ReviewMolecular oncology2022
MYC and therapy resistance in cancer: risks and opportunities.
Review in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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
72 citing papers in PubMed, 95 citations in OpenAlex.
- Transcription factor targeting strategies in cancer: mechanisms, challenges and cutting-edge progress.Acta pharmacologica Sinica · 2026Review
- c-Medical sciences (Basel, Switzerland) · 2026Review
- A 3D Bioprinted Platform That Maintains the Functional Integrity of Primary AML Cells.Cell proliferation · 2026Article
- Single-Cell Transcriptomic Profiling Reveals Dual Antitumor and Adaptive Resistance Mechanisms of a Novel HSP90 Inhibitor, SP11, in T-Cell Acute Lymphoblastic Leukemic Cells and DLA Mouse Model.International journal of molecular sciences · 2026Article
- Article
- Comprehensive Genomic Characterization Between Urothelial Carcinoma Subtypes/Divergent Differentiation (S/DD) and Pure Urothelial Carcinoma Using a Large-Scale Japanese Genomic Panel Dataset.International journal of urology : official journal of the Japanese Urological Association · 2026Observational
- c-Myc regulated long noncoding RNA TRD-AS1 to affect the progression of oral squamous cell carcinoma.Genes & genomics · 2026Article
- Identification of Critical miRNAs miR-4652 and miR-1304 as Novel Diagnostic Markers for Oral Squamous Cell Carcinoma.Cancer reports (Hoboken, N.J.) · 2026Article
- c-MYC enhances transcription of the type 1 diabetes mellitus associated gene BATF3 via promoter binding.Scientific reports · 2026Article
- Stability of c-Myc Protein in Early S Phase Is Regulated by the Interaction with PCNA.International journal of molecular sciences · 2026Article
- Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy.Molecular therapy. Nucleic acids · 2026Article
- Mitophagy-driven multidimensional regulation of tumor immune evasion and context-dependent therapeutic strategies.Journal of translational medicine · 2026Review
- Targeting NHEJ activates STING signaling through MYC degradation to boost antitumor immunity in SCLC.Nature communications · 2026Article
- Combinatorial targeting of MYC/BCL2-associated vulnerabilities in high-grade B-cell lymphoma.British journal of haematology · 2026Article
- Epigenetic modulation in cancer drug discovery: promising targets and clinical applications.Pharmacological reports : PR · 2026Review
- Splice-switching ASOs targeting the AURKA 5' UTR collapse an SRSF1-AURKA-MYC oncogenic circuit in pancreatic cancer.Molecular cell · 2026Article
- High-throughput drug screening identifies EGFR/MAPK pathway targeting sensitivities in organoid models of ovarian carcinosarcoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Integrative Bioinformatics Reveals Novel Molecular Mechanisms and Therapeutic Targets in Acute Myeloid Leukaemia.Journal of cellular and molecular medicine · 2026Article
- MYC as a key target for melanoma therapy.Frontiers in cell and developmental biology · 2026Review
- Adenylosuccinate lyase in pancreatic ductal adenocarcinoma chemoresistance: from purine metabolism to metabolic vulnerability.Cancer drug resistance (Alhambra, Calif.) · 2026Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MYC transcription factor, encoded by the c-MYC proto-oncogene, is activated by growth-promoting signals, and is a key regulator of biosynthetic and metabolic pathways driving cell growth and proliferation. These same processes are deregulated in MYC-driven tumors, where they become critical for cancer cell proliferation and survival. As other oncogenic insults, overexpressed MYC induces a series of cellular stresses (metabolic, oxidative, replicative, etc.) collectively known as oncogenic stress, which impact not only on tumor progression, but also on the response to therapy, with profound, multifaceted consequences on clinical outcome. On one hand, recent evidence uncovered a widespread role for MYC in therapy resistance in multiple cancer types, with either standard chemotherapeutic or targeted regimens. Reciprocally, oncogenic MYC imparts a series of molecular and metabolic dependencies to cells, thus giving rise to cancer-specific vulnerabilities that may be exploited to obtain synthetic-lethal interactions with novel anticancer drugs. Here we will review the current knowledge on the links between MYC and therapeutic responses, and will discuss possible strategies to overcome resistance through new, targeted interventions.
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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.