Cancer Arising After Pancreas and/or Kidney Transplantation in a Series of 99 Diabetic Patients

Martinenghi, Sabina; Dell’Antonio, Giacomo; Secchi, Antonio; Carlo, V. Di; Pozza, G.

doi:10.2337/diacare.20.3.272

Cited by 42 publications

(12 citation statements)

References 14 publications

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“…The literature, however, regarding cancer mortality among individuals with type 1 diabetes, is limited by small sample size and short length of follow-up (Mihara et al, 1986;Martinenghi et al, 1997) and therefore do not preclude a Ragozzino (F), 1982Whittemore, 1983Rulyak, 2003Ragozzino (M), 1982Hiatt, 1988Balkau, 1993, Shibata, 1994Inoue (F), 2003Batty, 2004, Mills, 1988 …”

Section: Level Of Adjustmentmentioning

confidence: 99%

Type-II diabetes and pancreatic cancer: a meta-analysis of 36 studies

et al. 2005

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Pancreatic cancer is the eighth major form of cancer-related death worldwide, causing 227 000 deaths annually. Type-II diabetes is widely considered to be associated with pancreatic cancer, but whether this represents a causal or consequential association is unclear. We conducted a meta-analysis to examine this association. A computer-based literature search from 1966 to 2005 yielded 17 case -control and 19 cohort or nested case -control studies with information on 9220 individuals with pancreatic cancer. The age and sex-adjusted odds ratio (OR) for pancreatic cancer associated with type-II diabetes was obtained from each study. The combined summary odds ratio was 1.82 (95% confidence interval (95% CI) 1.66 -1.89), with evidence of heterogeneity across the studies (P ¼ 0.002 for case -control and P ¼ 0.05 for cohort studies) that was explained, in part, by higher risks being reported by smaller studies and studies that reported before 2000. Individuals in whom diabetes had only recently been diagnosed (o4 years) had a 50% greater risk of the malignancy compared with individuals who had diabetes for X5 years (OR 2.1 vs 1.5; P ¼ 0.005). These results support a modest causal association between type-II diabetes and pancreatic cancer. British Journal of Cancer (2005) (Parkin et al, 2002), its poor prognosis makes it the eighth major form of cancer-related death worldwide, causing more than 220 000 deaths annually. Apart from cigarette smoking, which has been estimated to cause about 30% of pancreatic cancers (Doll and Peto, 1976; Baghurst et al, 1991), relatively little is known about the other chief determinants of the disease, although other lifestyle factors have been implicated, including obesity (Berrington de Gonzalez et al, 2003) and type-II diabetes (Everhart and Wright, 1995).As type-II diabetes frequently occurs with pancreatic cancer, it is considered by many to be an important risk factor for the malignancy. A meta-analysis of 20 studies conducted a decade ago estimated that individuals with diabetes have a two-fold greater relative risk (RR) of pancreatic cancer compared with individuals without diabetes (Everhart and Wright, 1995). However, there is also good evidence that pancreatic cancer is causally linked to the onset of diabetes (Wang et al, 2003) and is possibly associated with an abnormality of islet cell function.A large number of new studies have since published on the association between type-II diabetes and pancreatic cancer. Therefore, the purpose of the current study was to update the earlier meta-analysis to provide the most reliable information on the size of the association, and to explore any underlying sources of heterogeneity, including variations in the strength of the relationship with duration of diabetes. MATERIALS AND METHODS Data sourcesRelevant studies were identified through EMBASE, PUBMED and MEDLINE using a combined text word and MESH heading search strategy of pancreatic cancer (pancreas, tumour, malignancy) and type-II diabetes (NIDDM, diabetes, adult-onset diabetes). Ref...

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Section: Level Of Adjustmentmentioning

confidence: 99%

Type-II diabetes and pancreatic cancer: a meta-analysis of 36 studies

et al. 2005

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“…[5][6][7] Correspondence: S Martinenghi, Alternative therapeutic approaches based on allogenic transplantation are indeed a clinical option, but only in selected cases. Pancreas transplantation is able to completely normalize glucose metabolism, but is a major surgical procedure and requires permanent immunosuppression, 8 which is associated with increased risk of cancer 9 and infections. 10,11 The less invasive human islet transplantation has been shown to be successful in a specific setting, although still requiring immunosuppression and two/three donor pancreata per recipient.…”

Section: Introductionmentioning

confidence: 99%

Human insulin production and amelioration of diabetes in mice by electrotransfer-enhanced plasmid DNA gene transfer to the skeletal muscle

et al. 2002

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“…At present, the full replacement of failed b -cell function can be provided only by the transplantation of allogeneic pancreatic tissue, either as a vascularized pancreas (Sutherland, 1993;Landgraf, 1996) or as isolated Langerhans islets graft (Alejandro et al, 1997;Secchi et al, 1997). Unfortunately, relevant drawbacks of these procedures include surgical complications and the adverse effects of continuous immunosuppr essive therapy (Martinenghi et al, 1997), needed to prevent graft rejection and autoimmunity recurrence.…”

mentioning

confidence: 96%

Reversal of Diabetes in Mice by Implantation of Human Fibroblasts Genetically Engineered to Release Mature Human Insulin

Falqui

Martinenghi²,

Severini³

et al. 1999

Human Gene Therapy

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Autoimmune destruction of pancreatic beta cells in type I, insulin-dependent diabetes mellitus (IDDM) results in the loss of endogenous insulin secretion, which is incompletely replaced by exogenous insulin administration. The functional restoration provided by allogeneic beta-cell transplantation is limited by adverse effects of immunosuppression. To pursue an insulin replacement therapy based on autologous, engineered human non-beta cells, we generated a retroviral vector encoding a genetically modified human proinsulin, cleavable to insulin in non-beta cells, and a human nonfunctional cell surface marker. Here we report that this vector efficiently transduced primary human cells, inducing the synthesis of a modified proinsulin that was processed and released as mature insulin. This retrovirally derived insulin displayed in vitro biological activity, specifically binding to and phosphorylation of the insulin receptor, comparable to human insulin. In vivo, the transplantation of insulin-producing fibroblasts reverted hyperglycemia in a murine model of diabetes, whereas proinsulin-producing cells were ineffective. These results support the possibility of developing insulin production machinery in human non-beta cells for gene therapy of IDDM.

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Cancer Arising After Pancreas and/or Kidney Transplantation in a Series of 99 Diabetic Patients

Abstract: Increased dosage of immunosuppressive agents may be necessary in some patients of prevent or treat rejection in view of their reduced survival on hemodialysis.

Cited by 42 publications

References 14 publications

Type-II diabetes and pancreatic cancer: a meta-analysis of 36 studies

Type-II diabetes and pancreatic cancer: a meta-analysis of 36 studies

Human insulin production and amelioration of diabetes in mice by electrotransfer-enhanced plasmid DNA gene transfer to the skeletal muscle

Reversal of Diabetes in Mice by Implantation of Human Fibroblasts Genetically Engineered to Release Mature Human Insulin

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