ArticleCancer cell2020
MAX Functions as a Tumor Suppressor and Rewires Metabolism in Small Cell Lung Cancer.
Article in Cancer cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Multiple Endocrine Neoplasia Type 5 due to Germline MAX Mutations: A Systematic Review of Tumor Spectrum and Clinical Features.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2026Pooled it
- Loss of the USP22 deubiquitylase confers resistance to chemotherapy in small cell lung cancer.Nature communications · 2026Article
- c-MYC is an aggregation-prone, amyloidogenic protein.bioRxiv : the preprint server for biology · 2026Article
- Multiple endocrine neoplasia type 5: emerging evidence and clinical perspectives.Endocrine-related cancer · 2026Review
- Probing the Structural Dynamics of the Unbound MAX Protein: Insights from Well-Tempered Metadynamics.Journal of chemical information and modeling · 2026Article
- Metabolic reprogramming and lung cancer focused on roles, mechanism, and clinical prospects of circRNAs: a narrative review.Frontiers in oncology · 2026Review
- Loss of heterozygosity and absence of MAX immunostaining in a prolactinoma associated with multiple endocrine neoplasia type 5 (MEN5).Pituitary · 2025Article
- Lineage plasticity and histological transformation: tumor histology as a spectrum.Cell research · 2025Review
- Extramedullary myeloma is genomically complex and characterized by near-universal MAPK pathway alterations.Blood advances · 2025Article
- Article
- In vivo functional screens revealScience advances · 2025Article
- MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues.Science advances · 2025Article
- Super-enhancer MYCNOS-SE promotes chemoresistance in small cell lung cancer by recruiting transcription factors CTCF and KLF15.Oncogene · 2025Article
- Selinexor as a Therapeutic Target: Advances in Non-small Cell and Small Cell Lung Cancer Treatment Strategies.Recent patents on anti-cancer drug discovery · 2025Review
- Circulating non-coding RNA biomarkers of endocrine tumours.Nature reviews. Endocrinology · 2024Review
- Childhood Multiple Endocrine Neoplasia (MEN) Syndromes: Genetics, Clinical Heterogeneity and Modifying Genes.Journal of clinical medicine · 2024Review
- Comprehensive molecular profiling of multiple myeloma identifies refined copy number and expression subtypes.Nature genetics · 2024Observational
- Article
- The transcriptional co-repressor Runx1t1 is essential for MYCN-driven neuroblastoma tumorigenesis.Nature communications · 2024Article
- Hypermethylated Colorectal Cancer Tumours Present a Myc-Driven Hypermetabolism with a One-Carbon Signature Associated with Worsen Prognosis.Biomedicines · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Small cell lung cancer (SCLC) is a highly aggressive and lethal neoplasm. To identify candidate tumor suppressors we applied CRISPR/Cas9 gene inactivation screens to a cellular model of early-stage SCLC. Among the top hits was MAX, the obligate heterodimerization partner for MYC family proteins that is mutated in human SCLC. Max deletion increases growth and transformation in cells and dramatically accelerates SCLC progression in an Rb1/Trp53-deleted mouse model. In contrast, deletion of Max abrogates tumorigenesis in MYCL-overexpressing SCLC. Max deletion in SCLC resulted in derepression of metabolic genes involved in serine and one-carbon metabolism. By increasing serine biosynthesis, Max-deleted cells exhibit resistance to serine depletion. Thus, Max loss results in metabolic rewiring and context-specific tumor suppression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.