Your topics. New publications.

A compact browser notification when there’s something new. At most once a day — no account needed.

What interests you?

Optional and switchable off here at any time. We save your selected topics and device subscription; no email address is required. Privacy

Search the harborEN/DEAccount
NAD⁺ & NMN
Research brief

Abstract: NMN-responsive aging pathways and inherited triple-negative breast cancer susceptibility

In this abstract-only genetic association analysis, an autophagy-related inherited expression pattern was linked to triple-negative breast cancer susceptibility, and MAP2K2 was nominated for follow-up; the authors state this does not show that NMN prevents or treats breast cancer. [1]

Automatic summary · not editorially reviewed

The key findings

  1. The analysis applied a multi-gene-set transcriptome-wide association study pipeline to overall breast cancer and triple-negative breast cancer summary statistics from Zhang et al. (2020), evaluating ten KEGG pathways nominated through 35 NMN-responsive genes. [1]

  2. Autophagy showed the strongest supported result in triple-negative breast cancer (Stouffer Z −8.98; bootstrap 95% CI −14.78 to −3.09; permutation p .0022; pathway false discovery rate .022). [1]

  3. The authors state the results do not show that NMN prevents or treats breast cancer and that gene-level colocalization, case-case analyses and functional validation are required. [1]

The source at a glance

Study type / format
Abstract of a multi-gene-set transcriptome-wide association study
Population / context
Summary statistics for overall breast cancer and triple-negative breast cancer from Zhang et al. (2020); NMN-responsive genes from long-term NMN treatment in mice.
Summary based on
Study abstract
Publication status
Preprint · peer-review status not confirmed
Original publication
September 10, 2026

NMN-responsive genes tested against breast cancer genetics

The authors asked whether pathways changed by long-term nicotinamide mononucleotide (NMN) treatment in mice overlap with inherited susceptibility to triple-negative breast cancer. They applied a multi-gene-set transcriptome-wide association study pipeline to overall breast cancer and triple-negative breast cancer summary statistics from Zhang et al. (2020). Ten full KEGG pathways nominated through 35 NMN-responsive genes were evaluated with several statistical approaches, including permutation and bootstrap confidence intervals. The abstract does not report sample sizes or the number of participants behind the summary statistics.

Supporting source [1]

Autophagy signal strongest; MAP2K2 oppositely signed

Autophagy gave the strongest supported result in triple-negative breast cancer: a Stouffer Z of −8.98, a bootstrap 95% confidence interval of −14.78 to −3.09, a permutation p value of .0022 and a pathway false discovery rate of .022. The difference between overall breast cancer and triple-negative breast cancer was consistent across 11 tissues, with a mean gap of +2.83 and the same direction in 82% of tissues. MAP2K2 appeared across autophagy, Ras/MAPK and cytoskeletal pathways and had oppositely signed associations in the two phenotypes. Endocytosis was suggestive but did not survive pathway correction; fatty-acid degradation was not enriched but showed marked cross-phenotype anticorrelation.

Supporting source [1]

Convergence claim, not evidence NMN treats cancer

The authors conclude that the results identify an autophagy-related germline expression pattern associated with triple-negative breast cancer susceptibility and nominate MAP2K2 for focused follow-up. They describe the findings as supporting cross-context convergence between NMN-responsive aging biology and breast cancer genetics. They explicitly state that the results do not show that NMN prevents or treats breast cancer. Gene-level colocalization, case-case analyses and functional validation are required. This is an abstract; the full text was not reviewed, and the associations are not causal.

Supporting source [1]

How to interpret this

Abstract only; the full text was not reviewed. Sample sizes, participant numbers and follow-up are not reported in the abstract. The findings are genetic associations, not causal effects, and the NMN link comes from long-term treatment in mice, not human evidence.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    35 NMN-responsive genes were evaluated
  2. Finding 2 ↑

    Autophagy produced the strongest supported result
  3. Finding 3 ↑

    do not show that NMN prevents

AI-assisted summary with linked source passages. No independent editorial or clinical review.

Our editorial method

Discussion

Community discussions

0 topics

Member contributions. Share sources, disclose commercial interests, and avoid personal medical or dosing advice.

Loading…