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A Randomized Trial of Laparoscopic versus Open Surgery for Rectal Cancer To the editor: The primary outcome in the Colorectal Cancer Laparoscopic or Open Resection (COLOR) II trial by Bonjer et al. (April 2 issue)1 was locoregional recurrence 3 years after the index surgery. Although the percentages of patients who received preoperative chemotherapy and radiotherapy are reported (33% and 59%, respectively), the percentage of patients who received adjuvant chemotherapy is not. In the European Organisation for Research and Treatment of Cancer (EORTC) Radiotherapy Group Trial 22921, investigators found that in patients with rectal cancer who underwent radiotherapy preoperatively, both preoperative and postoperative chemotherapy had a significant effect on loco­ regional recurrence.2 After 5 years of follow-up, patients in the EORTC trial who received preoperative radiotherapy alone had a local recurrence rate of 21.9%, as compared with 10.9% of those who received preoperative chemoradiotherapy, 13.7% of those who received preoperative radiotherapy and adjuvant chemotherapy, and 10.7% of those who received preoperative chemoradiotherapy and adjuvant chemotherapy. These effects persisted at the 10-year follow-up.3 Thus, we believe that it is important to clarify the percentage of patients who received adjuvant chemotherapy and whether the rate was similar in the laparoscopic-surgery group and the open-surgery group. David E. Kearney, M.B., M.D. J. Calvin Coffey, M.B., Ph.D. University Hospital Limerick Limerick, Ireland No potential conflict of interest relevant to this letter was reported. 1. Bonjer HJ, Deijen CL, Abis GA, et al. A randomized trial of

laparoscopic versus open surgery for rectal cancer. N Engl J Med 2015;372:1324-32.

2. Bosset JF, Collette L, Calais G, et al. Chemotherapy with

preoperative radiotherapy in rectal cancer. N Engl J Med 2006;355: 1114-23. 3. Bosset JF, Calais G, Mineur L, et al. Fluorouracil-based adjuvant chemotherapy after preoperative chemoradiotherapy in rectal cancer: long-term results of the EORTC 22921 randomised study. Lancet Oncol 2014;15:184-90. DOI: 10.1056/NEJMc1505367

The authors reply: We agree with Kearney and Coffey that adjuvant chemotherapy could affect the rates of locoregional recurrence of rectal cancer. In our study, preoperative and postoperative protocols were administered equally in the laparoscopic-surgery group and the open-surgery group.1 Adjuvant chemotherapy was administered in 32.4% of patients in the laparoscopic-surgery group and in 33.6% of patients in the open-surgery group. Since the rates of adjuvant chemotherapy were similar in the two study groups, between-group differences in outcome cannot be attributed to adjuvant chemotherapy. H. Jaap Bonjer, M.D., Ph.D. Charlotte L. Deijen, M.D. VU University Medical Center Amsterdam, the Netherlands [email protected]

Eva Haglind, M.D., Ph.D. Sahlgrenska University Hospital–Östra Gothenburg, Sweden

for the COLOR II Study Group Since publication of their article, the authors report no further potential conflict of interest. 1. van der Pas MH, Haglind E, Cuesta MA, et al. Laparoscopic

versus open surgery for rectal cancer (COLOR II): short-term outcomes of a randomised, phase 3 trial. Lancet Oncol 2013;14:210-8.

DOI: 10.1056/NEJMc1505367

Cancers Complicating Inflammatory Bowel Disease To the Editor: Beaugerie and Itzkowitz (April 9 basis of colorectal cancer associated with inissue)1 describe the importance of genetic factors flammatory bowel disease should not be overin the colorectal cancers associated with inflam- looked. matory bowel disease. However, the immunologic Two recent studies have shown that T-helper

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correspondence

type 17 (Th17) cells play a key role in colorectal cancer associated with inflammatory bowel disease.2,3 Martin et al.2 reported that ROR-γt– dependent Th17 lymphocytes supported the growth of colorectal cancer in patients with colitis. Punkenburg et al.3 investigated basic leucine zipper transcription factor, ATF-like (Batf), the activating protein 1 family member, in a mouse model to evaluate the role of Th17 cells in inflammation-induced colon carcinogenesis. They also studied the expression of Batf and ROR-γt in patients with inflammatory bowel disease and colorectal cancer. They concluded that Batf-dependent interleukin-23R+interleukin6+CD4+ Th17 cells critically control interleukin-23–driven colitis-associated tumor formation. Though they are slightly different from each other, these two studies stressed that the Th17 cell is a potential future therapeutic target to limit colorectal carcinogenesis in inflammatory bowel disease.

