Cancer pain relief from opioids varies substantially between patients on the same dose. An explicitly exploratory 71-patient study found a candidate variant in ABAT (GABA transaminase) — reported here as a candidate needing validation, exactly as the study itself frames it, not a finding ready to guide dosing.
Cancer pain relief from opioids varies substantially between patients on the same dose — some get good relief with minimal side effects, others need much higher doses or tolerate them poorly. Understanding why matters clinically: untreated cancer pain is common, and dose titration by trial and error costs patients time spent in pain.
Yokoshima et al. 2018 ran a genome-wide association study in 71 cancer patients, rating pain before and after opioid dose increases on an 11-point scale, looking for genetic predictors of who gets good relief. They identified two candidate SNPs — one in ABAT (GABA transaminase) on chromosome 16, the variant on this page, and one on chromosome 3 — and explicitly describe both as candidate loci needing validation in larger studies, not a finding ready for clinical use. The paper's own title says "exploratory study," and this page keeps that framing rather than upgrading it.
ABAT's connection to GABA metabolism is a plausible, though unconfirmed, link to how the nervous system processes pain signals — GABA is a major inhibitory neurotransmitter, and enzymes that regulate its levels are a reasonable place to look for variation in pain processing, even though this study alone does not establish the mechanism.
Cancer pain management follows established titration protocols, adjusted by a clinician based on response and side effects — this page's variant is not used to guide dosing anywhere. It comes from a 71-patient exploratory study, described by its own authors as needing validation, not a result strong enough to act on.
A study this size is a pilot by any standard in genetics research. It is reported here because it is a real, published, peer-reviewed finding worth tracking as the field develops — not because 71 patients is enough to draw a conclusion an individual reader should act on.
OPRM1, the opioid receptor gene, has its own better-studied pharmacogenomic page elsewhere on this catalogue — a different, more established line of evidence about opioid response genetics than this exploratory finding.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Response to Opioid Analgesics in Cancer Pain comes down to these specific, well-studied positions — not a diagnosis.
ABAT · rs1641025
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Response to Opioid Analgesics in Cancer Pain. MyGeneLog™. https://www.mygenelog.com/conditions/opioid-analgesic-response-in-cancer-pain
No. It comes from a 71-patient exploratory study whose own authors describe it as a candidate needing validation, not a predictive tool. Opioid dosing follows established clinical titration protocols regardless of genotype.
Because it is a real, peer-reviewed result worth tracking as the field develops, and the paper itself is transparent about its exploratory scale — this page keeps that same framing rather than overstating it.
It encodes GABA transaminase, an enzyme involved in breaking down GABA, a major inhibitory neurotransmitter. Its link to opioid pain response is biologically plausible but not established by this study alone.
Yes — OPRM1, the opioid receptor gene, has its own page with a more established evidence base. This ABAT finding is a separate, earlier-stage line of research.
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