Eric A. Collisson
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
Eric A. Collisson has a total of 357 co-authors. Here are the top co-authors by number of shared publications:
- Amanda L. Koehne
Fred Hutchinson Cancer Center 6 Experimental Histopathology Seattle, Washington
20 shared publications - Emily Beirne
Department of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington
20 shared publications - Heidi L. Kenerson
Department of Surgery, University of Washington, Seattle, Washington
20 shared publications - Ian Nicholas Crispe
Department of Surgery, University of Washington, Seattle, Washington
20 shared publications - Jack Cernak
Department of Surgery, University of Washington, Seattle, Washington
20 shared publications - Jacqueline L. Mudd
Alvin J. Siteman Cancer Center, Washington University School of Medicine, St. Louis, Missouri
20 shared publications
Latest Publications
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figures1 from Efficacy of the ATR Inhibitor Ceralasertib in Patients with ARID1A-Deficient Gynecologic and Other Solid Tumor Malignancies
Supplementary Fig 1-9 with legends
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figures1 from Efficacy of the ATR Inhibitor Ceralasertib in Patients with ARID1A-Deficient Gynecologic and Other Solid Tumor Malignancies
Supplementary Fig 1-9 with legends
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from Efficacy of the ATR Inhibitor Ceralasertib in Patients with ARID1A-Deficient Gynecologic and Other Solid Tumor Malignancies
Study Representativeness Table
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from Efficacy of the ATR Inhibitor Ceralasertib in Patients with ARID1A-Deficient Gynecologic and Other Solid Tumor Malignancies
Study Representativeness Table
- 24 March 2026
- Published by American Association for Cancer Research (AACR) in Clinical Cancer Research
- p. OF1-OF9
Efficacy of the ATR Inhibitor Ceralasertib in Patients with ARID1A-Deficient Gynecologic and Other Solid Tumor Malignancies
Purpose: ARID1A is frequently mutated in cancer. Motivated by the preclinical synthetic lethality between ARID1A loss and ataxia telangiectasia and Rad3-related (ATR) inhibition, we performed an investigator-initiated phase II study of the ATR inhibitor (ATRi) ceralasertib in ARID1A-deficient solid tumors (NCT03682289). Patients and Methods: This was a phase II, Simon two-stage study with a planned sample size of 29 evaluable patients. Eligible patients had locally advanced or metastatic solid tumors with measurable disease by Response Evaluation Criteria in Solid Tumors 1.1 and radiographic progression at study entry. Patients were required to have ARID1A loss as determined by immunohistochemistry analysis of tumor tissue. Patients received ceralasertib 160 mg twice daily on days 1 to 14 every 28 days. RNA sequencing (RNA-seq) and cyclic immunofluorescence were performed on tumor tissue to identify potential biomarkers of treatment response. Results: The confirmed objective response rate (ORR) was 14% among the 29 efficacy-evaluable patients. All four responses, including three complete responses, occurred in endometrioid endometrial carcinoma or ovarian clear-cell carcinoma, with an ORR of 33% and a median duration of response of 33.7 months in this subset. Including one patient with uterine carcinosarcoma who had stable disease, the ORR was 31% among the 13 patients with gynecologic malignancies. Exploratory RNA-seq analysis of pretreatment archival tumor tissue identified upregulated G2–M checkpoint and DNA double-strand break-sensing pathways in patients who responded. Immune profiling revealed tumor immune microenvironment changes associated with the response to ceralasertib. Conclusions: Ceralasertib monotherapy demonstrated promising antitumor activity in ARID1A-deficient gynecologic malignancies. Tumor molecular and immune correlates may inform the further development of ATRis in this patient population.
- 24 March 2026
- Published by American Association for Cancer Research (AACR) in Clinical Cancer Research
- p. OF1-OF9
Efficacy of the ATR Inhibitor Ceralasertib in Patients with ARID1A-Deficient Gynecologic and Other Solid Tumor Malignancies
Purpose: ARID1A is frequently mutated in cancer. Motivated by the preclinical synthetic lethality between ARID1A loss and ataxia telangiectasia and Rad3-related (ATR) inhibition, we performed an investigator-initiated phase II study of the ATR inhibitor (ATRi) ceralasertib in ARID1A-deficient solid tumors (NCT03682289). Patients and Methods: This was a phase II, Simon two-stage study with a planned sample size of 29 evaluable patients. Eligible patients had locally advanced or metastatic solid tumors with measurable disease by Response Evaluation Criteria in Solid Tumors 1.1 and radiographic progression at study entry. Patients were required to have ARID1A loss as determined by immunohistochemistry analysis of tumor tissue. Patients received ceralasertib 160 mg twice daily on days 1 to 14 every 28 days. RNA sequencing (RNA-seq) and cyclic immunofluorescence were performed on tumor tissue to identify potential biomarkers of treatment response. Results: The confirmed objective response rate (ORR) was 14% among the 29 efficacy-evaluable patients. All four responses, including three complete responses, occurred in endometrioid endometrial carcinoma or ovarian clear-cell carcinoma, with an ORR of 33% and a median duration of response of 33.7 months in this subset. Including one patient with uterine carcinosarcoma who had stable disease, the ORR was 31% among the 13 patients with gynecologic malignancies. Exploratory RNA-seq analysis of pretreatment archival tumor tissue identified upregulated G2–M checkpoint and DNA double-strand break-sensing pathways in patients who responded. Immune profiling revealed tumor immune microenvironment changes associated with the response to ceralasertib. Conclusions: Ceralasertib monotherapy demonstrated promising antitumor activity in ARID1A-deficient gynecologic malignancies. Tumor molecular and immune correlates may inform the further development of ATRis in this patient population.
- Open Access
- 3 February 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure S10 from Intratumoral Three-Cell-Type Clusters Are a Conserved Feature of Endogenous Antitumor Immunity
Supplemental Figure S10. Role of APC:Treg:CTL three-cell-type clusters.
- 3 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure S10 from Intratumoral Three-Cell-Type Clusters Are a Conserved Feature of Endogenous Antitumor Immunity
Supplemental Figure S10. Role of APC:Treg:CTL three-cell-type clusters.
- Open Access
- 3 February 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure S11 from Intratumoral Three-Cell-Type Clusters Are a Conserved Feature of Endogenous Antitumor Immunity
Supplemental Figure S11. Correlation of spatial niches with T cell receptor repertoire clonality.
- 3 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure S11 from Intratumoral Three-Cell-Type Clusters Are a Conserved Feature of Endogenous Antitumor Immunity
Supplemental Figure S11. Correlation of spatial niches with T cell receptor repertoire clonality.
- Open Access
- 3 February 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure S5 from Intratumoral Three-Cell-Type Clusters Are a Conserved Feature of Endogenous Antitumor Immunity
Supplemental Figure S5. Spatial transcriptomics of CRC and NSCLC using Xenium immuno-oncology panel.
- 3 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure S5 from Intratumoral Three-Cell-Type Clusters Are a Conserved Feature of Endogenous Antitumor Immunity
Supplemental Figure S5. Spatial transcriptomics of CRC and NSCLC using Xenium immuno-oncology panel.
- Open Access
- 3 February 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure S4 from Intratumoral Three-Cell-Type Clusters Are a Conserved Feature of Endogenous Antitumor Immunity
Supplemental Figure S4. Spatial transcriptomics of PDAC using Xenium immuno-oncology panel.
- 3 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure S4 from Intratumoral Three-Cell-Type Clusters Are a Conserved Feature of Endogenous Antitumor Immunity
Supplemental Figure S4. Spatial transcriptomics of PDAC using Xenium immuno-oncology panel.