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Although tumor budding is linked to adverse prognosis in colorectal cancer, it remains largely unreported in daily diagnostic work due to the absence of a standardized scoring method. Our aim was to assess the interobserver agreement of a novel 10-high-power-fields method for assessment of tumor budding at the invasive front and to confirm the prognostic value of tumor budding in our setting of colorectal cancers. Whole tissue sections of 215 colorectal cancers with full clinico-pathological and follow-up information were stained with cytokeratin AE1/AE3 antibody. Presence of buds was scored across 10-high-power fields at the invasive front by two pathologists and two additional observers were asked to score 50 cases of tumor budding randomly selected from the larger cohort. The measurements were correlated to the patient and tumor characteristics. Inter-observer agreement and correlation between observers' scores were excellent (Po0.0001; intraclass correlation coefficient ¼ 0.96). A test subgroup of 65 patients (30%) was used to define a valid cutoff score for high-grade tumor budding and the remaining 70% of the patients were entered into the analysis. High-grade budding was defined as an average of Z10 buds across 10-high-power fields. High-grade budding was associated with a higher tumor grade (Po0.0001), higher TNM stage (P ¼ 0.0003), vascular invasion (Po0.0001), infiltrating tumor border configuration (Po0.0001) and reduced survival (Po0.0001). Multivariate analysis confirmed its independent prognostic effect (P ¼ 0.007) when adjusting for TNM stage and adjuvant therapy. Using 10-high-power fields for evaluating tumor budding has independent prognostic value and shows excellent inter-observer agreement. Like the BRE and Gleason scores in breast and prostate cancers, respectively, tumor budding could be a basis for a prognostic score in colorectal cancer.

Weekly administration of gemcitabine provides a safe, well-tolerated, and effective treatment for chemotherapy naïve patients with advanced cholangiocarcinoma, particularly with a gallbladder origin.

The purpose of the present study was to investigate the association between performance status (PS) and mean dose of irinotecan (CPT-11) in patients with recurrent advanced colorectal cancer relapsing after 5-fluorouracil and leucovorin chemotherapy. Patients who had completed their last chemotherapy course with 5-fluorouracil and leucovorin for at least 6 weeks and progressed were included. Based on PS, we administered a starting dose of 250 mg/m² in patients with a PS 70–80 (group A), and 350 mg/m² for those with a PS > 80 (group B). Of a total of 90 treated patients, all were evaluable, 18 had a partial response (PR) (20%), 39 stable disease (43%), and 15 progressed (37%). No significant difference was noticed between patients with PS ≧ 90 or ≤ 80 (p = 0.925), or between those who received a mean dose of CPT-11 ≧300 or ≤300 (p = 0.602), for response, survival and time to progression. Toxicity was increased in group B as expected, with significant differences for acute cholinergic syndrome (p = 0.02), diarrhea after the first 24 h (p = 0.03) and severe diarrhea (p = 0.03). According to these results, we conclude that response to CPT-11 is independent of its dose, and that a dose of 250 mg/m² every 3 weeks might be a cost-effective and less toxic alternative in this setting. However, further adequately powered phase II or III randomized studies might be required in order to confirm this observation.

Gastrointestinal stromal tumors (GISTs) are rare mesenchymal neoplasms of the gastrointestinal tract (1%), and stomach is the most common location involved. However, the co-existence of gastric adenocarcinoma and GIST is very rare. A case of an 80-year-old male with a simultaneous presentation of a gastric adenocarcinoma and GIST is presented. Various hypotheses have been proposed in order to explain this rare simultaneous development, but even though it's cause has not been proven yet.

Most pancreatic adenocarcinoma patients present with locally advanced or metastatic disease at diagnosis. in this retrospective study the authors evaluated the prognostic significance of the CEA and CA-19.9 serum tumor markers in advanced (unresectable) pancreatic cancer in correlation to other prognostic factors (demographic data, clinical parameters, treatment modality) and survival time using univariate and multivariate methods, in 215 patients with locally advanced (unresectable) or metastatic pancreatic adenocarcinoma. median survival was 29.0 weeks, with 21.9% of patients surviving 36 weeks. Among 24 potential prognostic variables, 19 were associated with shorter survival. Multivariate analysis indicated that ten factors had a significant independent effect on survival: chemotherapy, surgery, tumor localization, elevated C-reactive protein, elevated CeA, CA 19-9 (>30 x nl), jaundice at diagnosis, weight loss >10%, distant metastases, and Karnofsky performance status. Patients who had only palliative therapy had a hazard ratio of 8.94 versus those who underwent palliative surgery and chemotherapy. Although certain clinical, biochemical and biological factors remain important predictors of survival in patients with advanced pancreatic cancer, CA-19.9 serum tumor marker levels retain independent prognostic value for poor survival.

362 evaluable node-positive patients with stage II breast cancer were randomized, receiving either 6 cycles of conventional CMF or 6 cycles of the combination of cyclophosphamide (500 mg/m²), mitoxantrone (Novantrone 10 mg/ m²), and fluorouracil (500 mg/m²; CNF). After a median follow-up of 51 months, 64 (36%) patients relapsed in the CMF group and 60 (33%) in the CNF group (p = 0.8276). By Cox multivariate analysis, tumor size, menopausal status and number of involved nodes were retained as independently significant variables. Toxicities were remarkably similar in both groups. It appears that after a median follow-up of 51 months there is no significant difference in relapse-free survival between node-positive patients with breast cancer who received either 6 cycles of the conventional CMF or the CNF combination as adjuvant treatment.

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