Cancer Epidemiol Biomarkers Prev. 2026 May 14. doi: 10.1158/1055-9965.EPI-25-1836. Online ahead of print.

ABSTRACT

BACKGROUND: Depression is a leading global health burden and has been linked to chronic diseases, including cancer. Chronic stress may promote colorectal carcinogenesis via hormonal, immune, and metabolic abnormalities. Evidence for depression and colorectal cancer (CRC) is inconsistent, and data on colorectal polyps are limited.

METHODS: We prospectively followed 91,383 women from the Nurses’ Health Study II (1993-2019) for CRC analyses, and 62,237 women (1993-2017) for adenoma and serrated polyp analyses. Depression was defined as a Mental Health Index-5 score ≤ 52, antidepressant use, or physician-diagnosed depression. Multivariable Cox proportional hazards models estimated hazard ratios (HRs) for CRC while logistic regression estimated odds ratios (ORs) for adenomas and serrated polyps.

RESULTS: Over 2.36 million person-years of follow-up, 474 CRC cases were documented. Depression was modestly associated with lower risk of CRC (HR=0.76, 95% CI: 0.59-0.97) and colon, but not rectal cancer. Among 62,237 women undergoing lower endoscopy over 24 years, 4,104 conventional adenomas and 4,563 serrated polyps were documented. Depression was modestly inversely associated with overall and large conventional adenomas (OR = 0.76, 95% CI: 0.63-0.92). No consistent association was observed with serrated polyps in primary models, although some sensitivity analyses suggested possible positive associations.

CONCLUSIONS: Depression was inversely associated with CRC and large conventional adenomas. Associations with serrated polyps were not evident in primary models but varied across sensitivity analyses, requiring further study.

IMPACT: These findings suggest potential differences across colorectal neoplastic pathways, indicate that the relationship between depression and colorectal carcinogenesis may be more complex than previously appreciated.

PMID:42132476 | DOI:10.1158/1055-9965.EPI-25-1836

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Oncologist. 2026 May 8;31(6):oyag148. doi: 10.1093/oncolo/oyag148.

ABSTRACT

BACKGROUND: Anal cancer incidence is rising in the United States, now exceeding 10 000 cases annually. Chemoradiation (CRT) is the standard curative-intent treatment for non-metastatic squamous cell carcinoma of the anus (SCCA), with surgery generally reserved for non-responders with persistent or progressive disease. Recent trials have refined management, supporting the assessment of response at 26 weeks before considering surgery. However, contemporary population-level patterns of upfront primary surgery and associated survival trends remain incompletely described.

METHODS: Using the Surveillance, Epidemiology, and End Results (SEER) registry (2004-2020), we identified adults with newly diagnosed non-metastatic anal squamous cell neoplasms (ICD-O-3 8050-8089). Outcomes were receipt of primary surgery as initial treatment and overall survival. We evaluated temporal trends (Cochran-Armitage), factors associated with primary surgery (multivariable logistic regression), and survival over time (Kaplan-Meier; multivariable Cox proportional hazards modeling).

RESULTS: Among 16 718 patients with non-metastatic anal cancer, 33.1% (n = 5529) underwent primary surgery and 83.7% (n = 13 997) received radiation as part of initial management. Primary surgery declined from 46.0% in 2004 to 28.7% in 2020 (trend P < 0.001), while radiation utilization was relatively stable over time (trend P = 0.106). In adjusted analyses, younger age (<50 vs 60-69 years; OR 1.614), male sex (OR 1.508), and Non-Hispanic Black race (vs Non-Hispanic White; OR 1.178) were associated with higher odds of primary surgery. Tumor factors were strongly associated with surgical use (eg, T1 vs T2: OR 3.072; higher N stage associated with lower odds). Overall survival improved across diagnosis periods (log-rank P = 0.0002); in adjusted Cox models, diagnosis in 2016-2020 (vs 2004-2007) was associated with lower mortality risk (HR 0.77).

CONCLUSIONS: From 2004 to 2020, primary surgery as initial management for non-metastatic anal cancer declined substantially, consistent with increasing adoption of CRT, while overall survival improved over time. Persistent use of upfront surgery in select subgroups warrants further study to clarify indications and ensure guideline-concordant care.

PMID:42101873 | DOI:10.1093/oncolo/oyag148

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Clin Cancer Res. 2026 May 8. doi: 10.1158/1078-0432.CCR-25-4370. Online ahead of print.

ABSTRACT

PURPOSE: Aberrant enhancer dynamics play a critical role in the initiation and progression of colorectal cancer (CRC), particularly in the BRAFV600E-mutated metastatic subtype, which uniquely exhibits a strong epigenetic phenotype. Building on this epigenetic vulnerability, bromodomain 2, a reader of H3K27ac-marked enhancers, was found to be synthetically lethal with BRAF + EGFR inhibition.

EXPERIMENTAL DESIGN: We evaluated the effectiveness of targeting aberrant enhancers with bromodomain and extraterminal (BET) + MAPK pathway inhibitors in patient-derived xenograft models of metastatic CRC, followed by comprehensive transcriptomic and chromatin profiling.

RESULTS: BET plus standard MAPK inhibitors demonstrated improved efficacy against BRAFV600E CRC and selective improvements against RAS-mutant CRC in vivo. This combination induced a more profound downregulation of the MAPK signaling pathway than MAPK inhibition alone. The loss of activation signal on H3K27ac-marked enhancers led to the dysregulation of core-regulatory circuitries, especially the MAPK downstream E26 transformation-specific transcription factor family and MYC. Single-nucleus RNA+ATAC sequencing distinguished differential transcriptomic and chromatin dynamics at the cell-type level. Profound downregulation of well-differentiated cell types confirmed deep inhibition of MAPK signaling and downstream transcription factors. Conversely, an abundance of dedifferentiated cell populations emerged after MAPK or combination inhibition, suggesting therapy-induced cell-state switching and adaptation.

CONCLUSION: Our work demonstrates that BET inhibition improves MAPK signaling blockade through profound epigenetic reprogramming of core transcription factor circuits. These findings provide a preclinical rationale for the evaluation of BET + BRAF + EGFR inhibition in patients with treatment-refractory BRAFV600E metastatic CRC (NCT06102902).

PMID:42101296 | DOI:10.1158/1078-0432.CCR-25-4370

The post Reprogramming of Cellular Plasticity via ETS and MYC Core-regulatory Circuits During Response to MAPK Inhibition in BRAF-mutant Colorectal Cancer appeared first on FightCRC.

