Evidence map›Paper›PMID 41849351›Full record

ArticleCell reports2026

Alanine catabolism as a targetable vulnerability for MYC-driven liver cancer.

Tonatiuh Montoya, Joyce V Lee, Longhui Qiu, Abigail Krall, Nedas Matulionis, Yurim Seo, Brian N Finck, Robin K Kelley, Heather Christofk, Andrei Goga

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Tonatiuh MontoyaDepartment of Cell & Tissue Biology, University of California, San Francisco, San Francisco, CA, USA; Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, CA, USA.
Joyce V LeeDepartment of Cell & Tissue Biology, University of California, San Francisco, San Francisco, CA, USA.
Longhui QiuDepartment of Medicine, University of California, San Francisco, San Francisco, CA, USA.
Abigail KrallDepartment of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA, USA.
Nedas MatulionisDepartment of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA, USA.
Yurim SeoDepartment of Medicine, University of California, San Francisco, San Francisco, CA, USA.
Brian N FinckDepartment of Medicine, Washington University, St. Louis, MO, USA.
Robin K KelleyUCSF Helen Diller Comprehensive Cancer Center, San Francisco, CA, USA; Division of Hematology-Oncology, Department of Medicine, University of California, San Francisco, San Francisco, CA, USA.
Heather ChristofkDepartment of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA, USA.
Andrei GogaDepartment of Cell & Tissue Biology, University of California, San Francisco, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA; UCSF Helen Diller Comprehensive Cancer Center, San Francisco, CA, USA; Division of Hematology-Oncology, Department of Medicine, University of California, San Francisco, San Francisco, CA, USA. Electronic address: andrei.goga@ucsf.edu.

Funding

UCSF Liver Core CenterP30DK026743 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Holger Willenbring · 1986 to 2026
$30.7M
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Dominic N Reeds · 1999 to 2026
$30.2M
Molecular and Cellular Mechanisms in CancerT32CA108462 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOGA, ANDREI · 2004 to 2024
$10.4M
NCI NIH HHS T32 CA108462NIDDK NIH HHS P30 DK026743NIDDK NIH HHS P30 DK056341
6 · The paper itself

Abstract

Liver cancer is a leading cause of cancer-related death due to the shortage of effective therapies, and MYC overexpression defines an aggressive and difficult-to-treat subset of patients. Given MYC's ability to reprogram cancer metabolism and the liver's role in coordinating systemic metabolism, we hypothesized that MYC induces metabolic dependencies that could be targeted to attenuate tumor growth. We discovered that MYC-driven liver cancers catabolize alanine in a GPT2-dependent manner. GPT2 is the predominant alanine-catabolizing enzyme expressed in MYC-driven liver tumors and genetic ablation of GPT2 limited liver tumorigenesis. In vivo isotope tracing identified alanine as a substrate for a repertoire of pathways including the tricarboxylic acid cycle and biosynthesis. Finally, treating a MYC-driven liver tumor model with L-cycloserine diminished the frequency of mouse tumor formation and attenuated the growth of established human liver tumors. Thus, we identify a targetable metabolic dependency that MYC-driven liver tumors usurp to ensure their survival.

Indexed as

alanine metabolismCP: cancerCP: metabolismGPT2liver cancerMYC

Identifiers

PMID41849351
PMCPMC13264379

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.