Esophageal cancer (EC) is an aggressive tumor that represents the 6th most common cause of cancer death worldwide. The estimated incidence in Spain is 2090 cases/year. Two main pathological subtypes exist, squamous cell carcinoma and adenocarcinoma. The main differences between them are localization and underlying factors which are the principal cause of the recent incidence changes observed in west countries. Staging techniques and treatment options which combine surgery, chemotherapy and radiotherapy, reflected the high complexity of the EC management. An undeniably multidisciplinary approach is, therefore, required. In this guide, we review the status of current diagnosis and treatment, define evidence and propose recommendations.
Treatment options for patients with clinically localized c a n c e r d i a g n o s i s i n c l u d e r a d i a t i o n t h e r a p y a n d chemotherapy. Each option is associated with side effects. Progress in cancer therapy has increased multimodality approach such as chemoradiotherapy, and patient's life expectancy as well. However aggressive treatments and prolonged survival may cause growing concern about late effect of treatments. An important complication for patients submitted to combined approaches is the potential development of a second primary cancer (SPC). The appearance of SPCs is considered a late radiation effect only if it fits certain predetermined criteria. Some of these criteria include the timing of SPCs development (>5 years after radiation), the origin from tissues within the irradiated fields and the different histopathological features compared to primary tumors (1,2). The process of radio-carcinogenesis is not clearly understood, and accurate risk models do not exist; the best data for radiation-induced carcinogenic risk come from A-bomb survivor studies, although these are subject to big limitations (3). Carcinogenesis risk after radiotherapy seems to be highest for tissues receiving even low doses (≤6 Gy) (4). However, there seems to be a tissues-specific dose-response relationship for radiocarcinogenesis, whit radiation-induced sarcomas developing in tissues receiving higher doses (30 to 60 Gy) and carcinomas induced in tissues receiving much lower doses (5,6). Both the integral dose to normal tissue and its dose distribution therefore influence the risk. Recently it has been demonstrated that multiple primary tumors
rate (ORR), TTP, and OS: RAS (KRAS/NRAS) mutational status, primary tumour location and metastases site, efficacy of first-line treatment, sex, age, body mass index, lactate dehydrogenase (LDH), alkaline phosphatase, CEA, lymphocytes and haemoglobin level at the time of beginning second line treatment. Median follow-up was 35 months. Results: In whole group median TTP was 5.1 months and OS -12.9. Response rates: CR -1%, PR -18%, NC -40%, PD -40%. For patients who achieved ORR (CR or PR) median TTP and OS was 7.8 and 19.3 months while for patients with PD -2.8 and 9.9. Hepatic location of metastases was associated with the highest rate of ORR, while peritoneal with the lowest: 46% and 0% (p ¼ 0.041) respectively. Median TTP for patients who gained CR, PR or NC (DCR -disease control) while first-line treatment was 6.7 compared with 3.3 months for patients with PD (p < 0,0001). TTP under/equal 6 months and PD during first-line treatment were associated with shorter OS: 12.9 vs 15.3 months (p ¼ 0.049) and 9.9 vs 14.2 months (p ¼ 0.007). Age over 70 and BMI !25 were good prognostic factors with OS 19.6 months vs 10.4 (p ¼ 0.01) and 18.4 months vs 9.1 (p ¼ 0.039) respectively. There was no difference between patients in terms of KRAS and NRAS mutational status. For wild type and mutant tumours it was 6.6 months vs 6.1 (p ¼ 0.098) and 17.9 vs 12.9 (p ¼ 0.183) respectively in TTP and OS. Right-side primary tumours were associated with worse DCR, TTP and OS compared to left-side primary; 45%, 2.3 months and 11.2 months vs 61%, 4.9 months and 12.8 months, but the differences were not statistically significant. Other factors did not occur relevant. Sixteen patients (20%) discontinued treatment due to adverse events. There were no toxic deaths. Conclusion: Positive prognostic impact on second-line treatment with bevacizumab and FOLFOX4 in mCRC have: first-line treatment response, hepatic site of metastases, age over 70 and BMI !25. Worse prognosis was observed in group of patients with peritoneal metastases and poor response for first-line chemotherapy. RAS mutational status seemed to not influence prognosis in the analysed cohort. Location of the primary tumour in the right side of the colon was not proven to be a negative prognostic factor. P À 231 Clinical significance of microsatellite instability in Introduction: Colorectal cancer (CRC) with microsatellite instability (MSI) are known to have better prognosis compared to those with microsatellite stable (MSS). Recent studies reported that there are biological differences according to tumor location in CRC. In this study, we aimed to identify the clinical significance of MSI in patients with right-sided CRC. Methods: Between October 2004 and December 2016, medical records from a total of 1,009 patients with CRC were retrospectively reviewed. Patients with MSI testing were included in the analysis. We assessed the long-term outcomes of MSI according to the tumor location using the Kaplan-Meier curves and Cox regression models. Results: The median follow-up duration was 25 ...
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