Improves Early Detection of Hereditary Condition Linked to Increased Risk of Colorectal Cancer

Fight Colorectal Cancer (Fight CRC) announced that its Genetics and Family History Advisory Council, working alongside a group of nearly 150 patient advocacy organizations, medical societies, and medical professionals, successfully petitioned the International Classification of Diseases (ICD-10) Coordination and Maintenance Committee to establish a code specifically for Lynch syndrome and allows a path for inclusion of  BRCA 1, BRCA 2 and Li-Fraumeni.

The new ICD-10 codes represent a critical advancement in the identification, tracking, surveillance, and study of hereditary cancer syndromes. Accurate and specific coding will play a critical role in helping healthcare providers, researchers, health systems, and life sciences companies accurately identify genetic and hereditary syndromes earlier, leading to improved care and continued advances in research.

Specifically for colorectal cancer- Lynch syndrome, a hereditary condition, significantly increases the lifetime risk of colorectal cancer (CRC) and other cancers. It affects approximately 1 in every 279 individuals worldwide and is present in an estimated 1 in every 25-35 individuals diagnosed with colorectal cancer. Earlier identification through precise diagnostic coding can facilitate timely surveillance and intervention, ultimately saving lives. In addition, Li-Fraumeni syndrome is associated with a broad range of cancers, often occurring at unusually young ages.  Women with BRCA1 or BRCA2 mutations face up to a 60–70% lifetime risk of breast cancer.  Ensuring these genetic and hereditary syndromes have designated ICD-10 codes provides great paths to prevention and early detection strategies.

Accurate ICD-10 coding is crucial for monitoring genetic and hereditary syndromes, ensuring they receive appropriate surveillance, and enabling personalized treatment plans. Additionally, precise coding will facilitate the use of national-level data sets to monitor treatment outcomes, inform AI-powered analytics capabilities, and drive research and quality improvement efforts in the hereditary cancer community.

“Accurate, precise medical coding for a condition like Lynch syndrome and the additional hereditary syndromes is so critical because it is the foundation for how the patient journey is tracked over time, giving providers, researchers, and life sciences professionals a more granular, real-world understanding of how the disease presents and progresses, and its role as a precursor to other forms of cancer,” said Anjee Davis, CEO of Fight CRC. “I’m so proud of the work our team has done to rally a world-renowned group of experts to support this initiative and successfully secure an ICD-10 code for Lynch syndrome and then further support the inclusion of the BRCA 1, BRCA 2 and Li-Fraumeni codes.

Among the group of esteemed experts who worked with Fight CRC to secure the new ICD-10 codes were:

• Andrea Dwyer, MPH, Colorado University School of Public Health
• Heather Hampel, MS, CGC, City of Hope
• Bryson Katona, MD, PhD, University of Pennsylvania
• Elana Levinson, MS, MPH, CGC, Columbia University Irving Medical Center
• Swati Patel, MD, MS, University of Colorado Anschutz Medical Center
• Peter Stanich, MD, Ohio State University Wexner Medical Center
• Jennifer Weiss, MD, MS, University of Wisconsin School of Medicine and Public Health
• Beth Dudley Yurkovich, MS, MPH, CGC, University of Pittsburgh

“As a public health practitioner and advocate, I am excited about the impact we could have for stronger tracking of research and data that will drive better care for those with genetic syndromes and their families,” said Dwyer. “It is critical that Lynch is included as an ICD-10 measure.”

Fight CRC’s application to create specific ICD-10 coding for Lynch syndrome gathered broad support from the following organizations and individuals:

