Incidence of de-novo breast cancer in women chronically immunosuppressed after organ transplantation

Stewart, T. H. M.; Tsai, Shaw-Jeng; Grayson, H.; Henderson, Robin; Opelz, Gerhard

doi:10.1016/s0140-6736(95)91618-0

Cited by 208 publications

(123 citation statements)

References 19 publications

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“…However, the lower incidence of de novo breast cancer was also noted in the Collaborative Transplant Study registry. 89 The rate of genitourinary malignancy was 1.5 times less (SIR, 0.68) than expected, in contrast to the greater incidence of anogenital malignancies detected in renal transplant recipients. 90 Despite an apparent increased risk for colon cancer in liver transplant recipients with IBD, the rate for gastrointestinal malignancy was not significantly greater than that in the general population (SIR, 1.06).…”

Section: Discussionmentioning

confidence: 80%

De novo malignancies after liver transplantation: A major cause of late death

Fung

Jain

Kwak

et al. 2001

Liver Transplantation

181

145

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Section: Discussionmentioning

confidence: 80%

De novo malignancies after liver transplantation: A major cause of late death

Fung

Jain

Kwak

et al. 2001

Liver Transplantation

181

145

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“…Deleterious effects such as nephrotoxicity, hypertension, symptomatic hyper uricemy, and hyperlipidemia are associated with this treatment. More damaging, CSA-treated patients display an increased incidence of lympho-proliferative disorders and skin cancers, a common and dreaded complication (11,12). Different reports suggest that therapy with immunosuppressors can specifically stimulate the transcription of genes that may contribute to the onset of complications arising from therapy.…”

mentioning

confidence: 99%

Characterization of a Gene Encoding Two Isoforms of a Mitochondrial Protein Up-regulated by Cyclosporin A in Activated T Cells

Mascarell

Auger

Alcover

et al. 2004

Journal of Biological Chemistry

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Cyclosporin A (CSA) is an immunosuppressor used in organ transplantation. A recent proteomic analysis has revealed that activation of T cells in the presence of CSA induces the synthesis of hundreds of new proteins. Here we used representational difference analysis to characterize some of the corresponding induced genes. After cDNA bank screening we focused on one of these genes, which we named CSA-conditional, T cell activation-dependent (CSTAD) gene. This gene produces two mRNAs resulting from alternative splicing events. They encode two proteins of 104 and 141 amino acids, CSTADp-S and CSTADp-L, for the short and long forms, respectively. FK506 had the same effect as CSA, whereas rapamycin did not affect the level of CSTAD gene expression, demonstrating that inhibition of the calcineurin activation pathway is involved in CSTAD gene up-regulation. CSA also led to overexpression of CSTAD in mice immunized in the presence of CSA, confirming the in vitro analysis. Microscopic and cytofluorimetric analysis of cells expressing green fluorescent protein-tagged CSTADp-L and CSTADp-S showed that both proteins colocalize with mitochondrial markers and depolarize the mitochondrial transmembrane potential without causing release of cytochrome c, apoptosis, or necrosis. Both CSTADp isoforms are sensitive to proteinase K, implying that they are located in the mitochondrial outer membrane. These data reveal a new mechanism of action for CSA, which involves up-regulation of a gene whose products are sorted to mitochondria and depolarize the mitochondrial membrane.

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“…For example, that non-virus-associated cancers such as those of breast and lung, do not arise any more frequently in people with a defective immune system than in those with a fully functional system (Groopman 1987) argues against the immune surveillance hypothesis, instead suggesting that the immune system recognizes tumors more as self than as foreign. Also, results obtained in patients receiving therapeutic immunosuppression (cyclosporine A) after kidney or heart transplantation are conflicting, since a lower incidence of breast cancer was observed, while for all other major cancers, including breast fibroadenomas (Weinstein et al 2001) the incidence was higher (Stewart et al 1995). Potential mechanisms to explain these effects include production by inflammatory cell infiltrates of direct or indirect modulators of breast cell growth, e.g.…”

Section: Innate Immunity Versus Adaptive Immunitymentioning

confidence: 99%

Innate immunity in breast carcinoma.

Sfondrini¹,

Balsari²,

Ménard³

2003

Endocrine-Related Cancer

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The innate immune response, which depends on so-called pattern-recognition receptors (PRRs) is an evolutionarily old immune response able to elicit a defensive response against a vast array of pathogens. The purpose of this review is to revisit the role of innate immunity in breast carcinoma from the oldest therapeutic approach using bacillus Calmette-Guerin to the recent findings on the manipulation of the PRR pathways with unmethylated cytosine-guanosine dinucleotides (CpG motifs). Encouraging results have been obtained in prevention and local treatment of murine mammary tumors using tumor cells engineered to express stably mycobacterial antigens or directly using CpG-containing oligonucleotides. The experimental findings raise the possibility of successful anti-tumor management through stimulation of innate immunity in women at high risk of developing breast cancer and in breast cancer patients with reasonable immunological performance and low tumor load.

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Incidence of de-novo breast cancer in women chronically immunosuppressed after organ transplantation

Cited by 208 publications

References 19 publications

De novo malignancies after liver transplantation: A major cause of late death

De novo malignancies after liver transplantation: A major cause of late death

Characterization of a Gene Encoding Two Isoforms of a Mitochondrial Protein Up-regulated by Cyclosporin A in Activated T Cells

Innate immunity in breast carcinoma.

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