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by nonbel
3519 days ago
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Unless I am misunderstanding something, their figure 3 seems to be plotting effect size vs p-value... So all it would be showing is that they had more data from lung adenocarcinomas (ie sample size is larger for that cancer type). It isn't 100% clear to me if they shared the data used for that figure, but here are the frequencies each cancer type appeared in table S1: Acute myeloid leukaemia (AML) Bladder
202 399
Cervix Colorectal cancer
168 559
Esophageal Adenocarcinoma Esophageal Squamous
242 292
Gastric cancer Kidney
472 257
Larynx Liver
123 392
Lung Adeno Lung Squamous
678 175
Oral cavity Ovarian cancer
363 458
Pancreas Pharynx
239 76
Small Cell Lung Cancer
148
It is essentially just figure 1 from here:
https://arxiv.org/abs/1311.0081 |
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"Comparison of overall methylation between smokers and non-smokers was performed for all tobacco-associated cancer types for which there were available data from Illumina Infinium HumanMethylation450 BeadChip array, where each array contains 473,864 autosomal CpG probes. The examined data were downloaded from the original data source (Table S1)
[...]
distributions were subsequently compared between smokers and non-smokers using a two-sample Student’s t-test. Results were considered significant for Bonferroni threshold of 10-7."
So it is not like figure one from that Lew paper, because their effect size is not normalized to the inter-individual variance. This is a point in their favor.
However, the sample sizes do match up to those found in table S1 (which I posted above). From the data provided, we cannot tell whether that difference in p-values is solely due to sample size or not. They need to tell us the variance for each CpG/tissue combo as well.