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Life sciences · Journal article
Frontiers in Oncology · November 6, 2026
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Colorectal cancer with proficient mismatch repair (pMMR)/microsatellite stable (MSS) status is generally intrinsically resistant to immune checkpoint inhibitors; tumors with concomitant BRAF V600E mutations are highly aggressive, and conventional chemotherapy and targeted therapies have limited efficacy, resulting in a lack of effective personalized treatment options in clinical practice. This report describes a case of locally advanced right-sided colon adenocarcinoma that was pMMR/MSS, harbored a BRAF V600E mutation, and exhibited high programmed death-ligand 1 (PD-L1) expression (tumor proportion score [TPS] > 95%). The patient developed intestinal obstruction after failure of first-line conversion therapy. After undergoing palliative gastrojejunostomy and cecostomy, she developed gastroparesis and a liver abscess. Given the extremely high PD-L1 expression, tislelizumab monotherapy was initiated before the patient’s general condition had fully recovered. After three cycles, the patient’s performance status improved significantly. She then received a combination of tislelizumab and raltitrexed for two cycles; however, chemotherapy was discontinued due to raltitrexed-induced liver injury, and the patient continued maintenance therapy with tislelizumab monotherapy, achieving a partial response (PR) as the best outcome. After nine cycles of maintenance therapy, a new mass appeared in the right adnexal region, indicating disease progression; the overall progression-free survival (PFS) was 14 months. To the best of our knowledge, this is the first reported case of a patient with colorectal adenocarcinoma harboring a BRAF V600E mutation, characterized by extremely high PD-L1 expression and pMMR/MSS status, who achieved a PR with a regimen centered on programmed cell death protein 1 (PD-1) inhibitor monotherapy. This case suggests that for BRAF V600E-mutated colorectal cancer, assessment of PD-L1 expression levels should be considered regardless of mismatch repair status; if extremely high PD-L1 expression is present, even in the pMMR/MSS phenotype, PD-1 inhibitors may offer a potential personalized treatment option for these patients with poor prognosis and limited therapeutic choices.