Glucose-6-Phosphate Dehydrogenase Deficiency and the Incidence of Cancer

Beaconsfield, Peter; Rainsbury, Rebecca; Kalton, Graham

doi:10.1159/000224280

Cited by 48 publications

(13 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, epidemiological evidence of protective effect of G6PD deficiency against human tumorigenesis [12] has been recently disproved by Cocco [13] and by Cocco et al [14], Our results show that G6PD and 6PGD not only enhance in lung tumoral tissues of G6PD-normal sub jects, but also in lung tumoral tissues taken from patients with inherited enzymatic deficiency, strongly supporting the concept that these enzymes are neces sary requisites for tumoral cell proliferation.…”

Section: Discussionsupporting

confidence: 81%

“…Further, Schwartz et al [10] have shown that the administration of this steroid compound is able to cause a marked reduction in the incidence of tumors in a number of different organs, including lung tumors [11]. Epidemiological data also seemed to demonstrate a negative correla tion of cancer incidence in G6PD-deficient subjects [12], However, a critical survey by Cocco [13] com pletely revised these epidemiological data, and further studies have not proved a clear-cut negative correla tion between G6PD deficiency and cancer incidence [14].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Hexose Monophosphate Shunt Enzymes in Lung Tumors from Normal and Glucose-6-Phosphate-Dehydrogenase-Deficient Subjects

Dessı̀

Batetta

Cherchi³

et al. 1988

Oncology

View full text Add to dashboard Cite

Glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate, dehydrogenase the key enzymes of the hexose monophosphate shunt pathway, were measured in both surrounding and tumoral lung tissues from normal and G6PD-deficient subjects. A significant increase of these enzymatic activities in tumoral tissue was found not only in G6PD-normal patients, but also in G6PD-deficient patients with very low or nonmeasurable G6PD activity in both erythrocytes and normal lung tissue.

show abstract

Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Hexose Monophosphate Shunt Enzymes in Lung Tumors from Normal and Glucose-6-Phosphate-Dehydrogenase-Deficient Subjects

Dessı̀

Batetta

Cherchi³

et al. 1988

Oncology

View full text Add to dashboard Cite

show abstract

“…However, it is interesting to note that a decrease of tumor incidence has been demonstrated in GGPD-deficient patients (21)(22)(23). Long term p .~.…”

Section: Discussionmentioning

confidence: 99%

Modulatory Mechanisms of Chemical Carcinogenesis: The Role of the NADPH Pool in the Benzo(a)pyrene Activation

et al. 1984

View full text Add to dashboard Cite

A EST RA CT Human lymphocytes and human skin fibroblasts isolated in vilro from subjects carrying the Mediterranean variant of glucose-6-phosphate dehydrogenase (CCPD) exhibit an 86-87% decrease of this enzymatic activity. This is coupled with 51% and 61% decreases of the NADPH/NADP+ ratio in the GCPD-deficient human lymphocytes (HL) and human skin fibroblasts (HSF), respectively. There also occurs a 63-67% decrease of the hexose monophosphate shunt (HMS) in the deficient cells. Incubation with 0.1 mM methylene blue stimulates the HMS of normal HL 15-fold and that of deficient lymphocytes only 2.4-fold. These figures are, respectively, 7 and 2.2 in the case of HSF. This behavior of CCPDdeficient HL and HSF is coupled with an increase of the resistance to the cell death induced by benzo(a)pyrene (BP). This effect is mimicked by the incubation of normal HSF with dehydroepiandrosterone (DEA) which strongly inhibits GCPD. In contrast, no differences between normal and deficient HSF occur as a result of the effect of methylnitrosourea (MNU), a carcinogen that does not need metabolic activation.The NADPH-cytochrome c (P450) reductase of CCPD-deficient HL and HSF homogenates becomes lower than that of controls when endogenous GCPD and exogenous glucose 6-phosphate (CCP) and NADP' are used as a hydrogen donor system in place of NADPH. Normal and CCPD-deficient HL, having comparable BP-hydroxylating activities, in the presence of exogenous GCP, NADP+, and GCPD, were studied to determine the effect of the absence of exogenous GCPD in the reaction system. When exogenous CCPD is omitted, the deficient HL exhibit a BP hydroxylase activity sharply lower than controls. GCPD-deficient HL and HSF are less prone than controls to produce BP water-soluble metabolites. A decrease in the synthesis of BP metabolites, mutagenic for his-Salmonella typhimurium in CCPD-deficient HL, has also been observed.These results suggest that the decreased susceptibility of GCPD-deficient cells and HSF to the toxic effect of BP and that of deficient HSF to its previously observed transforming effect, could depend on a reduced BP metabolism in the deficient cells. Session I: 'Genetic Expression and Cell Transformation." October 12-15, Alghero. Italy. This symposium section will be continued in

show abstract

“…These enzymes inter vene in the metabolism of human erythro cytes; GSSG-R catalyzes the reduction of oxidized glutathione, PK catalyzes the con version of phosphoenolpyruvate to pyruvate in the Embden-Meyerhoff pathway, and G6PD catalyzes the first step in the phosphogluconate oxidative pathway. Their lack has been considered responsible for a varie ty of non-spherocytic congenital hemolytic anemias [Lohr and Waller, 1962;Britlinger et al, 1965;Valentine et al, 1961;Bussel, 1969;Woessner et al, 1961], as well as being associated with other effects, both hematological and extrahematological [Waller et al, 1965[Waller et al, , 1967Hayduk et al, 1968;Staal et al, 1968;Boivin, 1971;Beaconsfield et al, 1965]. So far, less than 100 cases of deficiency of erythrocyte GSSG-R have been pub lished.…”

Section: Introductionmentioning

confidence: 99%

Frequency of Glutathione Reductase, Pyruvate Kinase and Glucose-6-Phosphate Dehydrogenase Deficiency in a Spanish Population

García¹,

Moragón²,

López‐Fernández³

1979

Hum Hered

View full text Add to dashboard Cite

The frequencies of deficiencies of glutathione reductase (GSSG-R), pyruvate kinase (PK) and gIucose-6-phosphate dehydrogenase (G6PD) in a Spanish sample are presented. A total of 2,129 individuals was analyzed for GSSG-R, 1,636 for PK, and 1,066 (629 males and 437 females) for G6PD. Beutler’s method was used. The frequencies obtained for these deficiencies were: GSSG-R, 0.09%; PK, 0.24%; and G6PD, 0.79%. The results are discussed.

show abstract

Glucose-6-Phosphate Dehydrogenase Deficiency and the Incidence of Cancer

Cited by 48 publications

References 9 publications

Hexose Monophosphate Shunt Enzymes in Lung Tumors from Normal and Glucose-6-Phosphate-Dehydrogenase-Deficient Subjects

Hexose Monophosphate Shunt Enzymes in Lung Tumors from Normal and Glucose-6-Phosphate-Dehydrogenase-Deficient Subjects

Modulatory Mechanisms of Chemical Carcinogenesis: The Role of the NADPH Pool in the Benzo(a)pyrene Activation

Frequency of Glutathione Reductase, Pyruvate Kinase and Glucose-6-Phosphate Dehydrogenase Deficiency in a Spanish Population

Contact Info

Product

Resources

About