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Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas
Open accessAbstract
Although the MYC oncogene has been implicated in cancer, a systematic assessment of alterations of MYC, related transcription factors, and co-regulatory proteins, forming the proximal MYC network (PMN), across human cancers is lacking. Using computational approaches, we define genomic and proteomic features associated with MYC and the PMN across the 33 cancers of The Cancer Genome Atlas. Pan-cancer, 28% of all samples had at least one of the MYC paralogs amplified. In contrast, the MYC antagonists MGA and MNT were the most frequently mutated or deleted members, proposing a role as tumor suppressors. MYC alterations were mutually exclusive with PIK3CA, PTEN, APC, or BRAF alterations, suggesting that MYC is a distinct oncogenic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such as immune response and growth factor signaling; chromatin, translation, and DNA replication/repair were conserved pan-cancer. This analysis reveals insights into MYC biology and is a reference for biomarkers and therapeutics for cancers with alterations of MYC or the PMN.
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“The Myc oncogene, including its three subtypes C-Myc, N-Myc, and L-Myc, is believed to act as a transcriptional “amplifier” that can trigger a variety of oncogenic transcriptional programs in different types of cancer.410,411”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [411]
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“Overexpression or hyperactivation of Myc is one of the most common occurrences in cancer, making it a key factor in oncogenesis.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [411]
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“Gene ampli fi cation can result from DNA replication errors, chromosome translocations or gene rearrangements (Albertson, 2006; Beroukhim et al., 2010; Matsui et al., 2013; Schaub et al., 2018).”
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“Discussion Pan-cancer analysis can reveal similarities and differences in tumors, providing insights into cancer prevention and the design of therapeutic targets [30].”
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“Given that MYC family members are focally amplified in 28% of human cancers (87), these results have broad implications for metastasis in tumor types other than PDAC (88).”
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Self-citationMAX Functions as a Tumor Suppressor and Rewires Metabolism in Small Cell Lung Cancer
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“The MYC oncogene is part of the gene superfamily, and its product is commonly activated in human cancers (94, 95).”
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“c-MYC is a strong oncogenic driver in many cancers including acute leukemia [79].”
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“Notably, chr8 harbors the MYC gene, which is one of the most frequently amplified genes in human cancers (17), whereas chr17 contains the ERBB2 gene, which is amplified in about 20% of all invasive breast cancers (18).”
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“Genomic and proteomic features associated with MYC and the proximal MYC network were defined across the 33 cancers of TCGA by using computational approaches [8].”
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“A recent systematic genomic analysis has demonstrated that altered expression and mutations in other members of this network expand the range of tumors in which MYC function is perturbed (Schaub et al. 2018).”
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Two diphosphorylated degrons control c-Myc degradation by the Fbw7 tumor suppressor
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“A recent analysis of TCGA revealed that gene amplification of Myc paralogs occurs in 28% of samples analyzed, spanning the 33 solid cancer types available in TCGA, emphasizing the importance of this genetic alteration in tumorigenesis (Schaub et al., 2018).”
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Self-citationWidespread hypertranscription in aggressive human cancers
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“Indeed, common genetic alterations such as amplification of the MYC oncogenes, (~28% pan-cancer) [15], mutations of the RAS family (~16% of cancers) [22], or alterations of tumor suppressor genes such as TP53 (mutated in 50% of cancers) [23] are difficult to target directly and currently lack FDA approved drugs.”
BackgroundSelf-citationRethinking glutamine metabolism and the regulation of glutamine addiction by oncogenes in cancer
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Self-citationGenetic and Environmental Determinants of Immune Response to Cutaneous Melanoma
Poźniak, J., Nsengimana, J., Laye, J. P., O'Shea, S. J., Diaz, J. M. S., Droop, A., Filia, A., Harland, M., Davies, J. R., Mell, T., et al. (2019) · Cancer Research · doi:10.1158/0008-5472.can-18-2864 · Cited by 51
“MYC is a proproliferative oncogene, which has in recent years been reported to have various immunosuppressive functions (27, 35, 36, 37), and to have specific involvement in melanoma metastasis and invasiveness (38).”
BackgroundGanci, F., Pulito, C., Valsoni, S., Sacconi, A., Turco, C., Vahabi, M., Manciocco, V., Mazza, E. M. C., Meens, J., Karamboulas, C., et al. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-2485 · Cited by 51
“MYC oncoproteins in solid tumors are frequently activated by copy gains but may be also induced by a variety of other mechanisms (24); importantly, it is well established that even small changes in MYC levels can drive ectopic proliferation of somatic cells and oncogenesis (25–27).”
