AACR Project GENIE: Powering Precision Medicine through an International Consortium
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Abstract
The AACR Project GENIE is an international data-sharing consortium focused on generating an evidence base for precision cancer medicine by integrating clinical-grade cancer genomic data with clinical outcome data for tens of thousands of cancer patients treated at multiple institutions worldwide. In conjunction with the first public data release from approximately 19,000 samples, we describe the goals, structure, and data standards of the consortium and report conclusions from high-level analysis of the initial phase of genomic data. We also provide examples of the clinical utility of GENIE data, such as an estimate of clinical actionability across multiple cancer types (>30%) and prediction of accrual rates to the NCI-MATCH trial that accurately reflect recently reported actual match rates. The GENIE database is expected to grow to >100,000 samples within 5 years and should serve as a powerful tool for precision cancer medicine. Significance: The AACR Project GENIE aims to catalyze sharing of integrated genomic and clinical datasets across multiple institutions worldwide, and thereby enable precision cancer medicine research, including the identification of novel therapeutic targets, design of biomarker-driven clinical trials, and identification of genomic determinants of response to therapy. Cancer Discov; 7(8); 818–31. ©2017 AACR. See related commentary by Litchfield et al., p. 796. This article is highlighted in the In This Issue feature, p. 783
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KRAS is the oncogenic protein most often altered in solid tumours.
“Despite being the most frequently altered oncogenic protein in solid tumours, KRAS has historically been considered ‘undruggable’”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [16]
About 20% of all malignancies have a RAS abnormality, and about 17% of solid tumours have KRAS mutations, including about 90% of pancreatic, 50% of colon and 25% of lung adenocarcinomas.
“each dataset indicates that ~20% of all malignancies have a RAS abnormality. Overall, ~17% of solid tumours have KRAS mutations, including ~90% of pancreatic, ~50% of colon and ~25% of lung adenocarcinomas16,17”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [16]
KRAS is among the most frequently mutated oncogenes in human cancer.
“KRAS is the most frequently mutated oncogene”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [5]
About one in seven human cancers carry a KRAS alteration.
“approximately one in seven of all human cancers harbor KRAS (Kirsten rat sarcoma virus) alterations”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [5]
Based on AACR GENIE release 9.0-public, up to 210,000 new annual US diagnoses across non-hematological cancers have KRAS alterations.
“we estimate up to 210,000 new annual diagnoses/patients showing alterations in KRAS in the US across all non-hematological cancers, weighting by their respective baseline incidence rates.”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [5]
TP53 co-mutation frequency is comparable in non-G12C KRAS-mutated NSCLC (32-35%), while STK11 (G12C 23%, G12D 14%) and KEAP1 (G12C 8%, G12D 4%) differ.
“While the frequency of TP53 co-occurring mutations is comparable in non-G12C-KRAS mutated NSCLC (32%−35%), differences can be observed for the tumor suppressors STK11 (co-mutation rates: G12C, 23%; G12D, 14%) and KEAP1 (co-mutation rates: G12C, 8%; G12D, 4%).”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [5]
Non-G12C KRAS mutant NSCLC tumors differ from KRASG12C-mutated lung cancers in co-mutation of tumor suppressor genes.
“Non-G12C KRAS mutant NSCLC tumors are distinct from KRASG12C-mutated lung cancers in terms of co-mutation of tumor suppressor genes.”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [5]
In mouse models, combined PI3K and MEK inhibition has been reported to treat KRAS-driven lung cancers.
“For example, using a combination of PI3K and MEK inhibitors has been shown to treat KRAS-driven lung cancers in mouse models149.”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [149]
The digitalization of oncology, including electronic medical records, radiology and pathology imaging, and routine genomic profiling, is advancing but is uneven across data types and clinical sites.
“This includes the storage of patient data in electronic medical record (EMR) systems, the digitization of radiology and pathology imaging (3), and the increasing adoption of routine genomic profiling (4).”
