Cancer Research and Treatment

Original Articles

Non-Operative Management of Rectal Cancer with Adjuvant Chemotherapy after Chemoradiotherapy (NORMANDY): Prospective Study: Hyebin Lee, Hyung Ook Kim, Jason Joon Bock Lee, In-Gu Do, Heon-Ju Kwon, Mi Sung Kim, Soo-Kyung Park, Hyo-Joon Yang, Yoon Suk Jung, Jung Ho Park, Dong-Il Park, Kyung Uk Jung, Eo Jin Kim, Dong-Hoe Koo, Hungdai Kim, Ho-Kyung Chun, KBSMC Colorectal Cancer Team, Gastrointestinal Cancer Center; Received February 8, 2025 Accepted May 13, 2025 Published online May 15, 2025; DOI: https://doi.org/10.4143/crt.2025.148 [Accepted]

Abstract PDF: Purpose
Non-operative management (NOM) has emerged as a promising organ-preserving strategy for patients with rectal cancer who achieve a clinical complete response (cCR) after neoadjuvant chemoradiotherapy (CRT). However, no standardized treatment protocol has been established for watch-and-wait strategies.
Materials and Methods
This prospective study evaluated oncological outcomes of NOM combined with four months of adjuvant capecitabine. Patients with resectable rectal cancer (≤8 cm from the anal verge, cT2-4 or N+) underwent CRT (50-54 Gy in 25–27 fractions with capecitabine). Eight weeks post-CRT, a multidisciplinary team assessed cCR. Patients achieving cCR received six cycles of capecitabine (2 weeks on/1 week off) and were actively monitored.
Results
Among 89 patients receiving CRT (2018–2023), 17 (19%) achieved cCR and were included. The median age was 65 years, and 65% were male. Eleven (65%) completed all six cycles of adjuvant therapy. After a median follow-up of 31.4 months, 11 patients (65%) remained disease-free. Local regrowth occurred in six patients (35%) with 2- and 4-year rates of 34.5% and 47.6%, respectively. Five underwent radical surgery, and one received transanal excision with systemic chemotherapy. At the time of assessment, 15 patients (88%) showed no evidence of disease, while two (12%) received palliative chemotherapy. All patients were alive.
Conclusion
NOM with adjuvant capecitabine showed promising oncological outcomes, offering an alternative to passive watch-and-wait approaches. Further refinement through multidisciplinary strategies is warranted.

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General

Increased Radiosensitivity of Solid Tumors Harboring ATM and BRCA1/2 Mutations: Kyung Hwan Kim, Han Sang Kim, Seung-seob Kim, Hyo Sup Shim, Andrew Jihoon Yang, Jason Joon Bock Lee, Hong In Yoon, Joong Bae Ahn, Jee Suk Chang; Cancer Res Treat. 2022;54(1):54-64. Published online June 4, 2021; DOI: https://doi.org/10.4143/crt.2020.1247

Abstract PDF Supplementary Material PubReader ePub

Purpose
Preclinical data indicate that response to radiotherapy (RT) depends on DNA damage repair. In this study, we investigated the role of mutations in genes related to DNA damage repair in treatment outcome after RT.
Materials and Methods
Patients with solid tumor who participated in next generation sequencing panel screening using biopsied tumor tissue between October 2013 and February 2019 were reviewed and 97 patients that received RT were included in this study. Best response to RT and the cumulative local recurrence rate (LRR) were compared according to absence or presence of missense, nonsense, and frameshift mutations in ATM and/or BRCA1/2.
Results
Of the 97 patients, five patients harbored mutation only in ATM, 22 in only BRCA1/2, and six in both ATM and BRCA1/2 (ATM^mtBRCA^mt). Propensity score matching was performed to select the control group without mutations (ATM^wtBRCA^wt, n=33). In total, 90 RT-treated target lesions were evaluated in 66 patients. Highest objective response rate of 80% was observed in ATM^mtBRCA^mt lesions (p=0.007), which was mostly durable. Furthermore, the cumulative 1-year LRR was the lowest in ATM^mtBRCA^mt lesions and the highest in ATM^wtBRCA^wt lesions (0% vs. 47.9%, p=0.008). RT-associated toxicities were observed in 10 treatments with no significant difference among the subgroups (p=0.680).
Conclusion
Tumors with ATM and BRCA1/2 mutations exhibited superior tumor response and local control after RT compared to tumors without these mutations. The results are hypothesis generating and suggest the need for integrating the tumor mutation profile of DNA repair genes during treatment planning.

Citations

Citations to this article as recorded by

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