Evidence map›Paper›PMID 42521252›Full record

ArticleCancer science2026

Nicotinic Acid Restriction Enhances the Therapeutic Benefit of NAMPT Inhibition in Small-Cell Lung Cancer Models.

Kyoji Tsurumi, Miyuki Nomura, Mai Ouchi, Shigehiro Yagishita, Naohiko Kikuchi, Taku Sato, Mami Morita, Yoji Yamashita, Kayoko Hayashi, Tomoyoshi Soga and 3 more

Abstract read
In one paragraph

Article in Cancer science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Kyoji TsurumiDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.
Miyuki NomuraDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.
Mai OuchiDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.
Shigehiro YagishitaDivision of Molecular Pharmacology, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0002-1277-1203
Naohiko KikuchiDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.
Taku SatoDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.
Mami MoritaDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.
Yoji YamashitaDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.
Kayoko HayashiDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.
Tomoyoshi SogaHuman Biology-Microbiome-Quantum Research Center, Keio University, Tsuruoka, Japan.
Akinobu HamadaDivision of Molecular Pharmacology, National Cancer Center Research Institute, Tokyo, Japan.
Tatsuro FukuharaDepartment of Respiratory Medicine, Miyagi Cancer Center Hospital, Natori, Japan.
Nobuhiro TanumaDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, Japan.ORCID https://orcid.org/0000-0001-7914-1380

Funding

Japan Agency for Medical Research and Development 25ama221145h0001Japan Agency for Medical Research and Development 25ama221145h0002Japan Agency for Medical Research and Development JP21zf0127001Japan Science and Technology Agency JPMJCR2123Japan Society for the Promotion of Science 22K08989Japan Society for the Promotion of Science 23K07613Japan Society for the Promotion of Science 23K08577Japan Society for the Promotion of Science 23K18248Japan Society for the Promotion of Science 23K27448Japan Society for the Promotion of Science 25K12120Japan Society for the Promotion of Science 26K02285Japan Society for the Promotion of Science JP23H04939Japan Society for the Promotion of Science JP23H04946Ministry of Education, Culture, Sports, Science and TechnologyNaito FoundationPrincess Takamatsu Cancer Research FundTakeda Foundation
6 · The paper itself

Abstract

Small-cell lung cancer (SCLC) is an aggressive malignancy with limited therapeutic options. We previously showed that nicotinic acid riboside (NAR) sustains NAD biosynthesis in vivo and compensates for NAMPT inhibition in SCLC models. Here, we evaluated combining NAMPT inhibition with dietary nicotinic acid (NA) restriction to suppress NAR-dependent NAD biosynthesis. This combination showed enhanced antitumor activity consistent with synthetic lethality in SCLC CDX models and showed robust efficacy in PDX models, including those derived from chemotherapy-refractory tumors. In most CDX models examined, combination therapy showed greater antitumor activity than standard chemotherapy with cisplatin and etoposide. Although we did observe transient leukopenia, the treatment was otherwise better tolerated than chemotherapy, with less impact on body weight and platelet counts. These findings support NAD metabolism-targeted therapy as a promising strategy to treat SCLC.

Indexed as

dietary interventionmetabolismNADNAMPTsmall‐cell lung cancer

Identifiers

PMID42521252
PMCPMC13413092

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.