• Association of Black Gastroenterologists and Hepatologists
• AliveAndKickn
• American Cancer Society
• American Cancer Society Cancer Action Network
• American College of Gastroenterology
• American Gastroenteroligical Association
• American Society for Gastrointestinal Endoscopy
• California Colorectal Cancer Coalition
• CancerCare
• Catch It In Time
• Cheeky Charity
• Collaborative Group of the Americas on Inherited Gastrointestinal Cancer
• Colon Cancer Alliance for Research & Education for Lynch Syndrome
• Colon Cancer Coalition
• Colon Cancer Prevention Project
• Colorectal Cancer Alliance
• Colorectal Cancer Equity Foundation
• GH Foundation
• Hitting Cancer Below the Belt
• Jacqueline Rush Foundation
• Lynch Syndrome Screening Network
• Man Up to Cancer
• National Comprehensive Cancer Network
• National Society of Genetic Counselors
• NCGenetics
• OECI Comprehensive Cancer Centre, St James Hospital
• One Cancer Place
• Paltown Development Foundation
• Raymond Foundation & GI Cancers Alliance
• Ruesch Center for the Cure of GI Cancers
• The Blue Hat Foundation
• The Hereditary GI Cancer Prevention Program at the Ohio State University Wexner Medical Center
• The Lynch Syndrome Screening Network
• UCHealth University of Colorado Hospital
• United Ostomy Associations of America, Inc.
• Washington Colon Cancer Stats
• West Virginia University Cancer Institute
• Alexandra Capasso, Genetic Counselor, City of Hope
• Andrea Dwyer, MPH, Colorado University School of Public Health, Member University of Colorado Cancer Center
• Ann Bunnell, Genetic Counselor, Texas Oncology
• Anu Chittenden, Genetic Counselor, Dana-Farber Cancer Institute
• Aparajita Singh, Associate Clinical Professor, University of California San Francisco
• Ashley Mochizuki, Associate Genetic Counselor, City of Hope
• Beth Dudley Yurkovich, MS, MPH, CGC, University of Pittsburgh
• Bethany Kelly, MS, CGC, Genetic Counselor, CHI Saint Joseph Health Cancer Care
• Bita Nehoray, Manager, Genetic Counseling, City of Hope
• Brittany Glassett, PA-C, UCHealth
• Brittany Szymaniak, Genetic Counselor, Northwestern Medicine
• Bryson Katona, MD, PhD, Assistant Professor of Medicine, University of Pennsylvania
• Carly Grant, Cancer Genetic Counselor, Massachusetts General Hospital Cancer Center
• Carol Burke, MD, Cleveland Clinic
• Carol Ko, Genetic Counselor Supervisor, Providence
• Carol Koch, Patient
• Catherine Whitworth, Program Coordinator, WV Program to Increase Colorectal Cancer Screening
• Cheryl Lauren Meguid, Nurse Practitioner, University of Colorado Hospital
• Christina Fujii, Genetic Counselor, City of Hope
• Christine Drogan, Certified Genetic Counselor, University of Chicago
• Cindy L. O’Bryant, Professor/Clinical Pharmacist, University of Colorado Cancer Center
• Connie Zuo, Physician Assistant, University of Colorado Medicine (CU Medicine)
• Crystal Fogleman, Oncology Nurse, Invitae
• Danielle Marino, MD, University of Rochester
• Danielle Pastor, Associate Program Director, National drInstitutes of Health Hematology Oncology Fellowship Program; Chief, Medical Oncology Consult Service, National Cancer Institute, National Institutes of Health
• Dawn Nixon, Genetic Counselor, Ascension St. Vincent Cancer Care
• Deborah Cragun, Director, Genetic Counseling Graduate Program, University of South Florida
• Deepika Nathan, HS Associate Clinical Professor, Genetic Counselor, University of California Irvine School of Medicine
• Devin Cox, Genetic Counselor, University of Kansas Cancer Center
• Dillon van den Berg, Genetic Counselor, Providence Mission Hospital
• Douglas Riegert-Johnson, MD, Consultant of Gastroenterology, Mayo Clinic
• Ed Esplin, Physician, Clinical Geneticist, Invitae
• Elena Strait, Genetic Counselor, Penrose Hospital / CommonSpirit Health
• Elise Sobotka, MS, MPH, CGC, Genetic Counselor, City of Hope National Medical Center
• Elizabeth Lynn, Nurse Practitioner, University of California, San Francisco (UCSF) Hereditary Cancer Clinic
• Elyssa Zukin, Genetic Counselor, City of Hope
• Emily Toegel, MD, University of Colorado Anschutz Medical Campus
• Emma Keel, Genetic Counselor, University of Chicago
• Francesca Tubito-Massarano, Genetic Counselor, Weill Cornell Medicine
• Gayle Patel, Certified Genetic Counselor, Texas Oncology
• Gregory Austin, Professor Medicine, University of Colorado
• Gregory Idos, Associate Professor of Medicine, City of Hope National Medical Center
• Holli Loomans-Kropp, Assistant Professor, The Ohio State University
• Hunaydah Elfarawi, Genetic Counselor, City of Hope National Medical Center
• Jaime Jessen, Genetic Counselor, Dynacare
• Jamilyn Zepp, Genetic Counselor, Kaiser Permanente Center for Health Research
• Jamina Oomen-Hajagos, PhD, MS, Genetic Counselor, GeneDx
• Jennifer Weiss, MD, MS, Director, University of Wisconsin GI Genetics Clinic, University of Wisconsin School of Medicine and Public Health
• Jordyn Koehn, Clinical Genetic Counselor, The University of Kansas Cancer Center
• Joshua Smith, Resident Physician, University of Michigan Medicine
• Julia Martinez, Genetic Counselor, University of California Davis Health
• Karen Vikstrom, Genetic Counselor, NorthBay Cancer Center
• Kathryn Reyes, Genetic Counselor, City of Hope
• Kathryn Valdez, RSM, Invitae
• Kristen Shannon, Director, Massachusetts General Hospital Cancer Center Genetics Program, Mass General Cancer Center
• Kristina Markey, Genetic Counselor, University of Colorado S
• Lauren Gima, Senior Genetic Counselor, City of Hope
• Lee-may Chen, MD, Professor, UCSF Helen Diller Family Comprehensive Cancer Center
• Leigh Stout, Genetic Counselor, Indiana University Health
• Leila Jamal ScM, PhD, Genomics Education Specialist, National Cancer Institute
• Leslie Van Nostrand, RN – Nurse Navigator, UCHealth
• Leticia Valadez, Manager, Practice Management, City of Hope National Medical Center, Division of Clinical Cancer Genetics
• Linda H Rodgers-Fouche, Genetic Counselor, Massachusetts General Hospital
• Lisa Ku, Genetic Counselor, University of Colorado
• Lisen Axell, Instructor, Medicine-Medical Oncology, University of Colorado
• Lucia Richter Paz, MD, Instituto Oncológico del Oriente Boliviano
• Marcela Mora, RN, UCHealth
• Margaret R. Klehm, Nurse Practitioner, Dana-Farber Cancer Institute
• Melany Cruz, Genetic Counselor, Massachusetts General Hospital
• Melissa Fuller, Program Manager Oncology Service Line, UCHealth
• Michael Restrepo, Licensed Certified Genetic Counselor, City of Hope
• Michelle Hall, Genetic Counselor, Mercy Health
• Michelle Springer, Genetic Counselor, University of Colorado
• Mohammad Ali Abbass, Surgeon, Northwestern University
• Natalie Sivak, M.D., University of Colorado Denver
• Natalya Veneychuk, RN, UCHealth
• Nicholas Bartell, MD, University of Rochester Medical Center
• Nikhil Madhuripan, MD, Interim Section Chief of Abdominal Imaging, University of Colorado Anschutz Medical Campus School of Medicine
• Paul E. Wise, MD, Professor of Surgery, Washington University in St. Louis School of Medicine
• Peter P Stanich, MD, Associate Professor, The Hereditary GI Cancer Prevention Program, The Ohio State University Wexner Medical Center
• Priyanka Kanth, MD, MedStar Georgetown University Hospital
• Rachel Hodan, Genetic Counselor IV, Stanford Health Care
• Reed Weiss, DNP, ARNP, University of Colorado Cancer Center
• Rikki Caffrey, Director, Ethics, Advocate Health
• Robert Hollis, Assistant Professor, University of Alabama at Birmingham
• Samantha Goold, Genetic Counselor, Providence
• Samara Rifkin, Gastroenterologist, University of Michigan
• Sanjana Mehrotra, Associate Professor, University of Colorado
• Sara Mokhtary, Genetic Counselor, Texas Oncology
• Sarah Lindsey Davis, MD, University of Colorado Cancer Center
• Sarah Sturm, Genetic Counselor, University of California, San Francisco
• Stephanie Cohen, Genetic Counselor, Ascension St. Vincent
• Steven H. Erdman, Professor-Clinical, Pediatrics, The Ohio State University
• Sudeep Banerjee, MD, Kaiser Permanente
• Susan C Eason, Program Director, WV Program to Increase Colorectal Cancer Screening, WVU Cancer Institute
• Swati G. Patel, Associate Professor of Medicine, University of Colorado Anschutz Medical Center
• Timothy Yen, MD, Loma Linda University
• Trisha Nichols, MS, CGC, Certified Genetic Counselor/Program Coordinator, Texas Oncology (The US Oncology Network)
• Wells Messersmith, MD, Professor and Division Head of Medical Oncology, University of Colorado School of Medicine
• Wendy Rubinstein, Senior Scientific Officer, National Cancer Institute
• Xavier Llor, Professor of Medicine, Yale University

For more information on Fight CRC’s advocacy efforts to improve early detection and treatment of colorectal cancer, please visit www.fightcolorectalcancer.org.