BackgroundMYC in liver cancer: mechanisms and targeted therapy opportunities
Liu, F., Liao, Z., & Zhang, Z. (2023) · Oncogene · doi:10.1038/s41388-023-02861-w · Cited by 53
“This balance process is disrupted in tumor development since ampli fi cation of MYC and loss of MXD family genes occur during tumorigenesis, leading to the magni fi cation of MYC function [46].”
BackgroundTurning Up the Heat on MYC: Progress in Small-Molecule Inhibitors
Truica, M. I., Burns, M. C., Han, H., & Abdulkadir, S. A. (2020) · Cancer Research · doi:10.1158/0008-5472.can-20-2959 · Cited by 51
“Cancer Res; 81(2) January 15, 2021 CANCER RESEARCH 250”
BackgroundInfluentialMYC-induced metabolic stress and tumorigenesis
Wolpaw, A. J., & Dang, C. V. (2018) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2018.05.003 · Cited by 52
TFEB Links MYC Signaling to Epigenetic Control of Myeloid Differentiation and Acute Myeloid Leukemia
Yun, S., Vincelette, N. D., Yu, X., Watson, G. W., Fernandez, M. R., Yang, C., Hitosugi, T., Cheng, C., Freischel, A. R., Zhang, L., et al. (2020) · Blood Cancer Discovery · doi:10.1158/2643-3230.bcd-20-0029 · Cited by 51
“Among these, MYC gene amplification, copy-number variation, and somatic mutations are frequent in both adult and pediatric AML (1, 3, 4).”
BackgroundSelf-citationWoo, X. Y., Srivastava, A., Graber, J. H., Yadav, V. K., Sarsani, V., Simons, A., Beane, G., Grubb, S. C., Ananda, G., Liu, R., et al. (2019) · BMC Medical Genomics · doi:10.1186/s12920-019-0551-2 · Cited by 48
Singh, S. P., Bhaskar, R., Ghosh, S., Yarlagadda, B., Singh, D. K. K., Verma, P., Sengupta, S., Mladenov, M. I., Hadzi‐Petrushev, N., Stojchevski, R., et al. (2025) · Cancers · doi:10.3390/cancers17071082 · Cited by 63
“…mechanisms, with nuances observed across di ff erent cancer types [17,20]. mechanisms, with nuances observed across different cancer types [17,20] For example, MYC amplification is particularly common in breast cancer, neuroblastoma and For example, MYC ampli fi cation is particularly common…”
Evolution and structure of clinically relevant gene fusions in multiple myeloma
Foltz, S. M., Gao, Q., Yoon, C. J., Sun, H., Yao, L., Li, Y., Jayasinghe, R. G., Cao, S., King, J. A., Kohnen, D. R., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-16434-y · Cited by 48
Self-citationNovel insights in cell cycle dysregulation during prostate cancer progression
Ben‐Salem, S., & Venkadakrishnan, V. B. (2021) · Endocrine Related Cancer · doi:10.1530/erc-20-0517 · Cited by 52
“Amplification of the gene encoding MYC is frequently observed in human cancers ((Dang et al., 2006, Schaub et al., 2018).”
BackgroundProtein phosphatase 2A activation as a therapeutic strategy for managing MYC-driven cancers
Farrington, C. C., Yuan, E., Mazhar, S., Izadmehr, S., Hurst, L., Allen-Petersen, B. L., Janghorban, M., Chung, E. M., Wolczanski, G., Galsky, M. D., et al. (2020) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)49933-9 · Cited by 47
Tilting MYC toward cancer cell death
Harrington, C. T., Sotillo, E., Dang, C. V., & Thomas‐Tikhonenko, A. (2021) · Trends in cancer · doi:10.1016/j.trecan.2021.08.002 · Cited by 48
A panel of noncoding RNAs in non–small‐cell lung cancer
Bagheri, A., Khorshid, H. R. K., Tavallaie, M., Mowla, S. J., Sherafatian, M., Rashidi, M., Zargari, M., Boroujeni, M. E., & Hosseini, S. M. (2018) · Journal of Cellular Biochemistry · doi:10.1002/jcb.28111 · Cited by 46
Somatic selection distinguishes oncogenes and tumor suppressor genes
Chandrashekar, P. B., Ahmadinejad, N., Wang, J., Sekulić, A., Egan, J. B., Asmann, Y. W., Kumar, S., Maley, C. C., & Liu, L. (2019) · Bioinformatics · doi:10.1093/bioinformatics/btz851 · Cited by 45
Self-citationLlabata, P., Mitsuishi, Y., Choi, P. S., Cai, D., Francis, J. M., Torres-Diz, M., Udeshi, N. D., Golomb, L., Wu, Z., Zhou, J. R., et al. (2019) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-19-0657 · Cited by 43
“The activity of the MYC protein is tightly regulated by a protein interaction network that is centered on the MAX protein (10).”
