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Cancer risk in HFE C282Y homozygotes: results from the HUNT 2 study.

https://arctichealth.org/en/permalink/ahliterature117608
Source
Scand J Gastroenterol. 2013 Feb;48(2):189-95
Publication Type
Article
Date
Feb-2013
Author
Arne Asberg
Ketil Thorstensen
Wenche Ø Irgens
Pål R Romundstad
Kristian Hveem
Author Affiliation
Department of Clinical Chemistry, Trondheim University Hospital, Trondheim, Norway. arne.aasberg@stolav.no
Source
Scand J Gastroenterol. 2013 Feb;48(2):189-95
Date
Feb-2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Breast Neoplasms - epidemiology - genetics
Carcinoma, Hepatocellular - epidemiology - genetics
Colorectal Neoplasms - epidemiology - genetics
Female
Follow-Up Studies
Genetic markers
Histocompatibility Antigens Class I - genetics
Homozygote
Humans
Incidence
Liver Neoplasms - epidemiology - genetics
Male
Membrane Proteins - genetics
Middle Aged
Multivariate Analysis
Mutation
Norway - epidemiology
Proportional Hazards Models
Registries
Risk factors
Abstract
In addition to hepatocellular cancer, HFE C282Y homozygotes are reported to have increased risk of colorectal cancer and breast cancer. This study was done to further explore the cancer risk in C282Y homozygotes.
We studied cancer incidence in 292 homozygotes and 62,568 others that participated in the HUNT 2 population screening in 1995-1997. Using Cox proportional hazard models, we estimated cancer hazard ratio as a function of C282Y homozygosity and several screening variables including serum transferrin saturation, alcohol consumption and daily smoking.
Cancer was diagnosed in 36 homozygotes, five of which had two cancer diagnoses. The overall cancer incidence was not increased in C282Y homozygotes (hazard ratio 1.10 [95% CI 0.60-2.03] in women and 0.94 [95% CI 0.53-1.66] in men). However, homozygous men had increased risk of colorectal cancer (hazard ratio 3.03 [95% CI 1.17-7.82], p = 0.022) and primary liver cancer (hazard ratio 54.0 [95% CI 2.68-1089], p = 0.009). The risk of breast cancer in homozygous women was not increased (hazard ratio 1.13 [95% CI 0.35-3.72]). Adjusted for other variables including C282Y homozygosity, very low and very high serum transferrin saturation were associated with increased overall cancer incidence.
C282Y homozygosity is associated with increased risk of colorectal cancer and hepatocellular cancer in men. In the general population, individuals with a very low or a very high serum transferrin saturation may have increased cancer risk.
PubMed ID
23281741 View in PubMed
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Familial liver and gall bladder cancer: a nationwide epidemiological study from Sweden.

https://arctichealth.org/en/permalink/ahliterature18564
Source
Gut. 2003 Apr;52(4):592-6
Publication Type
Article
Date
Apr-2003
Author
K. Hemminki
X. Li
Author Affiliation
Department of Biosciences at Novum, Karolinska Institute, 141 57 Huddinge, Sweden. kari.hemminki@cnt.ki.se
Source
Gut. 2003 Apr;52(4):592-6
Date
Apr-2003
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Biliary Tract Neoplasms - etiology - genetics
Carcinoma, Hepatocellular - epidemiology - genetics
Child
Child, Preschool
Female
Gallbladder Neoplasms - epidemiology - genetics
Humans
Incidence
Infant
Infant, Newborn
Liver Neoplasms - epidemiology - genetics
Male
Middle Aged
Neoplastic Syndromes, Hereditary - epidemiology
Registries
Research Support, Non-U.S. Gov't
Sweden - epidemiology
Abstract
BACKGROUND AND AIMS: Familial risks in liver and biliary cancers have been assessed in small case control studies, usually based on reported, but not medically verified, cancers in family members. Thus the degree of familial clustering for these cancers remains to be established. METHODS: The nationwide Swedish Family-Cancer Database was used, covering 10.2 million individuals for the years 1961-1998 from the Swedish Cancer Registry. Liver and biliary tract cancers were identified from 1121 offspring between the ages of 0 and 66 years and 17 131 parents. Standardised incidence ratios (SIRs) and 95% confidence intervals (CIs) were calculated for cancers in family members. RESULTS: All cancers in the liver and biliary system showed a familial SIR of 1.65 (95% CI 1.05-2.46). This was mainly explained by a high risk for familial gall bladder cancer (SIR 5.21 (95% CI 2.07-10.80)) and for familial primary liver cancer with hepatocellular carcinoma histology (SIR 4.69 (95% CI 1.48-11.04)). For gall bladder and hepatocellular cancer, maternal transmission appeared to be favoured. Gall bladder cancer was associated with pancreatic cancer (SIR 2.39 (95% CI 1.23-4.18)). Primary liver cancer was associated with cervical, urinary bladder, and endocrine gland tumours. Cancer in extrahepatic bile ducts was associated with ovarian cancer and that in ampulla of Vater with thyroid cancer; however, these associations may have been fortuitous. CONCLUSIONS: This study has provided the first data on familial clustering of liver and gall bladder cancers, based on medically confirmed records. The risks were so high that heritable factors were likely to contribute, possibly modified by environmental factors. The demonstration of candidate genes would help to further characterise the familial risks.
PubMed ID
12631675 View in PubMed
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Genetic studies of human primary hepatocellular carcinoma.

