Amanda Labora
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
Amanda Labora has a total of 77 co-authors. Here are the top co-authors by number of shared publications:
- Timothy R. Donahue
Division of Surgical Oncology, Department of Surgery, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, USA
50 shared publications - Caius G. Radu
Jonsson Comprehensive Cancer Center, University of California Los Angeles, Los Angeles, USA
49 shared publications - Evan R. Abt
Department of Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095
48 shared publications - Thuc Le
Department of Molecular and Medical Pharmacology, University of California
48 shared publications - Alykhan Premji
Veterans Health Administration, Greater Los Angeles Healthcare System, Los Angeles, USA
47 shared publications - Charlotte Chan
Department of Surgery, University of California Los Angeles, Los Angeles, California
47 shared publications
Latest Publications
- 1 February 2026
- Published by Journal of Graduate Medical Education in Journal of Graduate Medical Education
- Vol. 18 (1) , 59-63
DaRE to Approach Differently: Teaching the Digital Anorectal Examination Through a Trauma-Informed Framework
Background: The digital anorectal examination (DRE) is a valuable clinical tool but is often underutilized due to provider discomfort, lack of confidence, and concerns about patient experience. Trauma-informed care (TIC) frameworks have improved education for other sensitive examinations, but their application to DRE instruction remains limited. Objective: To evaluate whether a TIC-focused educational intervention improved resident physician comfort, confidence, and knowledge related to the DRE. Methods: From October 2024 to February 2025, a prospective study was conducted among family medicine, internal medicine, and surgery residents at a large academic medical center. Residents attended a 30-minute TIC-focused DRE didactic session. Surveys were administered at baseline, immediately after the session, and at 6 weeks. Outcomes included confidence using TIC principles and identifying pathology, changes in comfort performing the DRE, and frequency of deferring examinations. Results: A total of 136 residents participated; 99 (73%) had paired post-session responses, and 45 (33%) completed all 3 surveys. Six weeks after the session, participants reported higher average confidence employing TIC (5.09 to 6.79, scale 1-10), greater comfort performing the DRE (4.63 to 6.36), and improved confidence identifying anal (4.07 to 6.00) and rectal pathology (3.65 to 5.47), with all comparisons P <.001. At baseline, 88 of 130 residents (68%) reported deferring clinically indicated examinations at least sometimes, and, among these residents, only one resident (5%) reported doing so during the follow-up period. Conclusions: A brief, low-resource educational session incorporating TIC principles significantly improved resident confidence and comfort employing TIC and performing the DRE.
- 1 February 2026
- Published by Journal of Graduate Medical Education in Journal of Graduate Medical Education
- Vol. 18 (1) , 59-63
DaRE to Approach Differently: Teaching the Digital Anorectal Examination Through a Trauma-Informed Framework
Background: The digital anorectal examination (DRE) is a valuable clinical tool but is often underutilized due to provider discomfort, lack of confidence, and concerns about patient experience. Trauma-informed care (TIC) frameworks have improved education for other sensitive examinations, but their application to DRE instruction remains limited. Objective: To evaluate whether a TIC-focused educational intervention improved resident physician comfort, confidence, and knowledge related to the DRE. Methods: From October 2024 to February 2025, a prospective study was conducted among family medicine, internal medicine, and surgery residents at a large academic medical center. Residents attended a 30-minute TIC-focused DRE didactic session. Surveys were administered at baseline, immediately after the session, and at 6 weeks. Outcomes included confidence using TIC principles and identifying pathology, changes in comfort performing the DRE, and frequency of deferring examinations. Results: A total of 136 residents participated; 99 (73%) had paired post-session responses, and 45 (33%) completed all 3 surveys. Six weeks after the session, participants reported higher average confidence employing TIC (5.09 to 6.79, scale 1-10), greater comfort performing the DRE (4.63 to 6.36), and improved confidence identifying anal (4.07 to 6.00) and rectal pathology (3.65 to 5.47), with all comparisons P <.001. At baseline, 88 of 130 residents (68%) reported deferring clinically indicated examinations at least sometimes, and, among these residents, only one resident (5%) reported doing so during the follow-up period. Conclusions: A brief, low-resource educational session incorporating TIC principles significantly improved resident confidence and comfort employing TIC and performing the DRE.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 1 STING agonist diABZI synergizes with MAPK inhibition in PDAC by enhancing apoptosis.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 1 STING agonist diABZI synergizes with MAPK inhibition in PDAC by enhancing apoptosis.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. 4 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 4 Immunoblot analysis demonstrating the effect of ± 100 U/ml exogenous IFN on CFPAC-1 and SUIT2 parental cells compared to their respective IFNAR-deficient isogenic cell lines. (B) Immunoblot analysis of CFPAC-1 parental and IFNAR1-KO cells exposed to ± 1 µM diABZI ± 100 nM trametinib for 24 h (C)Immunoblot analysis of the effects of ± 100 U/ml exogenous IFN ± 1 µM diABZI for 24 h.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. 4 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 4 Immunoblot analysis demonstrating the effect of ± 100 U/ml exogenous IFN on CFPAC-1 and SUIT2 parental cells compared to their respective IFNAR-deficient isogenic cell lines. (B) Immunoblot analysis of CFPAC-1 parental and IFNAR1-KO cells exposed to ± 1 µM diABZI ± 100 nM trametinib for 24 h (C)Immunoblot analysis of the effects of ± 100 U/ml exogenous IFN ± 1 µM diABZI for 24 h.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. 2 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 2 Tumor growth is inhibited by STING agonism and MEK inhibition in vivo.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. 2 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 2 Tumor growth is inhibited by STING agonism and MEK inhibition in vivo.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. 3 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 3 MEK inhibition amplifies STING-induced transcription of IFNB1, IL-6, and TNFA in multiple PDAC cell lines.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. 3 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 3 MEK inhibition amplifies STING-induced transcription of IFNB1, IL-6, and TNFA in multiple PDAC cell lines.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. 5 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. 5 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Resources and Table
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 1 from MEK Inhibition Sensitizes Pancreatic Cancer to STING Agonism by Tumor Cell–intrinsic Amplification of Type I IFN Signaling
Supplementary Resources and Table
- Open Access
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. 3 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 3 MEK inhibition amplifies STING-induced transcription of IFNB1, IL-6, and TNFA in multiple PDAC cell lines.
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. 3 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 3 MEK inhibition amplifies STING-induced transcription of IFNB1, IL-6, and TNFA in multiple PDAC cell lines.
- Open Access
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Fig. 5 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig. 5 from MEK inhibition sensitizes pancreatic cancer to STING agonism by tumor-cell intrinsic amplification of type I interferon signaling
Supplementary Fig. 5 IL6 is not responsible for the synergistic effects of STING agonism and MEK inhibition.