On 5 April 2018, the US National Institute of Health (NIH) announced that the researchers funded by the NIH have completed the PanCancer Atlas, a database containing genomic and clinical information from more than 11,000 tumours representing 33 types of cancer. The results from this project have been published in 27 articles in the journals Cell, Cancer Cell, Cell Reports and Immunity.
The PanCancer Atlas is a product of The Cancer Genome Atlas (TCGA), a multi-institution collaboration initiated and supported by the US National Human Genome Research Institute (NHGRI) and the US National Cancer Institute (NCI), both part of NIH. The programme, with over 300 million USD in total funding, involved upwards of 150 researchers across North America.
The PanCancer Atlas provides a uniquely comprehensive, in-depth understanding of how, where, and why tumours arise in humans. It is an essential resource for the development of new treatments in the pursuit of precision medicine. The project focused not only on cancer genome sequencing but also on different types of data analyses, such as investigating gene and protein expression profiles and associating them with clinical and imaging data.
The PanCancer Atlas is divided into three main categories, each anchored by a summary paper that recaps the core findings of the topic. The main topics include the cell of origin, oncogenic processes, and oncogenic pathways. Multiple companion papers report in-depth explorations of individual topics within these categories.
In the first summary paper, the authors summarize the findings from a set of analyses that used molecular clustering, which groups tumours by parameters such as genes being expressed, abnormality of chromosome numbers in tumour cells, and DNA modifications. The paper’s findings suggest that tumour types cluster by their possible cells of origin, a result that adds to an understanding of how tumour tissue of origin influences a cancer’s features and could lead to more specific treatments for various cancer types.
The second summary paper presents a broad view of the TCGA findings on the processes that lead to cancer development and progression. Specifically, the authors noted that the findings identified three critical oncogenic processes: mutations, both germline (inherited) and somatic (acquired); the influence of the tumour’s underlying genome and epigenome on gene and protein expression; and the interplay of tumour and immune cells. These findings will help prioritize the development of new treatments and immunotherapies for a wide range of cancers.
The final summary paper details TCGA investigations on the genomic alterations in the signalling pathways that control cell cycle progression, cell death, and cell growth, revealing the similarities and differences in these processes across a range of cancers. Their findings reveal new patterns of cancer’s potential vulnerabilities that will aid in the development of combination therapies and personalised medicine.
The entire collection of papers comprising the PanCancer Atlas is available through a dedicated portal here.
The press release entitled NIH completes in-depth genomic analysis of 33 cancer types was originally published by the NCI. Carolyn Hutter, PhD, director of NHGRI’s Division of Genome Sciences and the NHGRI team lead for TCGA said in the press release that “TCGA was the first project of its scale to characterize – at the molecular level – cancer across a breadth of cancer types… At the project’s infancy 10 years ago, it wasn’t even possible, much less on such a scale, to do the types of characterization and analysis that were being proposed. It was a hugely ambitious project.”
As the decade-long TCGA effort wraps up, there will be a three-day symposium, TCGA Legacy: Multi-Omic Studies in Cancer, in Washington, D.C., US from 27 to 29 September 2018, that will discuss the future of large-scale cancer studies, with a session focusing on the PanCancer Atlas. The meeting will feature the latest advances on the genomic architecture of cancer and showcase recent progress toward therapeutic targeting.