BackgroundMiRNAs are often deregulated in colorectal cancer and might function as tumor suppressors or as oncogenes. They participate in controlling key signaling pathways involved in proliferation, invasion and apoptosis and may serve as prognostic and predictive markers. In this study we aimed to evaluate the role of miRNA-148a and miRNA-625-3p in metastatic colorectal cancer.MethodsFifty-four patients with a first-time diagnosed CRC receiving FOLFOX ± Bevacizumab were involved in the study. Tumor samples underwent routine pathology examination including evaluation for tumor budding and KRAS. MiRNA-148a and miRNA-625-3p expression analysis was done by RT-PCR. Associations between expression of both miRNAs and clinico-pathological factors, treatment outcomes and survival were analyzed.ResultsBoth miRNA-148a and miRNA-625-3p were down-regulated in the tumors compared to normal colonic mucosa. Significantly lower expression of both miRNAs was noticed in tumors with budding phenomenon compared to tumors without it (median values of miRNA-148a were 0.314 and 0.753 respectively, p = 0.011, and 0.404 and 0.620 respectively for miRNA-625-3p, p = 0.036). Significantly lower expression of miRNA-625-3p was detected in rectal tumors, compared to tumors in the colon (median 0.390 and 0.665 respectively, p = 0.037). Progression free survival was significantly lower in patients with high miRNA-148a expression (6 and 9 months respectively, p = 0.033), but there were no significant differences in PFS for miRNA-625-3p and in overall survival for both miRNAs.ConclusionsThere was a significant relationship between low miRNA-148a and miRNA-625-3p expression and tumor budding, which is thought to represent epithelial-mesenchymal transition. Both studied miRNAs may be associated with a more aggressive phenotype and could be the potential prognostic and predictive biomarkers in CRC. Further investigation is needed to confirm miRNAs involvement in EMT, and their prognostic and predictive value.Electronic supplementary materialThe online version of this article (10.1186/s12885-017-3575-z) contains supplementary material, which is available to authorized users.

No abstract

Background: The study aims to evaluate the lymph node (LN) response to preoperative chemotherapy and its impact on long-term outcomes in advanced gastric cancer (AGC). Methods: Histological specimens retrieved at gastrectomy from patients who received preoperative chemotherapy were evaluated. LN regression was graded by the adapted tumor regression grading system proposed by Becker. Patients were classified as node-negative (lnNEG) in the case of all negative LN without evidence of previous tumor involvement. Patients with LN metastasis were classified as nodal responders (lnR) in case of a regression score 1a-2 was detected in the LN. Nodal non-responders (lnNR) had a regression score of 3 in all of the metastatic nodes. Survival was compared using Kaplan-Meier and Cox regression analysis. Result s: Among 87 patients included in the final analysis 29.9 % were lnNEG, 21.8 % were lnR and 48.3 % were lnNR. Kaplan-Meier curves showed a survival benefit for lnR over lnNR (p=0.03), while the survival of lnR and lnNEG patients was similar. Cox regression confirmed nodal response to be associated with decreased odds for death in univariate (HR: 0.33; 95 % CI 0.11-0.96, p=0.04) and multivariable (HR 0.37; 95 CI% 0.14-0.99, p=0.04) analysis. Conclusions: Histologic regression of LN metastasis after preoperative chemotherapy predicts the increased survival of patients with non-metastatic resectable AGC.

Rhabdoid colonic tumors are very rare lesions with just a few publications describing such neoplasms. Even more unusual for these lesions are their primary rectal locations, with only two brief case reports having been published on that subject to date. We present a case of a composite rhabdoid rectal carcinoma in a 49-year-old male. The tumor behaved very aggressively, with rapid patient demise despite radical surgery and intensive postoperative chemotherapy (FOLFIRI [folinic acid {leucovorin}, fluorouracil {5-fluorouracil}, and irinotecan] and FOLFOX4 [folinic acid {leucovorin}, fluorouraci {5-fluorouracil}, and oxaliplatin]). Pathologic examination was supportive of a rhabdoid carcinoma, with a compatible immunohistochemical profile, demonstrating synchronous expression of vimentin and epithelial markers in the tumor cells. In addition, BRAF V600E gene mutation, together with a wild-type KRAS gene, was identified, and no evidence of microsatellite instability based on MLH1, MSH2, MSH6, and PMS2 immunophenotypes, i.e., no loss of expression for all 4 markers, was observed. Our reported case confirms previously published observations of the clinical aggressiveness and the poor therapeutic response for rhabdoid tumors.

GSH and GST levels change significantly during the treatment process and these changes depend on the response to treatment, treatment type, and site of metastases. Further analysis of the changes in GSH and GST levels during treatment would allow the assessment of the predictive potential of this molecular marker.