BackgroundInfluentialSelf-citationAn MXD1-derived repressor peptide identifies noncoding mediators of MYC-driven cell proliferation
Raffeiner, P., Hart, J. R., García-Caballero, D., Bar‐Peled, L., Weinberg, M. S., & Vogt, P. K. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1921786117 · Cited by 43
“A recent study found that across the 33 tumor types included in The Cancer Genome Atlas, 28% have amplifications of at least one of the MYC paralogs (4).”
BackgroundDerakhshani, A., Rostami, Z., Safarpour, H., Shadbad, M. A., Nourbakhsh, N. S., Argentiero, A., Taefehshokr, S., Tabrizi, N. J., Kooshkaki, O., Astamal, R. V., et al. (2021) · Molecules · doi:10.3390/molecules26082278 · Cited by 43
“Studies demonstrate that ovarian cancer and breast cancer cells highly depend on Myc for maintaining their tumoral growth, which can serve as a valuable target for the treatment of affected patients [26].”
BackgroundPan, S., Sun, S., Liu, B., & Hou, Y. (2022) · Journal of Translational Internal Medicine · doi:10.2478/jtim-2022-0013 · Cited by 42
Ribosome-Directed Therapies in Cancer
Temaj, G., Chichiarelli, S., Eufemi, M., Fabio Altieri, F., Hadžiselimović, R., Farooqı, A. A., Yaylım, İ., & Saso, L. (2022) · Biomedicines · doi:10.3390/biomedicines10092088 · Cited by 40
Mathsyaraja, H., Catchpole, J., Freie, B. W., Eastwood, E., Babaeva, E., Geuenich, M., Cheng, P. F., Ayers, J., Yu, M., Wu, N., et al. (2021) · eLife · doi:10.7554/elife.64212 · Cited by 40
Self-citationEmerging Pharmacotherapeutic Strategies to Overcome Undruggable Proteins in Cancer
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“Overall, N-MYC and L-MYC are reportedly amplified in less than 7% of cancers[79], whereas C-MYC is amplified in 21%[87].”
BackgroundSelf-citationVilar, J. B., Christmann, M., & Tomicic, M. T. (2022) · Cancers · doi:10.3390/cancers14102416 · Cited by 41
Tang, M., O’Grady, S., Crown, J. P., & Duffy, M. J. (2022) · Breast Cancer Research and Treatment · doi:10.1007/s10549-022-06673-6 · Cited by 39
Transcription factor RFX7 governs a tumor suppressor network in response to p53 and stress
Coronel, L., Riege, K., Schwab, K., Förste, S., Häckes, D., Semerau, L., Bernhart, S. H., Siebert, R., Hoffmann, S., & Fischer, M. (2021) · Nucleic Acids Research · doi:10.1093/nar/gkab575 · Cited by 39
“0 1000 2000 3000 Time since diagnosis (days) Su rv iv al p ro ba bi lit y low (61) medium (60) high (61) TCGA-PAAD +++++ ++ + ++++ ++++++++++++++ ++ ++ + ++ + + ++ + ++ ++ + + +++ + + + ++ + +++ + ++++++++++++++ + ++++ + + +++ ++ +++ ++ ++ + + +”
Sheikh‐Zeineddini, N., Bashash, D., Safaroghli‐Azar, A., Riyahi, N., Shabestari, R. M., Janzamin, E., & Safa, M. (2019) · Journal of Cellular Biochemistry · doi:10.1002/jcb.28675 · Cited by 38
“participation in cancer pathogenesis, most studies only focused on the interconnection of this factor with varied intra‐ and extracellular programs, considering this protein as an intermediate molecule.(2) The first breakthrough in the identification of a leading role for c‐Myc in the initiation of ALL placed this mol…”
BackgroundProtein phosphatase 2A activation as a therapeutic strategy for managing MYC-driven cancers
Farrington, C. C., Yuan, E., Mazhar, S., Izadmehr, S., Hurst, L., Allen-Petersen, B. L., Janghorban, M., Chung, E. M., Wolczanski, G., Galsky, M. D., et al. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra119.011443 · Cited by 42
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MYC the oncogene from hell: Novel opportunities for cancer therapy
Papadimitropoulou, A., Makri, M., & Zoidis, G. (2024) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2024.116194 · Cited by 40
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Yang, D., Liu, M., Jiang, J., Luo, Y., Wang, Y., Chen, H., Li, D., Wang, D., Wang, D., & Chen, H. (2022) · Cancers · doi:10.3390/cancers14246220 · Cited by 36
“TCGA analyzes 33 common tumor types using multi-omics data, offering the opportunity to uncover molecular aberrations across cancer types [34,35].”
