201 research outputs found
Two distinct aetiologies of cardia cancer, evidence from premorbid serological markers of gastric atrophy and Helicobacter pylori status
Background: Non-cardia gastric adenocarcinoma is positively associated with Helicobacter pylori infection
and atrophic gastritis. The role of H pylori infection and atrophic gastritis in cardia cancer is unclear.
Aim: To compare cardia versus non-cardia cancer with respect to the premorbid state of the stomach.
Methods: Nested case–control study. To each of 129 non-cardia and 44 cardia cancers, three controls were
matched. Serum collected a median of 11.9 years before the diagnosis of cancer was tested for anti-H pylori
antibodies, pepsinogen I:II and gastrin.
Results: Non-cardia cancer was positively associated with H pylori (OR 4.75, 95% CI 2.56 to 8.81) and
gastric atrophy (pepsinogen I:II ,2.5; OR 4.47, 95% CI 2.71 to 7.37). The diffuse and intestinal histological
subtypes of non-cardia cancer were of similar proportions and both showed a positive association with
H pylori and atrophy. Cardia cancer was negatively associated with H pylori (OR 0.27, 95% CI 0.12 to
0.59), but H pylori-positive cardia cancer showed an association with gastric atrophy (OR 3.33, 95% CI 1.06
to 10.5). The predominant histological subtype of cardia cancer was intestinal and was not associated with
gastric atrophy compared with the diffuse subtype ((OR 0.72, 95% CI 0.19 to 2.79) vs (OR 3.46, 95% CI 0.32
to 37.5)). Cardia cancer in patients with atrophy had an intestinal: diffuse ratio (1:1) similar to non-cardia
cancer (1.9:1), whereas cardia cancers in patients without atrophy were predominantly intestinal (7:1).
Conclusion: These findings indicate two aetiologies of cardia cancer, one associated with H pylori atrophic
gastritis, resembling non-cardia cancer, and the other associated with non-atrophic gastric mucosa,
resembling oesophageal adenocarcinoma. Serological markers of gastric atrophy may provide the key to
determining gastric versus oesophageal origin of cardia cancer
GLC of Serum Phenylalanine - a Gas Liquid Chromatographic Method for the Determination of Phenylalanine Serum
Gas liquid chromatographic method for quantitative analysis of phenylalanine in seru
Human papillomavirus infection as a risk factor for anal and perianal skin cancer in a prospective study
2-methylbutyryl-CoA dehydrogenase deficiency associated with autism and mental retardation: a case report
<p>Abstract</p> <p>Background</p> <p>2-methylbutyryl-CoA dehydrogenase deficiency or short/branched chain acyl-CoA dehydrogenase deficiency (SBCADD) is caused by a defect in the degradation pathway of the amino acid L-isoleucine.</p> <p>Methods</p> <p>We report a four-year-old mentally retarded Somali boy with autism and a history of seizures, who was found to excrete increased amounts of 2-methylbutyryl glycine in the urine. The SBCAD gene was examined with sequence analysis. His development was assessed with psychometric testing before and after a trial with low protein diet.</p> <p>Results</p> <p>We found homozygosity for A > G changing the +3 position of intron 3 (c.303+3A > G) in the SBCAD gene. Psychometric testing showed moderate mental retardation and behavioral scores within the autistic spectrum. No beneficial effect was detected after 5 months with a low protein diet.</p> <p>Conclusion</p> <p>This mutation was also found in two previously reported cases with SBCADD, both originating from Somalia and Eritrea, indicating that it is relatively prevalent in this population. Autism has not previously been described with mutations in this gene, thus expanding the clinical spectrum of SBCADD.</p
Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts
BACKGROUND: The magnitude of the association
between Helicobacter pylori and
incidence of gastric cancer is unclear. H
pylori infection and the circulating antibody
response can be lost with development
of cancer; thus retrospective studies
are subject to bias resulting from classifi-
cation of cases as H pylori negative when
they were infected in the past.
