In the present study the prognostic value of both DNA ploidy and the proliferative activity of tomour cells were studied in a series of 76 consecutive patients suffering from gastric tumours. DNA ploidy and the proliferative index (as measured by the percentage of S-phase cells) were determined by flow cytometry using fresh tumour specimens.The presence of DNA aneuploid clones by flow cytometry was detected in 62% of the cases (mean DNA index of 1.63 ± 0.46; range 1.08–2.92), the mean proportion of S-phase cells being of 18.4 ± 11.5%. In comparison with diploid cases, aneuploid tumours showed a higher proliferative activity (cases with more than 15% S-phase cells: 18.4% versus 6.1%, p = 0.0001) as well as a higher incidence of node involvement (95% versus 68%, p = 0.001). By contrast, no significant differences were detected with respect to sex, age, histologic grade and type, clinical stage, tumour size and the incidence of extranodal involvement.Upon grouping the patients according to the proportion of S-phase cells no significant differences were observed for the clinical and biological parameters explored except for an association between a high percentage of S-phase cells and the presence of DNA aneuploidy (40% versus 96%, p = 0.0001). Regarding survival the presence of DNA aneuploidy was significantly associated with poor outcome as compared to the diploid cases (median of 15 versus 26 months, p = 0.005). By contrast, the proportion of S-phase cells did not predict patients’s outcome.Multivariate analysis of prognostic factors showed that the presence of DNA aneuploidy (p = 0.003) together with the histologic type (p = 0.03) and the existence of extranodal metastases (p = 0.05) were the best combination of prognostic factors for survival prediction.

The HPA medium is superior to Skirrow's medium and nonselective media in promoting growth of H. pylori and, on the basis of these results, we recommended the use of HPA medium for primary isolation of H. pylori from gastric biopsies.

Previous research has demonstrated that chronic inflammation facilitates cancer progression and spread to other sites. The effect of acute inflammation in the microenvironment of the tumor that develops as a result of standard biopsy procedures has not been studied in detail. Recent studies demonstrated that acute inflammation in mouse models from a mammary biopsy increases the frequency of distal cancer metastasis. Core needle biopsies are the standard procedure for breast cancer diagnosis, but there have been no studies detailing the inflammatory response from the biopsy. The purpose of this study is to determine if core needle biopsies in breast cancer patients trigger an inflammatory response, determine the type of inflammatory response that occurs and study the potential effect of acute inflammatory response on tumor cells remaining. The biopsy wound site was identified in primary tumor resection samples from breast cancer patients. The inflammatory response adjacent and distant to the biopsy were studied via histology and immunohistochemistry. Tumor cell proliferation was studied as well. Our study demonstrated that diagnostic core needle biopsies trigger inflammatory cell recruitment at the site, and those cells remain over long periods of time. An unexpected increase in eosinophils were found to accumulate at the biopsy site. The biopsy also was shown to increase proliferation adjacent to the wound site. Overall, core needle biopsies used for breast cancer diagnosis induce a unique inflammatory environment at the site of the biopsy as well as the closely surrounding cells. Inflammation induced by the biopsy could lead to tumor cell progression or metastasis in breast cancer. These findings may be important for the clinical management of breast cancer. Citation Format: Spencer BL, Szalayova G, Ogodnik A, Rincon M, James T. Human breast cancer biopsies induce eosinophil recruitment and enhance adjacent cancer cell proliferation [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-03-09.