BackgroundHe, J., McLaughlin, R. P., van der Beek, L., Canisius, S., Wessels, L. F. A., Smid, M., Martens, J. W. M., Foekens, J. A., Zhang, Y.-H., & van de Water, B. (2020) · Oncogene · doi:10.1038/s41388-020-1279-3 · Cited by 36
Zañudo, J. G. T., Mao, P., Alcon, C., Kowalski, K. J., Johnson, G. N., Xu, G., Baselga, J. M., Scaltriti, M., Letai, A. G., Montero, J., et al. (2021) · Cancer Research · doi:10.1158/0008-5472.can-21-1208 · Cited by 37
Metadata
- Authors
- Schaub, F. X., Dhankani, V., Berger, A. C., Trivedi, M., Richardson, A. B., Shaw, R., Zhao, W., Zhang, X., Ventura, A., Liu, Y., Ayer, D. E., Hurlin, P. J., Cherniack, A. D., Eisenman, R. N., Bernard, B., Grandori, C., Caesar-Johnson, S. J., Demchok, J. A., Felau, I., Kasapi, M., Ferguson, M. L., Hutter, C. M., Sofia, H. J., Tarnuzzer, R., Wang, Z., Yang, L., Zenklusen, J. C., Zhang, J. (., Chudamani, S., Liu, J., Lolla, L., Naresh, R., Pihl, T., Sun, Q., Wan, Y., Wu, Y., Cho, J., DeFreitas, T., Frazer, S., Gehlenborg, N., Getz, G., Heiman, D. I., Kim, J., Lawrence, M. S., Lin, P., Meier, S., Noble, M. S., Saksena, G., Voet, D., Zhang, H., Bernard, B., Chambwe, N., Dhankani, V., Knijnenburg, T., Kramer, R., Leinonen, K., Liu, Y., Miller, M., Reynolds, S., Shmulevich, I., Thorsson, V., Zhang, W., Akbani, R., Broom, B. M., Hegde, A. M., Ju, Z., Kanchi, R. S., Korkut, A., Li, J., Liang, H., Ling, S., Liu, W., Lu, Y., Mills, G. B., Ng, K.-S., Rao, A., Ryan, M., Wang, J., Weinstein, J. N., Zhang, J., Abeshouse, A., Armenia, J., Chakravarty, D., Chatila, W. K., de Bruijn, I., Gao, J., Gross, B. E., Heins, Z. J., Kundra, R., La, K., Ladanyi, M., Luna, A., Nissan, M. G., Ochoa, A., Phillips, S. M., Reznik, E., Sanchez-Vega, F., Sander, C., Schultz, N., Sheridan, R., Sumer, S. O., Sun, Y., Taylor, B. S., Wang, J., Zhang, H., Anur, P., Peto, M., Spellman, P., Benz, C., Stuart, J. M., Wong, C. K., Yau, C., Hayes, D. N., Parker, J. S., Wilkerson, M. D., Ally, A., Balasundaram, M., Bowlby, R., Brooks, D., Carlsen, R., Chuah, E., Dhalla, N., Holt, R., Jones, S. J. M., Kasaian, K., Lee, D., Ma, Y., Marra, M. A., Mayo, M., Moore, R. A., Mungall, A. J., Mungall, K., Robertson, A. G., Sadeghi, S., Schein, J. E., Sipahimalani, P., Tam, A., Thiessen, N., Tse, K., Wong, T., Berger, A. C., Beroukhim, R., Cherniack, A. D., Cibulskis, C., Gabriel, S. B., Gao, G. F., Ha, G., Meyerson, M., Schumacher, S. E., Shih, J., Kucherlapati, M. H., Kucherlapati, R. 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- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Broad Institute (US)
- Memorial Sloan Kettering Cancer Center (US)
- University of Utah (US)
- Oregon Health & Science University (US)
- Fred Hutch Cancer Center (US)
- Corresponding author
- Grandori, Carla
- ORCID
- Schaub, Franz X.
