TY - JOUR
T1 - Learning to distinguish progressive and non-progressive ductal carcinoma in situ
AU - Grand Challenge PRECISION Consortium
AU - Casasent, Anna K.
AU - Almekinders, Mathilde M.
AU - Mulder, Charlotta
AU - Bhattacharjee, Proteeti
AU - Collyar, Deborah
AU - Thompson, Alastair M.
AU - Jonkers, Jos
AU - Lips, Esther H.
AU - van Rheenen, Jacco
AU - Hwang, E. Shelley
AU - Nik-Zainal, Serena
AU - Navin, Nicholas E.
AU - Wesseling, Jelle
AU - Sawyer, Elinor J.
AU - Davies, Helen R.
AU - Futreal, Andrew
AU - Navin, Nicholas E.
AU - Hwang, E. Shelley
AU - van Rheenen, Jacco
AU - Behbod, Fariba
AU - Schmidt, Marjanka
AU - Wessels, Lodewyk F.A.
AU - Rea, Daniel
AU - Stobart, Hilary
AU - Pinto, Donna
AU - Verschuur, Ellen
AU - van Oirsouw, Marja
N1 - Funding Information:
This work was supported by Cancer Research UK and by KWF Kankerbestrijding (reference C38317/A24043). A.K.C. acknowledges support from the CPRIT Single Cell Genomics Center (RP180684) for funding. N.E.N. acknowledges support from the US National Cancer Institute (RO1CA240526) and the CPRIT Single Cell Genomics Center (RP180684). E.S.H. is funded by RFA-CA-17-035 (NIH), 1505-30497 (PCORI), BCRF 19-074 (BCRF), DOD BC132057 and R01 CA185138-01. S.N.-Z. is funded by a Cancer Research UK Advanced Clinician Scientist Fellowship (C60100/A23916) and an NIHR Research Professorship (NIHR 301607) and is supported by the NIHR Cambridge Biomedical Research Centre (BRC-125-20014). D.C. is funded by the Cancer Research UK PRECISION award. E.S.H, A.M.T and D.C. are supported by the PCORI-funded COMET study through the Alliance for Clinical Trials in Oncology Foundation. J.J and J.v.R. acknowledge funding by the Oncode Institute. C.M. is supported by the AVL Donation Investment Fund of the AVL Foundation. The authors thank the Grand Challenge PRECISION Consortium Steering Group. They also thank T. Kumar and M. Edgerton from MD Anderson Cancer Center and E. J. Sawyer from King’s College London for their feedback and support in the preparation of the manuscript.
Funding Information:
This work was supported by Cancer Research UK and by KWF Kankerbestrijding (reference C38317/A24043). A.K.C. acknowledges support from the CPRIT Single Cell Genomics Center (RP180684) for funding. N.E.N. acknowledges support from the US National Cancer Institute (RO1CA240526) and the CPRIT Single Cell Genomics Center (RP180684). E.S.H. is funded by RFA-CA-17-035 (NIH), 1505-30497 (PCORI), BCRF 19-074 (BCRF), DOD BC132057 and R01 CA185138-01. S.N.-Z. is funded by a Cancer Research UK Advanced Clinician Scientist Fellowship (C60100/A23916) and an NIHR Research Professorship (NIHR 301607) and is supported by the NIHR Cambridge Biomedical Research Centre (BRC-125-20014). D.C. is funded by the Cancer Research UK PRECISION award. E.S.H, A.M.T and D.C. are supported by the PCORI-funded COMET study through the Alliance for Clinical Trials in Oncology Foundation. J.J and J.v.R. acknowledge funding by the Oncode Institute. C.M. is supported by the AVL Donation Investment Fund of the AVL Foundation. The authors thank the Grand Challenge PRECISION Consortium Steering Group. They also thank T. Kumar and M. Edgerton from MD Anderson Cancer Center and E. J. Sawyer from King’s College London for their feedback and support in the preparation of the manuscript.
Publisher Copyright:
© 2022, Springer Nature Limited.
PY - 2022/12
Y1 - 2022/12
N2 - Ductal carcinoma in situ (DCIS) is a non-invasive breast neoplasia that accounts for 25% of all screen-detected breast cancers diagnosed annually. Neoplastic cells in DCIS are confined to the ductal system of the breast, although they can escape and progress to invasive breast cancer in a subset of patients. A key concern of DCIS is overtreatment, as most patients screened for DCIS and in whom DCIS is diagnosed will not go on to exhibit symptoms or die of breast cancer, even if left untreated. However, differentiating low-risk, indolent DCIS from potentially progressive DCIS remains challenging. In this Review, we summarize our current knowledge of DCIS and explore open questions about the basic biology of DCIS, including those regarding how genomic events in neoplastic cells and the surrounding microenvironment contribute to the progression of DCIS to invasive breast cancer. Further, we discuss what information will be needed to prevent overtreatment of indolent DCIS lesions without compromising adequate treatment for high-risk patients.
AB - Ductal carcinoma in situ (DCIS) is a non-invasive breast neoplasia that accounts for 25% of all screen-detected breast cancers diagnosed annually. Neoplastic cells in DCIS are confined to the ductal system of the breast, although they can escape and progress to invasive breast cancer in a subset of patients. A key concern of DCIS is overtreatment, as most patients screened for DCIS and in whom DCIS is diagnosed will not go on to exhibit symptoms or die of breast cancer, even if left untreated. However, differentiating low-risk, indolent DCIS from potentially progressive DCIS remains challenging. In this Review, we summarize our current knowledge of DCIS and explore open questions about the basic biology of DCIS, including those regarding how genomic events in neoplastic cells and the surrounding microenvironment contribute to the progression of DCIS to invasive breast cancer. Further, we discuss what information will be needed to prevent overtreatment of indolent DCIS lesions without compromising adequate treatment for high-risk patients.
UR - http://www.scopus.com/inward/record.url?scp=85140208135&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85140208135&partnerID=8YFLogxK
U2 - 10.1038/s41568-022-00512-y
DO - 10.1038/s41568-022-00512-y
M3 - Review article
C2 - 36261705
AN - SCOPUS:85140208135
SN - 1474-175X
VL - 22
SP - 663
EP - 678
JO - Nature Reviews Cancer
JF - Nature Reviews Cancer
IS - 12
ER -