The post Fight CRC Secures ICD-10 Code for Lynch Syndrome, BRCA 1, BRCA 2. Li-Fraumeni appeared first on FightCRC.

Clinical Trials Roundup

Curated by Fight CRC’s Medical Advisory Board & Research Advocacy Training and Support (RATS) team.

This month, we’re spotlighting trials that reflect a growing national investment in colorectal cancer research, and what that means for you. From precision medicine to next-generation trial platforms, these studies are designed to expand options, personalize care, and improve how research works for patients. 

Clinical trials don’t just test treatments; they shape the future of care. And staying informed gives you more power in your treatment journey.  

Need help understanding clinical trials or biomarker testing? See our biomarker resources here.

May 2026

1. NCI ComboMATCH — Combination Therapy Based on Tumor Genetics 

Biomarker Focus: Actionable genetic alterations 
Phase / Sites: Screening trial supporting multiple Phase II treatment sub-studies  / U.S. NCI network 
Stage: Advanced solid tumors, including colorectal cancer when biomarker eligible 
Recruitment Status: Recruiting 
What it’s studying: ComboMATCH assigns patients to treatment combinations based on tumor genetic changes rather than cancer type alone, using a screening platform that matches patients to specific sub-studies. 
Why it matters: This builds on precision medicine by testing whether targeted drug combinations can improve outcomes for patients whose tumors have actionable alterations. 
Patient Tip: If you’ve had genomic testing, ask whether your results include an alteration that could match to a precision medicine trial. 
ClinicalTrials.gov: NCT05564377 
https://clinicaltrials.gov/study/NCT05564377 

2. BASECAMP-1 — Screening Study for Future CEA-Targeted Cell Therapy 

Biomarker Focus: CEA expression, HLA type (including HLA loss of heterozygosity), tumor immune markers 
Phase / Sites: Observational screening study / U.S. sites 
Stage: Solid tumors, including colorectal cancer 
Recruitment Status: Recruiting 
What it’s studying: BASECAMP-1 screens patients for biomarkers that may determine eligibility for future CEA-targeted cell therapy studies. 
Why it matters: This expands biomarker testing beyond tumor mutations to include immune matching and cell therapy eligibility. 
Patient Tip: If you’re interested in cell therapy trials, ask whether HLA typing or CEA testing could be relevant. 
ClinicalTrials.gov: NCT04981119 
https://clinicaltrials.gov/study/NCT04981119 

3. Onvansertib Combination Trial — KRAS-Mutant Metastatic Colorectal Cancer 

Biomarker Focus: KRAS mutation 
Phase / Sites: Phase II / U.S. and international sites 
Stage: Metastatic colorectal cancer 
Recruitment Status: Active, Not Recruiting 
What it’s studying: This study evaluates onvansertib with standard chemotherapy and bevacizumab in patients with KRAS-mutant metastatic colorectal cancer. 
Why it matters: KRAS mutations are common in CRC, but many KRAS-mutant tumors still lack effective targeted options. This study focuses on a biologically defined CRC group. 
Patient Tip: If your tumor has a KRAS mutation, ask whether the specific KRAS variant and prior treatments affect trial eligibility. 
ClinicalTrials.gov: NCT06106308 
https://clinicaltrials.gov/study/NCT06106308 

4. P-MUC1C-ALLO1 — Allogeneic CAR-T Cell Therapy Targeting MUC1-C 

Biomarker Focus: MUC1-C expression 
Phase / Sites: Phase I / Includes U.S. sites 
Stage: Advanced or metastatic solid tumors, including colorectal cancer 
Recruitment Status: Active, Not Recruiting 
What it’s studying: This study evaluates an allogeneic CAR-T cell therapy targeting MUC1-C, a tumor-associated marker expressed in several epithelial cancers. 
Why it matters: Cell therapy research in CRC is expanding, and biomarker testing may help identify patients whose tumors express targets like MUC1-C. 
Patient Tip: Ask whether your tumor testing includes protein-expression markers, not just DNA mutations. 
ClinicalTrials.gov: NCT05239143 
https://clinicaltrials.gov/study/NCT05239143 

5. GCC19CART — CAR-T Therapy Targeting GCC in Advanced Gastrointestinal Cancers 

Biomarker Focus: GCC / guanylyl cyclase C expression 
Phase / Sites: Phase I / U.S. sites 
Stage: Metastatic colorectal cancer 
Recruitment Status: Recruiting 
What it’s studying: This trial evaluates CAR-T cells targeting GCC, a marker commonly associated with colorectal cancer cells. 
Why it matters: GCC-targeted cell therapy is a CRC-relevant biomarker strategy and represents a newer research direction for patients with advanced disease. 
Patient Tip: If you are exploring cell therapy options, ask whether your tumor expresses GCC or whether a GCC-targeted study is available. 
ClinicalTrials.gov: NCT05319314 
https://clinicaltrials.gov/study/NCT05319314 

April 2026

1. JANUS Rectal Cancer Trial — Total Neoadjuvant Therapy in Locally Advanced Rectal Cancer 
Biomarker Focus: Response-adapted treatment and organ preservation strategy 
Phase / Sites: Phase II / U.S. cooperative group, multicenter 
Stage: Stage II-III / locally advanced rectal cancer 
Recruitment Status: Active, not recruiting 
What it’s studying: JANUS is comparing long-course chemoradiation followed by mFOLFIRINOX versus mFOLFOX6 to improve clinical complete response and organ preservation in locally advanced rectal cancer. 
Why it matters: This study is relevant right now because it focuses on treatment intensification and organ-preservation goals in rectal cancer—an area of strong interest for patients and clinicians alike. 
Patient Tip: If you are discussing treatment before rectal cancer surgery, ask whether total neoadjuvant therapy or organ-preservation strategies may be appropriate for you. 
ClinicalTrials.gov: NCT05610163 
https://clinicaltrials.gov/study/NCT05610163 