- Richardson, Anne B.
- Shaw, Reid
- Zhao, Wei
- Zhang, Xiaoyang
- Ventura, Andrea
- Ayer, Donald E.
- Hurlin, Peter J.
- Eisenman, Robert N.
- Grandori, Carla
- Felau, Ina
- Kasapi, Melpomeni
- Ferguson, Martin L.
- Sofia, Heidi J.
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- Ma, Deqin
- Milhem, Mohammed
- Godwin, Andrew K.
- Madan, Rashna
- Adebamowo, Clement
- Adebamowo, Sally N.
- Boussioutas, Alex
- Beer, David
- Giordano, Thomas
- Bocklage, Therese
- Landrum, Lisa
- Moxley, Katherine
- Walker, Joan
- Zuna, Rosemary
- Feldman, Michael
- Dhir, Rajiv
- Luketich, James
- Carlotti, Carlos Gilberto
- Kemp, Rafael
- Tirapelli, Daniela
- Catto, James
- Swisher, Elizabeth
- Creaney, Jenette
- Robinson, Bruce
- Shelley, Carl Simon
- Bradford, Carol
- Carey, Thomas
- Prince, Mark
- Rozek, Laura
- Wolf, Gregory
- Fong, Kwun M.
- Yang, Ian
- Rathmell, W. Kimryn
- Kovatich, Albert J.
- Shriver, Craig D.
- DiPersio, John
- Drake, Bettina
- Govindan, Ramaswamy
- Heath, Sharon
- Ley, Timothy
- Rubin, Mark A.
- Lee, Jung Il
- Aredes, Natália D.
- Mariamidze, Armaz
- Venue
- Cell Systems
- Publisher
- Elsevier BV
- Published
- 2018-03
- Volume
- 6
- Issue
- 3
- Pages
- 282-300.e2
- ISSN
- 2405-4712 (ISSN-L)
- PMC
- PMC5892207
- OpenAlex
- W2795073885
- Cited by
- 431
- References
- 112
- Citations by year
- 2026: 36 · 2025: 56 · 2024: 62 · 2023: 53 · 2022: 58 · 2021: 63 · 2020: 57 · 2019: 33 · 2018: 13
- FWCI
- 12.55
- Type
- journal article
- Language
- en
- Open access
- hybrid
- dx.doi.org
- Licence
- Locations
- Cell Systems (publishedVersion, cc-by)
- UWA Profiles and Research Repository (UWA) (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, other-oa)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Bern Open Repository and Information System (University of Bern) (submittedVersion, cc-by)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- Utrecht University Repository (Utrecht University) (submittedVersion, other-oa)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Florence Research (University of Florence) (submittedVersion, cc-by-nc-nd)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion, other-oa)
- Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion, other-oa)
- Spiral (Imperial College London) (submittedVersion, cc-by-nc-nd)
- Open Access CRIS of the University of Bern
- Funders
- NIH (4U01CA176303-04, U24CA143867, RO1CA57138, 5R01CA149707)
- SEngine Precision Medicine
- Cure First
- Shriners Hospitals for Children and Leukemia and Lymphoma Society
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- MYC oncogene, MGA, medical nutrition therapy, tumor suppressor, oncogenic drivers, MYC transcription factors, pan-cancer analysis, PIK3CA, PTEN, APC, BRAF, tumor subtypes, immune response, growth factor signaling, chromatin, translation (biology), DNA replication and repair, biomarkers, cancer therapeutics
- MeSH terms
- Chromatin, Humans, Neoplasms, Oncogenes, Repressor Proteins, Transcription Factors, Biomarkers, Tumor, Signal Transduction, Genes, myc, Proto-Oncogene Proteins c-myc, Computational Biology, Genomics, Proteomics, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Basic Helix-Loop-Helix Transcription Factors, Basic Helix-Loop-Helix Proteins, Carcinogenesis
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