LETTERS TO THE EDITOR 487 tumour cells. No additional metastases were identified in a thorough search. Such an occurrence may be coincidental but it makes one wonder whether intra-operative seeding of tumour cells should not be a real concern of the surgeon, and what can be done about it?Ami Schattner, Adi Shani Kaplan Hospital, 76100 Rehovot, Israel.Carcinoma of the splenic flexure -a case for extended right hemicolectomy?Sir, We have recently managed a patient with a splenic flexure colonic carcinoma, who had an unusual distribution of lymph node metastases. This questions the validity of transverse colectomy for this condition.The classical treatment of resectable colonic carcinoma has been excision in continuity with its vascular supply in an attempt at reducing local recurrence by removing involved or potentially involved lymph nodes. This is based on Jamieson and Dobson's work' which suggested that the lymphatic drainage ofthe colon followed its main blood supply. However, blood supply to the splenic flexure has been shown to be somewhat variable. Griffiths2 demonstrated that it was supplied by the inferior mesenteric artery via the left colic in 89% of cases and by the superior mesenteric artery via the middle colic in 11 %. He also noted that the middle colic was absent in 22% of cases. These findings were confirmed by Sierocinski3 who found in 100 post-mortem dissections that the middle colic vessel supplied the splenic flexure in only 19. Where the middle colic is absent, the ileocolic supplied the transverse colon and the left colic supplied the splenic flexure.Goligher4 has advocated transverse colectomy for splenic flexure carcinoma, ligating both middle colic at its origin and the ascending branch of the left colic to remove those nodes most likely to be involved.We report the case of an 83 year old female admitted as an emergency with vomiting and abdominal pain. Plain abdominal X-rays and a gastrografin enema revealed a stenotic lesion at the splenic flexure with complete obstruction. At laparotomy a splenic flexure carcinoma was found and an extended right hemicolectomy performed with an end to end ileocolic anastomosis. The patient made an uneventful recovery and was discharged home.Histological examination of the specimen showed a moderately differentiated adenocarcinoma of the splenic flexure with one of eight local lymph nodes involved (Duke's stage C Jass Class IV). However, one node at the ileo-colic junction showed adenocarcinomatous deposits.Aldridge5

BACKGROUND:Despite strict patient selection criteria, diabetes remission is not seen in all patients after gastric bypass. Can length of the common limb influence diabetes remission?AIM:To find if any correlation exists between the length of the common limb and remission of diabetes.STUDY DESIGN:Prospective study.MATERIALS AND METHODS:Twenty-five consecutive patients with Type II diabetes mellitus and a fasting C-peptide >1 ng/ml who underwent laparoscopic Roux-en-y gastric bypass were included. All patients had standard limb lengths and length of the common limb was measured in all patients. Patients were followed up and glycated haemoglobin (HbA1c) was repeated at 6 months postoperatively. Pre- and postoperative HbA1c were then correlated with the lengths of common limb to look for any relation.STATISTICAL ANALYSIS:Descriptive and inferential statistical analysis, analysis of variance (ANOVA).RESULTS:Of the 25 patients, 15 were females and 10 were males. The mean age was 44.16 years and the mean body mass index (BMI) was 43.96 kg/m2. Preoperative HbA1c varied from 5.8 to 12.3%. Length of the common limb varied from 210 to 790 cm (mean 470.4 cm). HbA1c at 6 months ranged from 4.8 to 7.7% (mean 5.81%). On comparison of preoperative and 6 months postoperative HbA1c and correlating with the length of common limb, we found that patients with a common limb of length <600 cm had a statistically significant improvement in HbA1c compared to those with >600 cm length (P = 0.004).CONCLUSION:A shorter common limb does appear to have better chances of resolution of Type II diabetes mellitus in our study, thus paving the way for further studies.

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She then received carboplatin/pemetrexed with a PR. Brief erlotinib rechallenge resulted in PD, with post-progression NGS revealing loss of EGFR T790M, presence of the original EGFR exon19del, and a new CBL C384R, a mutation located in the RING domain and predicted to result in the loss of CBL ligase adaptor function, resulting in sustained activation of relevant RTKs. The patient then started sitravatinib treatment in Study 516-001. After 36 days on-study, restaging demonstrated PR, which was later confirmed with a maximum decrease in unidimensional target lesion measurement of 77%. She remains on-study. Conclusion: Loss of function mutations in CBL represents a unique class of mutations that may be responsible for acquired resistance to 3 rd generation EGFR TKI. Sitravatinib has demonstrated clinical activity in a patient with NSCLC characterized by EGFR exon19del and CBL C384R mutations. The clinical trial with sitravatinib is currently enrolling patients with CBL loss of function mutations. (NCT02219711).