William Charles Hemming Cross
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
William Charles Hemming Cross has a total of 297 co-authors. Here are the top co-authors by number of shared publications:
- Trevor A. Graham
Centre for Evolution and Cancer, Institute of Cancer Research, London, UK
41 shared publications - Andrea Sottoriva
Computational Biology Research Centre, Human Technopole, Milan, Italy
37 shared publications - Giulio Caravagna
Department of Mathematics, Informatics and Geosciences, University of Trieste, Trieste, Italy
36 shared publications - Ann-Marie Baker
Centre for Evolution and Cancer, Institute of Cancer Research, London, UK
35 shared publications - Marc J. Williams
Memorial Sloan Kettering Cancer Center
34 shared publications - Chris Barnes
University College London
33 shared publications
Latest Publications
- Open Access
Protracted copy number alteration evolution in Barrett’s oesophagus leading to oesophageal cancer
Detection of copy number alterations (CNAs) in Barrett’s oesophagus (BO) predicts oesophageal adenocarcinoma (OAC) risk. When CNAs first occur is unknown. Here we show that CNAs typically form in BO many decades prior to first clinical detection of BO or cancer, and often during childhood. Using a novel molecular clock analysis, we analysed spatiotemporal longitudinal whole genome data from 80 individuals within BO surveillance. Chr 9p loss of heterozygosity (LOH) tended to be the first CNA event typically occurring at age 10-30 years. Genome doubling (GD) also typically originated multiple decades prior to cancer develop. Patients who progressed to OAC had an enrichment of CNAs late in life. CNA rate was more predictive of cancer risk than CNA burden. Analysis of OAC whole genomes confirmed the early-life origins of cancer-associated CNAs. The malignant transformation potential of BO may be set during the first decades of life, enabling early cancer interception.
Open AccessProtracted copy number alteration evolution in Barrett’s oesophagus leading to oesophageal cancer
Detection of copy number alterations (CNAs) in Barrett’s oesophagus (BO) predicts oesophageal adenocarcinoma (OAC) risk. When CNAs first occur is unknown. Here we show that CNAs typically form in BO many decades prior to first clinical detection of BO or cancer, and often during childhood. Using a novel molecular clock analysis, we analysed spatiotemporal longitudinal whole genome data from 80 individuals within BO surveillance. Chr 9p loss of heterozygosity (LOH) tended to be the first CNA event typically occurring at age 10-30 years. Genome doubling (GD) also typically originated multiple decades prior to cancer develop. Patients who progressed to OAC had an enrichment of CNAs late in life. CNA rate was more predictive of cancer risk than CNA burden. Analysis of OAC whole genomes confirmed the early-life origins of cancer-associated CNAs. The malignant transformation potential of BO may be set during the first decades of life, enabling early cancer interception.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per genomic bin copy number calls (gains=3, diploid=2, loss=1) for data presented in Figure 1.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per genomic bin copy number calls (gains=3, diploid=2, loss=1) for data presented in Figure 1.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 5 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per segment raw sWGS copy number data for patients presented in Figure 2.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 5 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per segment raw sWGS copy number data for patients presented in Figure 2.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 8 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per genomic bin copy number calls for single-cell data presented in Figure 3.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 8 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per genomic bin copy number calls for single-cell data presented in Figure 3.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 9 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Cohort information per sample for the longitudinal metastasis cohort (Figure 4), including description of organ, timepoint sampled, tumour stage at diagnosis, whether the sample is treatment naïve, if the sample was treated in the prior interval, the number of days and months elapsing since the first timepoint, in addition to per sample genomic metrics such as PGA, number of segments, patient ploidy, per sample GD classification and overall patient GD classification.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 9 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Cohort information per sample for the longitudinal metastasis cohort (Figure 4), including description of organ, timepoint sampled, tumour stage at diagnosis, whether the sample is treatment naïve, if the sample was treated in the prior interval, the number of days and months elapsing since the first timepoint, in addition to per sample genomic metrics such as PGA, number of segments, patient ploidy, per sample GD classification and overall patient GD classification.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Note on Modelling 1 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Supplementary note where we describe the gland mathematical modelling and simulations
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Note on Modelling 1 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Supplementary note where we describe the gland mathematical modelling and simulations
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 3 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Clinical information for CRC cohort presented in Figure 1.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 3 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Clinical information for CRC cohort presented in Figure 1.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 10 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per sample, per segment, raw copy number data (log2 ratios) and integer calls for the longitudinal metastasis cohort presented in Figure 4.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 10 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per sample, per segment, raw copy number data (log2 ratios) and integer calls for the longitudinal metastasis cohort presented in Figure 4.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 4 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per patient clinical information for the CRC cases presented in Figure 2.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 4 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per patient clinical information for the CRC cases presented in Figure 2.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Pairwise comparison metrics for data presented in Figure 1.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Pairwise comparison metrics for data presented in Figure 1.