Haptoglobin Groups and Lung Cancer

Beckman, G.; Eklund, Anders; Fröhlander, Nils; Stjernberg, N

doi:10.1159/000153638

Cited by 26 publications

(15 citation statements)

References 4 publications

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“…In some studies, the Hp2-2 frequency was significantly lower in patients with pulmonary adenocarcinoma and bladder carcinoma than in normal subjects (Beckman et al, 1986;Benkmann et al, 1987), whereas a significantly higher frequency of Hp2-1 and Hp2-2 phenotypes was found in patients with esophageal and gastric cancer (Jayanthi et al, 1989).…”

Section: Cancermentioning

confidence: 95%

Polymorphism of human haptoglobin and its clinical importance

2008

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Haptoglobin (Hp) is a plasma glycoprotein, the main biological function of which is to bind free hemoglobin (Hb) and prevent the loss of iron and subsequent kidney damage following intravascular hemolysis. Haptoglobin is also a positive acute-phase protein with immunomodulatory properties. In humans, the HP locus is polymorphic, with two codominant alleles (HP1 and HP2) that yield three distinct genotypes/phenotypes (Hp1-1, Hp2-1 and Hp2-2). The corresponding proteins have structural and functional differences that may influence the susceptibility and/or outcome in several diseases. This article summarizes the available data on the structure and functions of Hp and the possible effects of Hp polymorphism in a number of important human disorders.

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Section: Cancermentioning

confidence: 95%

Polymorphism of human haptoglobin and its clinical importance

2008

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“…A deficit of group 0 in lung cancer observed in the last study was not supported by the other seven, and various associations of blood groups with certain histological types and with proximal tumours reported by Ashley (1969) were again not present in the other studies. Beckman et al (1986) reported the distribution of haptoglobin groups in lung cancer patients and controls and reviewed three similar studies -an association in their own study was not present in the others. Of five studies that have sought associations between HLA antigens Bodmer (1986) has shown that such associations of two unrelated genes on the same chromosome could have persisted (in the absence of natural selection) only with extremely close linkage, with recombination fraction approaching 0.1%.…”

Section: Familial Clustering Of Lung Cancer Casesmentioning

confidence: 95%

Genetic predisposition to lung cancer

1990

Br J Cancer

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In Britain, the life-time risk of lung cancer in men who smoke 20 or more cigarettes per day is about 15%. That most smokers never develop lung cancer has promoted interest in the role of host factors. While chance, other environmental factors and the competing effect of other diseases, some of which are also smoking related, are all likely to affect individual lung cancer risk, genetic factors may also be important. This review examines the evidence for genetic predisposition to smoking related lung cancer.The review concentrates on the numerous metabolic studies that have sought differences between individuals in the genetic control of biochemical pathways that could be involved in the metabolism of carcinogens in tobacco smoke. Insights gained are likely to have wider implications for other environmental carcinogens. Other studies that have sought simple evidence, such as familial clustering or associations of lung cancer with blood group, HLA and other naturally occurring antigens, are also examined. The field of chromosomal abnormalities in lung cancer and the difficulties in interpreting them is reviewed only briefly, since this area may not directly relate to tobacco smoking and has been reviewed elsewhere (Birrer & Minna, 1988). Various sources of bias important in the interpretation of the metabolic studies in particular are outlined. Future research is likely to be dominated by the recent advances in molecular genetics that offer the possibility of circumventing bias by the direct identification of genes, but at present this is possible only to a limited extent. Familial clustering of lung cancer casesFamilial clustering of a cancer (or indeed of any disease) is an insensitive indicator of genetic predisposition. Peto (1980) and Bodmer (1986) have pointed out that a cancer can have a major genetic component yet show no detectable familial clustering. The ratio of the incidence of the cancer in relatives of known cases to that in age-matched controls is the only measure of familial clustering (in the absence of a marker). This ratio will be much smaller than the ratio of the incidence in genetically susceptible to non-susceptible individuals, which is the direct measure of the magnitude of the genetic effect. It is a question of dilution -not all patients with cancer will be genetically susceptible individuals, fewer of their relatives will be, and tne general population contains susceptibles as well as non-susceptibles. (1980) showed that even with a very large cancer risk in susceptibles, the incidence of cancer in relatives will generally be increased by no more than 1.5-3-fold. It is difficult in a family study to show that such a modest increase could not be due to chance, shared exposure or other bias.Five studies have examined lung cancer incidence in relatives of cases, but three (Tokuhata & Lilienfeld, 1963b;

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“…11,14) It is produced in the liver and immunological cells and secreted into serum. Its level changes in the serum in response to infection, inflammation, and various malignant diseases, including lung and bladder cancer, 15,16) leukemia, 17) breast cancer, 18) malignant lymphoma, 19) urogenital tumors, 20) and esophageal squamous cell carcinoma. 21) Of these 41 genes, we especially observed Hp gene.…”

Section: Haptoglobin Proved a Prognostic Biomarker In Peripheral Bloomentioning

confidence: 99%