Laura Riva
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
Laura Riva has a total of 297 co-authors. Here are the top co-authors by number of shared publications:
- Allan Balmain
Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California
16 shared publications - Giorgio E. M. Melloni
TIMI Study Group, Brigham and Women’s Hospital, Harvard Medical School, Boston, USA
16 shared publications - Ludmil B. Alexandrov
University of California San Diego
16 shared publications - Lucilla Luzi
Department of Experimental Oncology, European Institute of Oncology, Milan, Italy
15 shared publications - Pier Giuseppe Pelicci
European Institute of Oncology (IEO) IRCCS, Milan, Italy
15 shared publications - Di Wu
Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, USA
14 shared publications
Latest Publications
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 6 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Inflammation is the time limiting step in tumorigenesis in LGR5/6-Cre activated KRAS/HRAS mouse
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 6 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Inflammation is the time limiting step in tumorigenesis in LGR5/6-Cre activated KRAS/HRAS mouse
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Summary of SNV mutations observed by tumor model and subgroup
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Summary of SNV mutations observed by tumor model and subgroup
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 4 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Inflammation-driven mutations may be associated with timing of exposure during development
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 4 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Inflammation-driven mutations may be associated with timing of exposure during development
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Dinucleotide and insertion-deletion mutational signatures observed across the samples
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Dinucleotide and insertion-deletion mutational signatures observed across the samples
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 8 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Recurrently observed driver mutations and co-mutation frequencies
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 8 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Recurrently observed driver mutations and co-mutation frequencies
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Dataset from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
List of top differentially expressed genes in the high versus low BMI tumor study
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Dataset from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
List of top differentially expressed genes in the high versus low BMI tumor study
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 9 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Structural variants identified by whole genome sequencing
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 9 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Structural variants identified by whole genome sequencing
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 2 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Using pentanucleotide signature to define novel DMBA signature
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 2 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Using pentanucleotide signature to define novel DMBA signature
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Correlation between total mutational load and clock/clock-like mutational signatures
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Correlation between total mutational load and clock/clock-like mutational signatures
- Open Access
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 7 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Driver mutations observed in chemically induced tumors or spontaneously derived tumors
- 3 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 7 from Long-Term Latency of Highly Mutated Cells in Normal Mouse Skin Is Reversed by Exposure to Tumor Promoters and Chronic Tissue Damage
Driver mutations observed in chemically induced tumors or spontaneously derived tumors