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At least 1,297 records · Page 72Linked to original sources
PubMed1982

Genetics of teratocarcinoma transplantation. III. Genetic control of resistance to F9 tumor formation in allogeneic hosts.

Major F9 allograft resistance of strains C57Bl/6J, CBA/J, C3H/He and AKR/J has been shown to be controlled by a small number of recessive genes. These loci are not linked to H-2. Recombinational analysis suggests that the loci responsible for resistance in these strains are at least partially non-overlapping. These results obtained with the blocked F9 embryonal carcinoma cell line are discussed in relation to those reported for embryonal carcinoma strain PCC3/A/l and OTT6050 embryoid bodies, where recessive resistance is H-2 linked.

Animals↗
PubMed2006

Implications of small effect sizes of individual genetic variants on the design and interpretation of genetic association studies of complex diseases.

Accumulated evidence from searching for candidate gene-disease associations of complex diseases can offer some insights as the field moves toward discovery-oriented approaches with massive genome-wide testing. Meta-analyses of 50 non-human lymphocyte antigen gene-disease associations with documented overall statistical significance (752 studies) show summary odds ratios with a median of 1.43 (interquartile range, 1.28-1.65). Many different biases may operate in this field, for both single studies and meta-analyses, and these biases could invalidate some of these seemingly "validated" associations. Studies with a sample size of >500 show a median odds ratio of only 1.15. The median sample size required to detect the observed summary effects in each population addressed in the 752 studies is estimated to be 3,535 (interquartile range, 1,936-9,119 for cases and controls combined). These estimates are steeply inflated in the presence of modest bias. Population heterogeneity, as well as gene-gene and gene-environment interactions, could steeply increase these estimates and may be difficult to address even by very large biobanks and observational cohorts. The one visible solution is for a large number of teams to join forces on the same research platforms. These collaborative studies ideally should be designed up front to also assess more complex gene-gene and gene-environment interactions.

Alleles↗