Kaohsiung Medical University Hospital Kaohsiung, Taiwan

support for the role of both the innate and adaptive immune system, including Th17 cells, in colitis-associated carcinogenesis.1 Given the space limitations for our article, we were unable to provide details on Th17 cells in this field of research. It is established that Th17 cells play a pivotal role in intestinal inflammation in patients with inflammatory bowel disease, even if differences exist between Crohn’s disease and ulcerative colitis with respect to cell and cytokine pathways.2 In parallel, there is emerging evidence that Th17 cytokines could play a role in the control of colorectal-cancer carcinogenesis in general.3 However, to our knowledge, so far data suggesting a specific role of Th17 cells in colitis-associated carcinogenesis have been restricted mainly to animal models.4,5 Future investigations may elucidate the role of specific immunologic mechanisms in colitisassociated carcinogenesis, including Th17 overexpression. Data are also lacking on the interface between these mechanisms and molecular genetic changes of the colonic epithelial cells of inflamed tissues in patients with inflammatory bowel disease and the relationship between these mechanisms and the gut microbiome. Laurent Beaugerie, M.D., Ph.D.

Chung-Jen Chen, M.D.

Université Pierre et Marie Curie Paris, France

Yi-Ching Lin, M.D. Kaohsiung Medical University Kaohsiung, Taiwan

Yu-Chih Lin, M.D.

Kaohsiung Medical University Kaohsiung, Taiwan [email protected]

Steven H. Itzkowitz, M.D.

No potential conflict of interest relevant to this letter was reported. 1. Beaugerie L, Itzkowitz SH. Cancers complicating inflamma-

tory bowel disease. N Engl J Med 2015;372:1441-52. 2. Martin M, Kesselring RK, Saidou B, et al. RORγt(+) hematopoietic cells are necessary for tumor cell proliferation during colitis-associated tumorigenesis in mice. Eur J Immunol 2015; 45:1667-79. 3. Punkenburg E, Vogler T, Büttner M, et al. Batf-dependent Th17 cells critically regulate IL-23 driven colitis-associated colon cancer. Gut 2015 April 2 (Epub ahead of print). DOI: 10.1056/NEJMc1505689

The Authors Reply: In reply to Lin and colleagues about the potential role of Th17 cells in colitis-associated carcinogenesis: indeed, data from studies in animals and humans provide

Icahn School of Medicine at Mount Sinai New York, NY Since publication of their article, the authors report no further potential conflict of interest. 1. Ullman TA, Itzkowitz SH. Intestinal inflammation and can-

cer. Gastroenterology 2011;140:1807-16. 2. Troncone E, Marafini I, Pallone F, Monteleone G. Th17 cytokines in inflammatory bowel diseases: discerning the good from the bad. Int Rev Immunol 2013;32:526-33. 3. De Simone V, Franzè E, Ronchetti G, et al. Th17-type cytokines, IL-6 and TNF-α synergistically activate STAT3 and NF-kB to promote colorectal cancer cell growth. Oncogene 2014 September 1 (Epub ahead of print). 4. Martin M, Kesselring RK, Saidou B, et al. RORγt(+) hematopoietic cells are necessary for tumor cell proliferation during colitis-associated tumorigenesis in mice. Eur J Immunol 2015; 45:1667-79. 5. Punkenburg E, Vogler T, Büttner M, et al. Batf-dependent Th17 cells critically regulate IL-23 driven colitis-associated colon cancer. Gut 2015 April 2 (Epub ahead of print). DOI: 10.1056/NEJMc1505689

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Cancers Complicating Inflammatory Bowel Disease.

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