2. EA2201 — Immunotherapy in dMMR Stage II/III Rectal Cancer 
Biomarker Focus: Deficient mismatch repair (dMMR) / MSI-H 
Phase / Sites: Phase II / Multicenter U.S. trial 
Stage: Stage II–III locally advanced rectal adenocarcinoma 
Recruitment Status: Active, not recruiting 
What it’s studying: EA2201 is evaluating nivolumab + ipilimumab with short-course radiation in patients with MSI-H/dMMR rectal cancer, with the goal of improving response while potentially reducing the need for more intensive conventional treatment. 
Why it matters: dMMR rectal cancer is one of the clearest examples of biomarker-driven care in CRC. This trial reflects the shift toward tailoring treatment based on tumor biology. 
Patient Tip: If your tumor is dMMR or MSI-H, ask whether immunotherapy-based trials may be available before surgery. 
ClinicalTrials.gov: NCT04751370 
https://clinicaltrials.gov/study/NCT04751370 

3. COMMIT Study — First-Line Immunotherapy Strategy in Metastatic dMMR/MSI-H Colorectal Cancer 
Biomarker Focus: dMMR / MSI-H 
Phase / Sites: Phase III / national multicenter trial 
Stage: Metastatic colorectal cancer 
Recruitment Status: Active, not recruiting 
What it’s studying: COMMIT is testing atezolizumab-based first-line treatment strategies, including chemotherapy/bevacizumab-containing approaches, in metastatic dMMR CRC. 
Why it matters: Although immunotherapy is already important in dMMR/MSI-H CRC, not all patients have durable benefit. COMMIT is trying to refine the best first-line approach for this population. 
Patient Tip: If you have metastatic dMMR/MSI-H CRC and are starting treatment, ask whether a first-line immunotherapy trial is an option. 
ClinicalTrials.gov: NCT02997228 
https://clinicaltrials.gov/study/NCT02997228 

4. ERAS-007 Combination Trial in Advanced Gastrointestinal Malignancies, Including Colorectal Cancer 
Biomarker Focus: MAPK pathway / BRAF and RAS pathway signaling 
Phase / Sites: Phase Ib/II / Multicenter, including U.S. sites 
Stage: Advanced gastrointestinal malignancies, including metastatic CRC 
Recruitment Status: Completed 
What it’s studying: This study is evaluating ERAS-007, an ERK inhibitor, in combination regimens designed to interrupt downstream MAPK signaling in GI cancers, including CRC. 
Why it matters: Many CRC tumors are driven by pathway alterations that remain difficult to target directly. ERAS-007 reflects a newer strategy aimed at blocking downstream signaling to improve outcomes. 
Patient Tip: If your cancer has a BRAF or RAS-pathway alteration, ask whether downstream pathway-targeting trials may be appropriate. 
ClinicalTrials.gov: NCT05039177 
https://clinicaltrials.gov/study/NCT05039177 

5. Nous-209 Vaccine Prevention Study in Lynch Syndrome 
Biomarker Focus: Lynch syndrome / mismatch repair deficiency risk 
Phase / Sites: Phase Ib/II / U.S.-based prevention study 
Stage: High-risk individuals with Lynch syndrome 
Recruitment Status: Active, not recruiting 
What it’s studying: This study is evaluating the Nous-209 vaccine strategy for cancer prevention in Lynch syndrome carriers at elevated risk for colon and other Lynch-associated cancers. 
Why it matters: This is a prevention-focused trial rather than a treatment trial, but it is highly relevant to colorectal cancer because it aims to reduce future cancer risk in a well-defined high-risk population. 
Patient Tip: If you or your family members have Lynch syndrome, ask whether prevention studies or surveillance-focused research may be appropriate. 
ClinicalTrials.gov: NCT05078866 

https://clinicaltrials.gov/study/NCT05078866

March 2026

1. ARPA-H ADAPT Oncology Platform – Colorectal Cohort 

Biomarker Focus: Real-time biomarker integration and adaptive trial infrastructure 
Phase / Sites: Early research initiative / United States 
Stage: Colorectal cancer (see eligibility criteria in protocol) 
Recruitment Status: Not yet recruiting 
What it’s studying: This ARPA-H supported initiative is part of the ADAPT oncology platform, designed to modernize how cancer clinical trials are conducted. The platform integrates advanced biomarker monitoring, coordinated data systems, and adaptive treatment strategies to accelerate therapeutic development in CRC and other cancers. 
Why it matters: Rather than testing a single drug, this national investment focuses on transforming the clinical trial system itself — potentially speeding up how promising treatments move from concept to clinic. 
Patient Tip: Even if enrollment hasn’t begun, ask your care team about upcoming federally funded research programs that may open new opportunities. 
ClinicalTrials.gov: NCT07318389

2. Molecularly Guided Therapy Based on Tumor Genetics: NCI-MATCH 

Biomarker Focus: Actionable genetic mutations 
Phase / Sites: Phase 2 / Nationwide (NCI-sponsored) 
Stage: Advanced solid tumors, including colorectal cancer 
Recruitment Status: Active, not recruiting 
What it’s studying: NCI-MATCH assigns treatment based on specific genetic mutations found in a tumor rather than the cancer’s location in the body. Patients with colorectal cancer whose tumors harbor actionable mutations may be matched to targeted therapies designed for those alterations. 
Why it matters: This national precision-medicine trial helped redefine how we think about treatment selection. Instead of a one-size-fits-all approach, MATCH reflects a shift toward therapy guided by tumor biology. 
Patient Tip: If you’ve had comprehensive genomic testing, ask whether your tumor’s mutations may qualify you for a MATCH sub-study. 
ClinicalTrials.gov: NCT02465060

3. COBRA Trial: ctDNA-Guided Predictor in Stage IIA 

Biomarker Focus: Circulating tumor DNA (ctDNA) 
Phase / Sites: Phase 2/3 / U.S. cooperative groups 
Stage: Stage II colon cancer 
Recruitment Status: Active 
What it’s studying: The COBRA study evaluates whether ctDNA testing after surgery can identify patients who truly need chemotherapy and who may safely avoid it. 
Why it matters: This study reflects the growing role of blood-based biomarkers in guiding adjuvant therapy, with the goal of reducing overtreatment while maintaining excellent outcomes. 
Patient Tip: If you have stage II colon cancer, ask whether ctDNA testing is appropriate for you and whether participation in a biomarker-guided trial is an option. 
ClinicalTrials.gov: NCT04068103

