Autoimmune disease and subsequent digestive tract cancer by histology

Hemminki, Kari; Liu, Xiangdong; Ji, Jianguang; Sundquist, Jan; Sundquist, Kristina

doi:10.1093/annonc/mdr333

Cited by 83 publications

(93 citation statements)

References 22 publications

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“…The data sources and methods were exactly as described previously. 7 Briefly, the nationwide database used in this study contains data from the national MigMed 2 dataset maintained at the Center for Primary Health Care Research. Data on AI diseases were obtained from the Hospital Discharge Register, which contains data on all discharges, with dates of hospitalization and diagnoses, for some regions since 1964 and the whole of Sweden since 1986.…”

mentioning

confidence: 99%

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Kaposi sarcoma and Merkel cell carcinoma after autoimmune disease

Hemminki

Liu

et al. 2012

Intl Journal of Cancer

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mentioning

confidence: 99%

“…A total of 33 diseases were covered, as listed elsewhere. 7 As KS and MCC are rare cancers, two cases were recorded for only 13 AI diseases. Only these AI diseases are reported.…”

mentioning

confidence: 99%

Kaposi sarcoma and Merkel cell carcinoma after autoimmune disease

Hemminki

Liu

et al. 2012

Intl Journal of Cancer

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“…The deregulation of the immune system in autoimmune diseases could lead to cancer, and there is defi nitive evidence relating some autoimmune mechanisms to the occurrence of malignancies. 90 A signifi cant association of HLA-DRBI*02 and DRBI*03 has been found with the likely occurrence of malignancies (OR 5.2 and 9.9, respectively), independently of the family history of RA and cancer or the clinical RA activity. Thus, HLA class II alleles seem to be associated with the occurrence of malignancies in patients with RA.…”

Section: Malignanciesmentioning

confidence: 99%

“…89 Among patients with RA, the risk of death increased due to the causes listed in all chapters of the International Classifi cation of Diseases Hemminki et al 90 have also reported a reduction in the risk of colon and rectal adenocarcinomas in patients with RA, suggesting that the underlying infl ammatory mechanisms acting as risk factors in those patients could have been suppressed by the use of anti-infl ammatory drugs.…”

Section: Malignanciesmentioning

confidence: 99%

Consenso 2012 da Sociedade Brasileira de Reumatologia sobre o manejo de comorbidades em pacientes com artrite reumatoide

Pereira¹,

Mota²,

Cruz³

et al. 2012

Rev. Bras. Reumatol.

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Objective: To elaborate recommendations of the Rheumatoid Arthritis Committee of the Brazilian Society of Rheumatology (SBR) to manage comorbidities in rheumatoid arthritis (RA). Methods: To review the literature and the opinions of the SBR RA Committee experts. Results and conclusions: Recommendations: 1) Early diagnosis and proper treatment of comorbidities are recommended; 2) The specifi c treatment of RA should be adapted to the presence of comorbidities; 3) Angiotensin-converting-enzyme inhibitors or angiotensin II receptor blockers are preferred to treat systemic arterial hypertension; 4) In patients diagnosed with rheumatoid arthritis and diabetes mellitus, the continuous use of a high cumulative dose of corticoids should be avoided; 5) Statins should be used to maintain LDL cholesterol levels under 100 mg/dL and the atherosclerotic index lower than 3.5 in patients with RA who have other comorbidities; 6) Metabolic syndrome should be treated; 7) Performing non-invasive tests to investigate subclinical atherosclerosis is recommended; 8) Greater surveillance for the early diagnosis of occult malignancy is recommended; 9) Preventive measures of venous thrombosis are suggested; 10) Bone densitometry is recommended in RA patients over the age of 50 years and in younger patients on corticoid therapy at a dose greater than 7.5 mg for over three months; 11) Patients with RA and osteoporosis should be instructed to avoid falls, to increase their dietary calcium intake and sun exposure, and to exercise; 12) Calcium and vitamin D supplementation is suggested. Bisphosphonates are suggested for patients with T score < -2.5 on bone densitometry; 13) A multidisciplinary team, with the active participation of a rheumatologist, is recommended to treat comorbidities.

