observed/3.3 expected) and lymphoma and multiple myeloma (14 observed/5.8 expected). Evidence from other studies of rubber workers suggests that observed excesses in deaths from bladder cancer and leukemia are related to work-place exposures. The present findings suggest that occupational exposures etiologically relevant to these diseases may not have been reduced in recent years or that sufficient time has not elapsed for such reductions to result in decreased mortality. Further investigation is required to clarify the contribution of occupational factors to observed excesses in deaths form cancers of the esophagus and the biliary passages and liver and from lymphoma and multiple myeloma.
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PMID:Mortality among rubber workers. III. Cause-specific mortality, 1940-1978. 729 3

We have encountered two cases of bone tumors with high 18F-fluorodeoxyglucose (FDG) uptake and negative 99mTc-HMDP bone scintigraphy, including a patient with myeloma and a patient with a metastatic bone tumor from esophageal cancer. Bone scintigraphy with a 99mTc-phosphate complex reflects osteoblastic activity in the bone tissue surrounding the tumor, whereas the accumulation of FDG is associated with the metabolic activity of the tumor itself. An FDG-PET study can therefore be used as a complementary study for the detection and follow-up of bone tumors when a 99mTc-phosphate bone scintigram is negative.
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PMID:Fluorine-18-fluorodeoxyglucose positron emission tomography in technetium-99m-hydroxymethylenediphosphate negative bone tumors. 842 49

The cause-specific mortality (1940-1993) of 2,985 male workers employed in three oil refineries was examined using a proportionate mortality study design. Separate analyses were undertaken by race, refinery, employment status (active and retired), and time since entry into the Oil, Chemical, and Atomic Workers (OCAW) union. Proportionate cancer mortality ratio (PCMR) analyses also were conducted. Proportionate mortality ratios (PMR) were significantly increased (P < 0.05) for cancers of the lip (PMR = 384), stomach (PMR = 142), unspecified sites of the liver (PMR = 238), pancreas (PMR = 151), connective tissues (PMR = 243), prostate (PMR = 135), eye (PMR = 407), brain (PMR = 181), benign and unspecified neoplasms (PMR = 289), and leukemia (PMR = 175) for the entire cohort. Significantly decreased mortality was observed for respiratory tuberculosis (PMR = 29), esophageal cancer (PMR = 45), rectal cancer (PMR = 49), and cancers of the bladder and other urinary organs (PMR = 40). Skin cancer was observed to be significantly increased (PMR = 242) for workers with less than 20 years since union initiation. Significantly increased PCMRs were seen for cancers of unspecified sites of the liver (PCMR = 205), brain (PCMR = 147), benign and unspecified neoplasms (PCMR = 243), and leukemia (PCMR = 146). Among nonwhites, an increased risk of bone cancer was observed in the PCMR analysis (PCMR = 704), although based on only two deaths. Analyses of mortality patterns for white males by refinery revealed similar patterns in each refinery as was seen in the overall cohort of refinery workers. Mortality patterns for whites and nonwhites also were similar. Additional analyses of deaths between 1960 and 1993 demonstrated increased mortality due to asbestosis (PMR = 683) and multiple myeloma (PMR = 124), although the multiple myeloma excess was not statistically significant. Ten deaths due to mesotheliomas were observed among these refinery workers.
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PMID:Proportionate mortality among union members employed at three Texas refineries. 988 51

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

Cilium is a conservative cell organelle, found in many types of cell surfaces. Cilia are tail-like prominence protruding out of the cell surface, capable of locomotion and acting as the cell's signal transduction sensory organs with their complex structures and ingenious function. Studies have shown that ciliary pathological changes and defects are related to the development of many diseases, including renal cysts, infertility, organ reversal, obesity and so on. The inactivation and mutation of cilia-related proteins can cause tumors, such as neoplasms, intestinal cancer, myeloma, rhabdomyosarcoma and adenocarcinoma. Adenomatous polyposis coli (APC) is a kind of multifunctional protein encoded by the APC gene that participates in many vital activities of organisms. The mutation of APC can lead to familial adenomatous polyposis, and also has a role in the development of human tumors, such as gastric cancer, esophageal cancer and breast carcinoma. Recent studies indicate that the abnormal mutation of APC may lead to some diseases caused by abnormal growth of cilia. Herein, the development of studies on cilia, APC and associated diseases are summarized in brief.
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PMID:Cilia, adenomatous polyposis coli and associated diseases. 2186 Apr 14

It is now 40 years since bisphosphonates (BPs) were first used in the clinic. So, it is timely to provide a brief review of what we have learned about these agents in bone disease. BPs are bone-specific and have been classified into two major groups on the basis of their distinct molecular modes of action: amino-BPs and non-amino-BPs. The amino-BPs are more potent and they inhibit farnesyl pyrophosphate synthase (FPPS), a key enzyme of the mavalonate/cholesterol biosynthetic pathway, while the non-amino-BPs inhibit osteoclast activity, by incorporation into non-hydrolyzable analogs of ATP. Both amino-BPs and non-amino-BPs can protect osteoblasts and osteocytes against apoptosis. The BPs are widely used in the clinic to treat various diseases characterized by excessive bone resorption, including osteoporosis, myeloma, bone metastasis, Legg-Perthes disease, malignant hyperparathyroidism, and other conditions featuring bone fragility. This review provides insights into some of the adverse effects of BPs, such as gastric irritation, osteonecrosis of the jaw, atypical femoral fractures, esophageal cancer, atrial fibrillation, and ocular inflammation. In conclusion, this review covers the biochemical and molecular mechanisms of action of BPs in bone, particularly the discovery that BPs have direct anti-apoptotic effects on osteoblasts and osteocytes, and the current situation of BP use in the clinic.
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PMID:Basic research and clinical applications of bisphosphonates in bone disease: what have we learned over the last 40 years? 2433 Jul 28

Previous epidemiology reviews of exposure to styrene and the risk of cancer considered studies published through 13 November 2013. Since then, additional relevant research has been published. No review has included meta-analyses. The current systematic review considered research published through June 2017; included meta-analyses of the relationship between any exposure to styrene and cancers identified as being of concern, including non-Hodgkin lymphoma (NHL), leukemia and cancers of the esophagus, pancreas, lung and kidney; and evaluated several other forms of cancer. Meta-relative risks for all studies were 1.14 (95% confidence interval (CI), 0.91-1.43) for NHL, 1.00 (95% CI, 0.80-1.26) for multiple myeloma, 0.98 (95% CI, 0.87-1.09) for all leukemia, 1.03 (95% CI, 0.92-1.15) for esophageal cancer, 1.02 (95% CI, 0.93-1.12) for pancreatic cancer, 1.09 (95% CI, 0.95-1.24) for lung cancer and 1.10 (95% CI, 0.99-1.22) for kidney cancer. Individual studies provided little evidence of exposure-response or induction time trends. Limitations of the available research and of the meta-analyses included reliance in most studies on mortality data rather than on incidence data, lack of quantitative estimates of styrene exposure for individual subjects and lack of information on lifestyle factors. Consideration of all pertinent data, including substantial recent research, indicates that the epidemiologic evidence on the potential carcinogenicity of styrene is inconclusive and does not establish that styrene causes any form of cancer in humans.
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PMID:A systematic review of epidemiologic studies of styrene and cancer. 2958 66


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