4. SWOG S2107: Immunotherapy Strategies in MSS Metastatic CRC 

Biomarker Focus: Microsatellite stable (MSS) and BRAF V600E mutation 
Phase / Sites: Phase 2 / National cooperative group (SWOG) 
Stage: Previously treated metastatic colorectal cancer 
Recruitment Status: Recruiting 
What it’s studying: This study is testing whether adding nivolumab (immunotherapy) to encorafenib + cetuximab improves outcomes in BRAF V600E/MSS metastatic CRC. 
Why it matters: Approximately 85–90% of colorectal cancers are MSS. Expanding immunotherapy strategies for this population remains one of the most urgent research priorities in CRC, and to a population that historically does not benefit from single-agent checkpoint inhibitors. 
Patient Tip: If you’ve been told your tumor is MSS and that immunotherapy alone is unlikely to work, ask whether combination immunotherapy trials are available at your treatment center. 
ClinicalTrials.gov: NCT04963283 

5. CIRCULATE-US (NRG-GI008) — ctDNA-Guided Adjuvant Strategy in Stage II/III 

Biomarker Focus: Circulating tumor DNA (ctDNA) 
Phase / Sites: Phase II/III / North America (NRG Oncology) 
Stage: Stage II and III (resected) colon cancer 
Recruitment Status: Recruiting 
What it’s studying: This randomized study evaluates whether post-surgical ctDNA testing can guide escalation or de-escalation of chemotherapy in patients with stage II or III colon cancer. Patients who test ctDNA-positive may receive intensified therapy, while those who test ctDNA-negative may receive less intensive treatment. 
Why it matters: ctDNA is emerging as a precision tool to detect minimal residual disease and personalize adjuvant therapy decisions. 
Patient Tip: If you’ve had surgery for stage II or III colon cancer, ask whether ctDNA testing or enrollment in a ctDNA-guided trial is appropriate for you. 
ClinicalTrials.gov: NCT05174169 

February 2026

1. BRAFTOVI® + Cetuximab + FOLFIRI — New Triplet Regimen for BRAF V600E mCRC

Biomarker Focus: BRAF V600E mutation
Phase / Sites: Phase 2 / Multinational (Pfizer-sponsored)
Stage: Metastatic (mCRC)
Recruitment Status: Active, not recruiting
What it’s studying: This study evaluates the combination of encorafenib + cetuximab + FOLFIRI in patients with previously treated, BRAF V600E-mutated metastatic CRC.
Findings: Results from ASCO GI 2026 show a significant increase in overall response rates (ORR) and progression-free survival compared to historical controls.
Why it matters: Offers a promising targeted therapy option earlier in the treatment journey for patients with BRAF-mutant CRC.
Patient Tip: If your tumor is BRAF V600E-positive and you’ve been previously treated, ask your care team about this combination.
ClinicalTrials.gov: NCT04607421

2. CIRCULATE-North America (NRG-GI008) — ctDNA-Guided Adjuvant Therapy in Stage II/III CRC

Biomarker Focus: Circulating tumor DNA (ctDNA)
Phase / Sites: Phase II/III / North America (NRG Oncology)
Stage: Stage II and III (resected)
Recruitment Status: Recruiting
What it’s studying: This randomized trial evaluates whether ctDNA testing after surgery can guide the need for adjuvant chemotherapy in patients with stage II or III colon cancer. Patients with detectable ctDNA may receive intensified treatment, while ctDNA-negative patients may avoid unnecessary chemotherapy.
Presented: ASCO GI 2026
Why it matters: ctDNA is emerging as a precision tool for assessing minimal residual disease (MRD). This trial could help patients avoid overtreatment—or identify recurrence risk earlier.
Patient Tip: If you’ve had surgery for stage II or III colon cancer, ask if ctDNA testing might inform your follow-up care plan.
ClinicalTrials.gov: ASCO Abstract: NRG-GI008

3. KEYNOTE-975 Subanalysis — Pembrolizumab in dMMR/MSI-H mCRC

Biomarker Focus: dMMR / MSI-H
Phase / Sites: Phase 3 / Global
Stage: Metastatic
Recruitment Status: Ongoing
What it’s studying: Examining the efficacy of pembrolizumab as a first-line treatment for dMMR/MSI-H metastatic CRC.
Findings: Durable responses reported in previously untreated patients, including those with comorbidities and older age groups.
Why it matters: Validates immunotherapy as a frontline option in dMMR CRC—not just for ideal candidates.
Patient Tip: If your tumor is MSI-H or dMMR, ask if you qualify for first-line immunotherapy.
ClinicalTrials.gov: NCT04003636

4. BEACON-Lite Cohort A — Real-World Evaluation of Triplet Therapy in BRAF CRC

Biomarker Focus: BRAF V600E mutation
Phase / Sites: Phase 2 / Expanded access
Stage: Metastatic
Recruitment Status: Closed to new participants
What it’s studying: A cohort evaluating encorafenib + cetuximab + chemotherapy in patients not eligible for the original BEACON trial.
Findings: Preliminary real-world data shows efficacy in older patients and those with comorbidities.
Why it matters: Supports more inclusive criteria for accessing promising triplet regimens.
Patient Tip: If you were previously excluded from BRAF-targeted trials, ask if real-world data may now support this approach.
ClinicalTrials.gov: NCT02928224

January 2026

1. BREAKWATER Trial — Triplet Therapy Sets New Standard for BRAF V600E mCRC

Biomarker Focus: BRAF V600E mutation
Phase / Sites: Phase 3 / Multi-national
Stage: Stage IV (metastatic)
Recruitment Status: Completed (Phase 3)
What it’s studying: Encorafenib + cetuximab + FOLFIRI vs chemotherapy in first-line mCRC
Findings: PFS nearly doubled (12.8 vs 7.1 months); OS improved to 30.3 vs 15.1 months
Why it matters: A new triplet could replace chemo as the standard for BRAF-mutated mCRC
Patient Tip: If you have BRAF V600E-mutant CRC and are starting first-line treatment, ask whether this triplet regimen is being considered.
ClinicalTrials.gov: N/A

2. ATOMIC Trial — Atezolizumab + Chemo in Stage III dMMR CRC

Biomarker Focus: Mismatch repair deficiency (dMMR / MSI-H)
Phase / Sites: Phase 3 / Multi-center
Stage: Stage III (resected)
Recruitment Status: Completed
What it’s studying: mFOLFOX6 with or without atezolizumab after surgery in stage III colon cancer
Findings: 3-year disease-free survival improved to 86.4% vs 76.6%
Why it matters: May change adjuvant therapy for early-stage dMMR CRC
Patient Tip: If your tumor is MSI-H/dMMR and you’re receiving adjuvant chemo, ask whether immunotherapy was considered or studied in your care setting.
ClinicalTrials.gov: NCT02912559