AIMS: To combine data from all case control
studies nested within prospective
cohorts to assess more reliably the relative
risk of gastric cancer associated with H
pylori infection.To investigate variation in
relative risk by age, sex, cancer type and
subsite, and interval between blood sampling
and cancer diagnosis.
METHODS: Studies were eligible if blood
samples for H pylori serology were collected
before diagnosis of gastric cancer in
cases. Identified published studies and two
unpublished studies were included. Individual
subject data were obtained for
each. Matched odds ratios (ORs) and 95%
confidence intervals (95% CI) were calculated
for the association between H pylori
and gastric cancer.
RESULTS: Twelve studies with 1228 gastric
cancer cases were considered. The association
with H pylori was restricted to noncardia
cancers (OR 3.0; 95% CI 2.3–3.8)
and was stronger when blood samples for
H pylori serology were collected 10+ years
before cancer diagnosis (5.9; 3.4–10.3). H
pylori infection was not associated with an
altered overall risk of cardia cancer (1.0;
0.7–1.4).
CONCLUSIONS: These results suggest that
5.9 is the best estimate of the relative risk
of non-cardia cancer associated with H
pylori infection and that H pylori does not
increase the risk of cardia cancer. They
also support the idea that when H pylori
status is assessed close to cancer diagnosis,
the magnitude of the non-cardia
association may be underestimated
A prospective study of the relationship between prediagnostic Human Papillomavirus seropositivity and HPV DNA in subsequent cervical carcinomas
Several prospective studies with invasive carcinoma as endpoint have supported Human Papillomavirus as a cause of cervical carcinoma. However, the largest study used seroepidemiology and did not analyse presence of Human Papillomavirus DNA in the subsequent tumour. Linkage of serum bank registries and cancer registries had identified 196 women with a registered cervical carcinoma after donation of a serum sample. For the present study, biopsies for 127 cases could be located, verified to contain invasive carcinoma and be amplified by PCR. Three control women who had remained alive and without cervical carcinoma during an equal length of follow-up had been matched to each of the case women and tested for HPV antibodies. Presence of Human Papillomavirus DNA in the tumours was analysed by general primer and type specific PCR. HPV16-seropositive women had a relative risk of 4.4 (95% CI: 2.2–8.8) to develop cervical carcinoma carrying HPV16 DNA. By contrast, there was no excess risk for Human Papillomavirus 16-seropositive women to develop cervical carcinoma devoid of HPV16 DNA. Prediagnostic HPV16 seropositivity was strongly correlated with later HPV16 DNA positivity of the tumour (P<0.001) and prediagnostic HPV18 seropositivity correlated with HPV18 DNA in the tumour (P<0.03). The link between prediagnostic seropositivity and type of viral DNA in the cancer implies that the carcinogenic effect of infection with these viruses is dependent on persistent presence of type-specific viral DNA
Human papillomavirus infection as a risk factor for anal and perianal skin cancer in a prospective study
Human papillomavirus has emerged as the leading infectious cause of cervical and other anogenital cancers. We have studied the relation between human papillomavirus infection and the subsequent risk of anal and perianal skin cancer. A case–cohort study within two large Nordic serum banks to which about 760 000 individuals had donated serum samples was performed. Subjects who developed anal and perianal skin cancer during follow up (median time of 10 years) were identified by registry linkage with the nationwide cancer registries in Finland and Norway. Twenty-eight cases and 1500 controls were analysed for the presence of IgG antibodies to HPV 16, 18, 33 or 73, and odds ratios of developing anal and perianal skin cancer were calculated. There was an increased risk of developing anal and perianal skin cancer among subjects seropositive for HPV 16 (OR=3.0; 95%CI=1.1–8.2) and HPV 18 (OR=4.4; 95%CI=1.1–17). The highest risks were seen for HPV 16 seropositive patients above the age of 45 years at serum sampling and for patients with a lag time of less than 10 years. This study provides prospective epidemiological evidence of an association between infection with HPV 16 and 18 and anal and perianal skin cancer
BRCA1 mutations in ovarian cancer and borderline tumours in Norway: a nested case–control study
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