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“…Unexpectedly, there is lower incidence of adenocarcinomas (breast, colon, prostate) against the background of a bona fide autoimmune disease, treated or untreated (590,591). The German Cancer Research Center in Heidelberg suggests that the natural risk for cancers in autoimmune diseases is increased, but is artificially reduced by suppressing the inflammatory component of cancer induction by anti inflammatory medications (592). MicroRNA155 emerges as one of the master regulators of immune cell generation, as it has the ability to target mRNAs of a wide variety of the cellular immune system.…”

Section: Mechanisms Of Inflammatory Carcinogenesismentioning

confidence: 99%

Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review)

Sinkovics

2011

Int J Oncol

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Abstract. In some inflammasomes tumor cells are generated. The internal environment of the inflammasome is conducive to the induction of malignant transformation. Epigenetic changes initiate this process. The subverted stromal connective tissue cells act to promote and sustain the process of malignant trans formation. In its early stages, the premalignant cells depend on paracrine circuitries for the reception of growth factors. The ligands are derived from the connective tissue, and the receptors are expressed on the recipient premalignant cells. The initial events are not a direct attack on the protooncogenes, and thus it may be entirely reversible. Epigenetic processes of hypermethylation of the genes at the promoters of tumor suppressor genes (to silence them), and deacetylation of the histones aimed at the promoters of protooncogenes (to activate them) are ongoing. A large number of short RNA sequences (interfering, micro, short hairpin, noncoding RNAs) silence tumor suppressor genes, by neutralizing their mRNAs. In a serial sequence oncogenes undergo amplifications, pointmutations, translocations and fusions. In its earliest stage, the process is reversible by demethylation of the silenced suppressor gene promoters (to reactivate them), or reacetylation of the histones of the oncogene promoters, thus deactivating them. The external administration of histone deacetylase inhibitors usually leads to the restoration of histone acetylation. In time, the uncorrected processes solidify into constitutive and irreversible gene mutations. Some of the pathogens inducing inflammations with consquential malignant transformation contain oncogenic gene sequences (papilloma viruses, EpsteinBarr virus, Kaposi's sarcomaassociated herpesvirus, hepatitis B and C viruses, Merkel cell polyoma virus, Helicobacter pylori, enterotoxigenic Bacteroides fragilis). These induced malignancies may be multifocal. Other pathogens are devoid of any known oncogenic genomic sequences (mycoplasma vavcarcinogenesis, chlamydia MALTlymphoma genesis). In these cases the host's inflammatory reactions induce the malignant transformation in serial sequences of gene alterations initiated by hypoxia and reactive oxygen and nitrogen species generation. Carcinogenic intrinsic inflammatory processes endogenously initiated without a pathogen are recognized. Chronic inflammatory processes signal the RNA/DNA complex. In response, the DNA may revert into its ancient primordial 'immortal' format, which the clinics recognize as 'oncogenesis'. The DNA remains the ultimate master of bioengineering in order to sustain life. A discussion on the most versatile and resistant primordial RNA/ DNA complex and the pre, proto, and unicellular world in which they coexisted is included. Contents1. Pathogens without oncogenic genomic sequences activating cellular oncogenes 2. The inflammasome 3. Tumor cell colonies generated in the inflammasomes 4. Pathogens with potentially oncogenic genomic sequences 5. Mechanisms of inflammatory carcinogenesis Pathogens without oncogenic...

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Autoimmune disease and subsequent digestive tract cancer by histology

Cited by 83 publications

References 22 publications

Kaposi sarcoma and Merkel cell carcinoma after autoimmune disease

Kaposi sarcoma and Merkel cell carcinoma after autoimmune disease

Consenso 2012 da Sociedade Brasileira de Reumatologia sobre o manejo de comorbidades em pacientes com artrite reumatoide

Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review)

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