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The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist. Author summary Precision oncology relies on the capability of identifying and targeting tumor-specific aberrations resulting from causative genomic alterations in each tumor. Conventional cancer driver identification methods identify candidate cancer driver genes as those exhibit an alteration frequency significantly above the expected frequency that would occur by random chance in a population of tumor samples.
This population-based nature prevents them from performing instance-specific discovery, and alteration frequency does not contain information regarding the functional impact of candidate driver genes identified in this approach. Here, we report a novel Bayesian causal discovery framework, referred to as tumor-specific causal inference TCI , which identifies candidate driver genes as the ones that bear significant functional impact on cancer-related molecular phenotypes at the individual tumor level.
By discovering candidate drivers and their function impact in each individual tumor, TCI analysis reveals information that is of value for both general cancer biology research and precision oncology.
Introduction Cancer is mainly caused by a variety of SGAs, including, but not limited to, somatic mutations SMs [ 1 , 2 ], somatic DNA copy number alterations SCNAs [ 3 , 4 ], chromosome structure variations [ 5 — 7 ], and epigenetic changes [ 8 — 10 ].
Each tumor hosts a unique combination of SGAs ranging in number from hundreds to thousands, of which only a small fraction contributes to tumorigenesis drivers , while the rest are non-consequential passengers.
Identifying causative SGAs that underlie different oncogenic processes [ 11 ], such as metastasis or immune evasion, in an individual tumor is of fundamental importance in cancer biology and precision oncology [ 12 — 14 ].
Current methods for identifying cancer driver genes concentrate on finding those that have a higher than expected mutation rate in a cohort of tumor samples [ 15 — 17 ]. Some methods focus on specific mutation sites e.
These mutation-centric, frequency-based models have successfully identified many major oncogenes and tumor suppressors across cancer types. However, they do not directly determine the functional impact of mutations, because mutation frequency of a gene either at the gene or at the specific amino acid level does not directly reflect which molecular or cellular processes will be affected by the altered gene product. Besides mutations, other SGA events affecting driver genes also contribute to cancer development, such as SCNAs [ 3 , 4 , 23 ], chromosome structure variation [ 5 — 7 ], and epigenetic changes [ 8 — 10 ].
Currently, analyses of SMs, SCNAs, structure variation, and epigenetic data are usually carried out separately, with distinct statistical models for different types of data [ 1 , 2 , 16 , 24 , 25 ]. Such disconnection is largely due to the lack of a unifying statistical framework that is able to integrate diverse data.
Integrating diverse data can provide increased statistical power to detect biological function and to gain biological insights by pooling diverse information to assess the role of a driver gene in oncogenesis. A Bayesian approach has the potential to provide such a unifying framework. Some recent studies have started to employ a Bayesian framework to infer relationships between cancer driver mutations and other omics changes, such as transcriptomic changes. Razi et al. We hold stock of over , parts ready to ship from our worldwide network of repair centres and warehouses.
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Shop by category. The inferred causal relationships are statistically robust and biologically sensible, and multiple lines of experimental evidence support the predicted functional impact of both the well-known and the novel candidate drivers that are predicted by TCI.
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