https://arctichealth.org/en/permalink/ahliterature4129
Source
Prog Clin Biol Res. 1992;376:155-72
Publication Type
Article
Date
1992
Author
K H Buetow
Author Affiliation
Division of Population Science, Fox Chase Cancer Center, Philadelphia, PA 19111.
Source
Prog Clin Biol Res. 1992;376:155-72
Date
1992
Language
English
Geographic Location
U.S.
Publication Type
Article
Keywords
Alaska - epidemiology
Alleles
Carcinoma, Hepatocellular - epidemiology - genetics
Chromosomes, Human, Pair 4
Genes, Tumor Suppressor - genetics
Humans
Liver Neoplasms - epidemiology - genetics
PubMed ID
1326768 View in PubMed
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Somatic changes in primary liver cancer in Russia: a pilot study.

https://arctichealth.org/en/permalink/ahliterature112449
Source
Mutat Res. 2013 Aug 15;755(2):90-9
Publication Type
Article
Date
Aug-15-2013
Author
Olga Kalinina
Agnès Marchio
Aleksandr I Urbanskii
Aleksandra B Tarkova
Khadija Rebbani
Dmitri A Granov
Anne Dejean
Mikhail I Generalov
Pascal Pineau
Author Affiliation
Laboratory of Molecular Microbiology, Saint-Petersburg Pasteur Institute, Saint-Petersburg, Russian Federation, Laboratory of Molecular Biology, Almazov Centre for Heart, Blood and Endocrinology, Saint-Petersburg, Russian Federation.
Source
Mutat Res. 2013 Aug 15;755(2):90-9
Date
Aug-15-2013
Language
English
Publication Type
Article
Keywords
Adult
Aflatoxin B1 - toxicity
Aged
Aged, 80 and over
Axin Protein - genetics
Carcinoma, Hepatocellular - epidemiology - genetics - pathology - virology
Cholangiocarcinoma - epidemiology - genetics - pathology
Chromosomal Instability
Chromosomes, Human, Pair 18
Cohort Studies
Comorbidity
Female
Genes, p53
Genes, ras
Hepatitis B, Chronic - epidemiology
Hepatitis C, Chronic - epidemiology
Humans
Liver Neoplasms - epidemiology - genetics - pathology - virology
Loss of Heterozygosity
Male
Middle Aged
Monosomy
NF-E2-Related Factor 2 - genetics
PTEN Phosphohydrolase - genetics
Pilot Projects
Point Mutation
Proto-Oncogene Proteins B-raf - genetics
Risk factors
Russia - epidemiology
Young Adult
beta Catenin - genetics
Abstract
Primary liver cancer (PLC) is a major public health concern worldwide, ranking third among the causes of death from cancer. Molecular pathogenesis of PLC is known to be especially sensitive to ethno-environmental variations that modulate mutation spectra in tumours. Despite a high prevalence of chronic liver diseases, the molecular epidemiology of PLC is still poorly known in Russia. To characterize the major genetic features of liver tumours in Russian populations, we conducted a pilot study on 34 PLC cases (28 hepatocellular, two cholangiocellular, and four mixed cases) among patients attending the Radiology and Roentgenology Hospital in Saint Petersburg. Point mutations were searched in 9 genes that are commonly altered in PLC, viz. TP53, CTNNB1, AXIN1, H/K/N-RAS, BRAF, PTEN, and NFE2L2. The genes TP53 and AXIN1 were mutated in 16% and 10% of the cases, respectively, whereas mutations of ?-catenin were present in only 7% of samples, an unusual situation for Europe but common in East Asia. No R249S mutation indicative of exposure to aflatoxin B1 was detected in TP53. A single case harboured an NFE2L2 mutation. The loss of chromosome 18q was associated with early onset of tumours (mean 50 vs 62yrs, p=0.0252) and with the patient's place of birth in Caucasus or Siberia. A lack of any risk factor was noted in 47% of the patients, whereas only 23% of the patients were infected either by hepatitis virus B or C. An extension of the present cohort as well as further molecular studies are now warranted in order to understand the processes governing liver carcinogenesis affecting Russian populations.
PubMed ID
23830926 View in PubMed
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