3. IVX037 + Sintilimab in MSS CRC — RNA Virus Therapy for IO-Resistant Tumors

Biomarker Focus: Microsatellite stable (MSS), KRAS mutations
Phase / Sites: Phase 1 / Single site (expansion)
Stage: Stage IV (refractory)
Recruitment Status: Expansion underway (Phase 1a complete)
What it’s studying: A bio-selected, receptor-targeted oncolytic RNA virus (IVX037) injected into tumors, combined with anti-PD-1 sintilimab
Findings: Disease control in patients with MSS and KRAS G12D CRC; early immune activation observed
Why it matters: One of the first intratumoral viral therapies showing benefit in MSS CRC: a population typically unresponsive to immunotherapy
Patient Tip: If your tumor is MSS and you’ve exhausted chemo options, ask your care team about clinical trials exploring novel immunotherapy combinations or virus-based therapies.
ClinicalTrials.gov: N/A

4. DYNAMIC-III Trial — ctDNA-Guided Escalation in Stage III CRC

Biomarker Focus: Circulating tumor DNA (ctDNA)
Phase / Sites: Phase 2 / Australia
Stage: Stage III (resected)
Recruitment Status: Completed
What it’s studying: Use of post-surgical ctDNA to guide chemotherapy intensity
Findings: Escalation based on ctDNA positivity improved outcomes; negative ctDNA patients avoided unnecessary chemo
Why it matters: Further validates ctDNA as a tool for adjuvant therapy decisions
Patient Tip: If you’ve had surgery for stage III CRC, ask if ctDNA testing could help tailor your chemotherapy plan.
ClinicalTrials.gov: NCT03803553

5. Tumor-Agnostic ADC Use in CRC – Real-World Data on KRAS G12C and HER2+ Subtypes
Biomarker Focus: KRAS G12C, HER2, and ADC-responsive profiles
Phase / Sites: Retrospective / Multiple centers
Stage: Stage IV (refractory)
Recruitment Status: Retrospective analysis of real-world patients (not an interventional trial)
What it’s studying: Outcomes among CRC patients treated with tumor-agnostic antibody-drug conjugates (ADCs) in third-line or later settings
Findings: HER2+ and KRAS G12C patients experienced stable disease or prolonged progression-free survival with investigational ADCs
Why it matters: Highlights the transition of novel ADCs from trials to practice and underscores the importance of biomarker matching in refractory mCRC
Patient Tip: If you’ve already tried standard treatments, ask your provider about biomarker testing for targets like HER2 or KRAS G12C, which may open access to novel ADC-based strategies through expanded access or real-world use.
ClinicalTrials.gov: N/A

The post On Our Radar: May 2026 Clinical Trials Roundup appeared first on FightCRC.

Fam Cancer. 2026 May 6;25(2):49. doi: 10.1007/s10689-026-00552-5.

ABSTRACT

BACKGROUND: The Lynch syndrome INtegrative Epidemiology And GEnetics (LINEAGE) consortium was established to address gaps in understanding genotype-specific cancer risks and risk-modifiers in contemporary North American Lynch syndrome (LS) populations. LINEAGE is a multi-center, longitudinal cohort to systematically collect data on risk factors, adherence to care, quality of surveillance, and patient-, provider-, and system-level factors associated with incident LS-associated cancers.

METHODS: LINEAGE recruits individuals with confirmed pathogenic or likely pathogenic variants in LS-associated genes from participating institutions. Data includes retrospective and prospective collection, encompassing clinical abstraction (demographics, surgical history, endoscopic data, treatments), patient-reported surveys (behavioral/lifestyle factors, quality of life, procedures), endoscopist-level data, and biosample metadata. A standardized REDCap database, data harmonization protocols, and a virtual biobank support reproducibility and linkage of clinical data and biosamples. Rigorous quality assurance/quality control processes are embedded for data integrity.

RESULTS: Participating centers will contribute data to determine gene-specific risks, and gene-environment interactions for Lynch-associated, and other cancers. We will evaluate associations with exposure to, and quality of cancer risk-reduction care, including endoscopic surveillance, risk-reduction surgery, and chemoprevention. The inclusion of provider-level variables, such as endoscopist training and experience, enables unique research into modifiers of post-endoscopy cancer risk. The linked biosample resources will further facilitate mechanistic studies and biomarker discovery.

CONCLUSIONS: LINEAGE provides a robust platform for advancing LS research by integration of clinical, pathological, epidemiological and genetic data across institutions. Its standardized, collaborative framework enhances the validity and generalizability of risk estimates that will guide decision-making and policy for surveillance to ultimately reduce morbidity and mortality for individuals with Lynch syndrome.

PMID:42089916 | DOI:10.1007/s10689-026-00552-5

The post Lynch syndrome integrative epidemiology and genetics (LINEAGE): rationale for cohort design appeared first on FightCRC.

JTCVS Open. 2026 Feb 27;30:101702. doi: 10.1016/j.xjon.2026.101702. eCollection 2026 Apr.

ABSTRACT

OBJECTIVE: Thoracic Surgery Oncology Group 103 was a prospective multi-institutional trial that aimed to (1) evaluate the role of perioperative chemotherapy for low-risk patients with metastatic colorectal cancer undergoing pulmonary metastasectomy and (2) characterize the impact of surgery on outcomes for high-risk patients with metastatic colorectal cancer receiving chemotherapy.

METHODS: From July 2018 to September 2023, patients with histologically confirmed primary colorectal cancer and lung metastases amenable to complete margin-negative resection from 3 institutions were enrolled and stratified by low- and high-risk clinical features and randomized accordingly within 2 treatment paradigms.

RESULTS: A total of 22 and 26 patients were enrolled in the low- and high-risk cohorts, respectively. Randomization within the low-risk cohort resulted in 8 individuals (40.0%) receiving perioperative chemotherapy and surgery (+Chemo) and 12 patients (60.0%) undergoing surgery alone (-Chemo). Median overall survival was unable to be calculated for either group, and median recurrence-free survival was 21.8 months for +Chemo and not yet reached for -Chemo (P = .33). Among high-risk patients receiving chemotherapy, 8 (36.4%) remained on chemotherapy only (-SX) and 14 (63.6%) underwent pulmonary metastasectomy (+SX). Partial response to initial chemotherapy was achieved in 4 (50.0%) -SX patients and 6 (42.9%, P = 1.00) +SX patients. No deaths occurred in either group, and median recurrence-free survival was 33.4 months in the -SX group and 55.8 (P = .95) months in the +SX group.