From Artificial Intelligence in Oncology: Current Landscape, Challenges, and Future Directions (2024) · cites this paper as [4]
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Thought leader perspectives on benefits and harms in precision medicine research
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HER3 Alterations in Cancer and Potential Clinical Implications
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- Authors
- The AACR Project GENIE Consortium, The AACR Project GENIE Consortium, André, F., Arnedos, M., Baras, A. S., Baselga, J., Bedard, P. L., Berger, M. F., Bierkens, M., Calvo, F., Cerami, E., Chakravarty, D., Dang, K. K., Davidson, N. E., Del Vecchio Fitz, C., Dogan, S., DuBois, R. N., Ducar, M. D., Futreal, P. A., Gao, J., Garcia, F., Gardos, S., Gocke, C. D., Gross, B. E., Guinney, J., Heins, Z. J., Hintzen, S., Horlings, H., Hudeček, J., Hyman, D. M., Kamel-Reid, S., Kandoth, C., Kinyua, W., Kumari, P., Kundra, R., Ladanyi, M., Lefebvre, C., LeNoue-Newton, M. L., Lepisto, E. M., Levy, M. A., Lindeman, N. I., Lindsay, J., Liu, D., Lu, Z., MacConaill, L. E., Maurer, I., Maxwell, D. S., Meijer, G. A., Meric-Bernstam, F., Micheel, C. M., Miller, C., Mills, G., Moore, N. D., Nederlof, P. M., Omberg, L., Orechia, J. A., Park, B. H., Pugh, T. J., Reardon, B., Rollins, B. J., Routbort, M. J., Sawyers, C. L., Schrag, D., Schultz, N., Shaw, K. R. M., Shivdasani, P., Siu, L. L., Solit, D. B., Sonke, G. S., Soria, J. C., Sripakdeevong, P., Stickle, N. H., Stricker, T. P., Sweeney, S. M., Taylor, B. S., ten Hoeve, J. J., Thomas, S. B., Van Allen, E. M., Van 'T Veer, L. J., van de Velde, T., van Tinteren, H., Velculescu, V. E., Virtanen, C., Voest, E. E., Wang, L. L., Wathoo, C., Watt, S., Yu, C., Yu, T. V., Yu, E., Zehir, A., & Zhang, H.
- ORCID
- André, Fabrice
- Baras, Alexander S.
- Bedard, Philippe L.
- Berger, Michael F.
- Bierkens, Mariska
- Calvo, Fabien
- Cerami, Ethan
- Chakravarty, Debyani
- Dang, Kristen K.
- Davidson, Nancy E.
- DuBois, Raymond N.
- Ducar, Matthew D.
- Futreal, P. Andrew
- Gao, Jianjiong
- Gocke, Christopher D.
- Gross, Benjamin E.
- Guinney, Justin
- Heins, Zachary J.
- Horlings, Hugo
- Hudeček, Jan
- Hyman, David M.
- Kandoth, Cyriac
- Kumari, Priti
- Kundra, Ritika
- Ladanyi, Marc
- LeNoue-Newton, Michele L.
- Lepisto, Eva M.
- Levy, Mia A.
- Lindeman, Neal I.
- Lindsay, James
- Liu, David
- Lu, Zhibin
- MacConaill, Laura E.
- Maxwell, David S.
- Meijer, Gerrit A.
- Micheel, Christine M.
- Mills, Gordon
- Nederlof, Petra M.
- Omberg, Larsson
- Park, Ben Ho
- Pugh, Trevor J.
- Reardon, Brendan
- Rollins, Barrett J.
- Routbort, Mark J.
- Sawyers, Charles L.
- Schrag, Deborah
- Schultz, Nikolaus
- Shaw, Kenna R Mills
- Siu, Lillian L.
- Solit, David B.
- Sonke, Gabe S.
- Soria, Jean Charles
- Stickle, Natalie H.
- Stricker, Thomas P.
- Sweeney, Shawn M.
- Taylor, Barry S.
- Thomas, Stacy B.
- Velculescu, Victor E.
- Virtanen, Carl
- Voest, Emile E.
- Wang, Lucy L.
- Yu, Celeste
- Yu, Thomas V.
- Zehir, Ahmet
- Zhang, Hongxin
- Venue
- Cancer Discovery
- Published
- 2017-08-01
- Volume
- 7
- Issue
- 8
- Pages
- 818-831
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC5611790
- OpenAlex
- W3217485783
- Cited by
- 1,964
- References
- 28
- Citations by year
- 2026: 166 · 2025: 238 · 2024: 310 · 2023: 335 · 2022: 295 · 2021: 248 · 2020: 196 · 2019: 90 · 2018: 67 · 2017: 19
- FWCI
- 34.54
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- American Association for Cancer Research
- New York Genome Center
- National Institutes of Health (5r01ca121113-15)
- National Human Genome Research Institute (U54HG008100)
- National Cancer Institute (R01CA182587, K08CA188615, P50CA098258, R01-CA121113, U24CA210950, U01CA168394, R01CA190642, U01CA217842, U24CA209851, U10CA180950, P50CA083639, P30CA008748, P30CA016672, P30CA068485, P30CA006973, P30CA006516)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomics and Rare Diseases
- Keywords
- AACR Project GENIE, precision oncology, clinical actionability, NCI-MATCH trial, therapeutic target, biomarker-driven clinical trials, data standards
- MeSH terms
- Humans, Neoplasms, Databases, Factual, Genomics, Information Dissemination, Precision Medicine
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