CONCLUSIONS: Patient accrual targets were not reached, leaving this study underpowered; as such, all analyses are descriptive and hypothesis generating. We were unable to determine differences in survival in the high-risk cohort; however, our findings suggest that adequately selected low-risk individuals can be treated with up-front pulmonary metastasectomy without additional lung-directed chemotherapy.

PMID:42079931 | PMC:PMC13131173 | DOI:10.1016/j.xjon.2026.101702

The post Outcomes of Thoracic Surgical Oncology Group 103: Multimodality management in risk-stratified patients with lung-limited metastatic colorectal cancer appeared first on FightCRC.

Environ Pollut. 2026 Apr 27:128220. doi: 10.1016/j.envpol.2026.128220. Online ahead of print.

ABSTRACT

Evidence indicates that cigarette smoking affects anti-tumor immunity. We tested a hypothesis that the association of smoking with long-term colorectal cancer (CRC) incidence might differ by myeloid cell infiltrates, which may play roles in cancer immune evasion. We utilized the prospective cohort incident-tumor biobank method on two longitudinal prospective cohort studies, namely the Nurses’ Health Study and the Health Professionals Follow-up Study. To identify myeloid cells in the tumor microenvironment, we applied multiplexed immunofluorescence (for ARG1, CD14, CD15, CD33, HLA-DR, and KRT) combined with digital image analysis and machine learning. We examined the association of smoking with long-term incidence of CRC subclassified by myeloid cell densities using the multivariable inverse-probability-weighted duplication-method Cox regression model. During the follow-up of 131,143 cohort participants (3,647,434 person-years), we documented 3,092 incident CRC cases, including 854 cases with available data on tissue myeloid cells. The association of pack-years smoked with long-term CRC incidence differed by intraepithelial CD14⁺HLA-DR^– cell densities (P_{heterogeneity}<0.001) but not by CD15⁺ cell densities (P_{heterogeneity}=0.32). Smoking pack-years were strongly associated with the incidence of tumors with high CD14⁺HLA-DR^– cell densities (multivariable HR for ≥40 vs. 0 pack-years, 1.86; 95% CI, 1.35-2.57; P_trend<0.001) but not with that of tumors with intermediate or low CD14⁺HLA-DR^– cell densities (P_trend≥0.1). These differential associations generally persisted in non-microsatellite instability-high tumors. In conclusion, the association of smoking with long-term CRC incidence was stronger for tumors with more abundant CD14⁺HLA-DR^– immature monocytes, highlighting the interplay of smoking and immature monocytic myeloid cells in colorectal tumorigenesis.

PMID:42055208 | DOI:10.1016/j.envpol.2026.128220

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Nat Rev Clin Oncol. 2026 Apr 28. doi: 10.1038/s41571-026-01149-8. Online ahead of print.

ABSTRACT

Globally, colorectal cancer (CRC) is the third most frequently diagnosed cancer and the second leading cause of cancer-related deaths, although these epidemiological patterns show substantial geographical variation. In this Review, we discuss the emerging global patterns of CRC incidence, which historically has been the highest among Western, high-income countries but is now increasing globally beyond these regions. This rise has mainly been driven by early-onset CRC – that is, cancers diagnosed in individuals aged <50 years. A birth cohort effect beginning with individuals born in the 1960s indicates that factors beyond genetic susceptibility or changes in screening practice underlie this increase. A changing landscape of established and emerging risk factors occurring worldwide has been proposed to underlie these epidemiological trends in CRC. Hypothesized risk factors include dietary and lifestyle aspects, shifts in the gut microbiota and the rise in environmental contaminants associated with the rapid urbanization occurring globally. Substantial advances in the characterization of genomic and epigenomic profiles of CRCs as well as their gut microbiomes not only hold potential for providing insight on the aetiology of this disease but could also be leveraged for early detection and interception strategies. The under-representation of non-Western populations in these studies, however, greatly limits progress and, if not addressed, could widen the existing gaps in global CRC prevention and control.

PMID:42050153 | DOI:10.1038/s41571-026-01149-8

The post Emerging trends in the global burden of colorectal cancer appeared first on FightCRC.

Clin Cancer Res. 2026 Apr 28. doi: 10.1158/1078-0432.CCR-25-4126. Online ahead of print.

ABSTRACT

PURPOSE: Familial adenomatous polyposis (FAP) confers a significant risk of colorectal/duodenal cancer. Encapsulated rapamycin (eRapa) has demonstrated promise as FAP chemoprevention in early clinical studies.

METHODS: 30 FAP patients enrolled to three dosing regimens of eRapa (0.5 mg): cohort 1 – every other day, cohort 2 – daily every other week, or cohort 3 – daily. The primary endpoints were safety/tolerability, pharmacokinetics, and percentage change from baseline (PCFB) in colorectal polyp burden (CPB) at 6 mos. Secondary endpoints included PCFB total (TPB) and duodenal (DPB) polyp burden, and change in InSiGHT stage and Spigelman score at 6 and 12 mos.

RESULTS: 29/ 30 patients (97%) completed the 12-mos study with predictable bioavailability. Low grade adverse events were frequent, but most pronounced in daily dosing. Two patients discontinued treatment related to toxicity. Cohort 1 had the largest decrease median PCFB CPB, DPB, and TPB at 6 mos: -39.4 % (IQR, 108.9; p = 0.28), -33.33 % (IQR, 90.0; p = 0.04), and -38.6 % (IQR, 88.5; p = 0.26), respectively. At 12 mos, Cohort 2 had the largest decrease median PCFB CPB and TPB: -29.3 % (IQR, 67.6; p = 0.37) and -26.3 % (IQR, 49.5; p = 0.29), respectively. Intermittent dosing cohorts (1 & 2) reduced DPB at 6 mos (p = 0.04), and improved TPB at 12 mos (p = 0.05) compared to daily dosing.

CONCLUSION: eRapa was safe, tolerable and showed preliminary efficacy for FAP chemoprevention. The 0.5 mg daily every-other-week schedule will be evaluated in an upcoming phase III trial.

PMID:42048421 | DOI:10.1158/1078-0432.CCR-25-4126

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