Cytogenetic analysis of epithelial ovarian cancer's stem cells: an overview on new diagnostic and therapeutic perspectives.

Ovarian cancer is one of the most frequent solid tumor that shows clearly biphasic behaviour in response to chemotherapy, with the majority of patients who achieved complete remission after the first cycle of chemotherapy, and subsequently present a relapse which, in most cases, leads to death. Epithelial ovarian cancer (EOC) arises as a consequence of genetic alterations that affect the cells of the ovarian surface, which leads to changes that occur through the activation of oncogenes and inactivation of tumor suppressor genes. The progression of EOC is characterized by a series of combined epigenetic aberrations, including the most important of those determined by the loss of methylation of certain regions of DNA encoding genes such as Ras-association domain-containing family 1 [(RASSF1A) tumor suppressor], death-associated protein kinase [(DAPK) protein kinase associated with the regulation of apoptosis], human sulfa- tase-I [(hSulf-1) sulfatase, which plays a key role in the regulation of apoptosis], breast cancer 1 gene [(BRCA1) tumor suppressor gene, involved in the processes of DNA repair], and HOXAI0 (gene required to promote many transcription factors). To date, accumulating evidence suggests that the initial clinical response is due primarily to the therapeutic efficacy of chemotherapy against differentiated can- cer cells that constitute the bulk of the tumor, whereas the high rate of recurrence is thought to be due to remaining drug-resistant cells, biologically distinct, identified as cancer stem cells (CSC). Current efforts are focusing on genetic and cytological definition of CSC, to guide the development of new diagnostic, and therapeutic perspectives.

Hematopoietic progenitor cells (HPCs) in node-negative invasive breast carcinomas: Immunohistochemical analysis and clinico-pathological correlations.

Using immunohistochemistry, we investigated 603 negative lymph nodes from 51 patients affected by invasive breast cancer (BC) to recognize bone marrow-derived hematopoietic progenitor cells (HPCs). HPC aggregates, revealed by CD34, CD133, VEGFR1, and CD117 antisera, were determined by an intensity-distribution score (ID). Cases with an ID-score >3 at least for one marker were considered to strongly express HPCs. Twenty-five of 51 (49%) high expressor patients were identified by CD34 antiserum, while 24/51 (47.1%), 17/51 (33.3%), and 15/51 (29.4%) were identified by CD117, CD133, and VEGFR1, respectively. No significant relationships were found between HPCs status and histotype, tumor grade, stage, and hormone receptors, as determined at the moment of the first diagnosis. A significant correlation was recorded for Ki-67 values, as well as for death from invasive BC. No statistical significance was achieved regarding HER2 status, although a tendency toward a statistically significant P value was obtained. A significant relationship (P<0.001) was found between high expressors of HPC and progression of disease, documented by the development of distant metastases. An equivalent P value was ascertained for osseous localizations, with a lesser value in other metastatic sites. Regarding the appearance of distant metastases, the greatest efficiency value was obtained by CD133 (85.7%). Overall survival (OS) and distant metastases-free survival (DMFS) revealed a high statistical significance for HPC expression, Ki-67 values, and HER2 status. By multivariate analysis, HPC expression and Ki-67 values emerged as the higher independent prognostic variables in the analysis of DMFS and OS, respectively.

Role of interleukin-23 circulating levels increase in resected colorectal cancer before and after chemotherapy: preliminary data and future perspectives.

Expression of IL-23, a heterodimeric cytokine involved in the induction of Th17 cells, is increased in human tumors. Although the endogenous IL-23 expression has been reported to promote tumor development and growth, the studies using local and systemic administration of IL-23 have shown that its application at the excessive amount induces antitumor immune responses. IL-23 is, today, considered the key driver of intestinal inflammation and its role in inflammatory responses is tissue-specific. The aim of this study was to investigate the role of circulating levels of IL-23 in patients with resected colorectal cancer (CRC) before and after chemotherapy, respect to healthy controls. Twenty-five patients were enrolled between June 2007 and January 2009, and followed through 2010. All patients underwent chemotherapy, mostly FOLFOX4. Twenty-sex and age-matched healthy donors were recruited as controls. IL-23 serum concentrations, measured by a quantitative enzyme immunoassay technique, were significantly higher in patients with resected CRC (26.02 ± 28.63 pg/ml versus 7.1 ± 6.4 pg/ml, P < 0.001) and after chemotherapy respect to controls (21.74 ± 23.82 pg/ml versus 7.17 ± 6.43 pg/ml, P < 0.001). An increase was documented also before chemotherapy (26.02 ± 28.63 pg/ml versus 21.74 ± 23.82 pg/ml, P = 0.7) but not statistically significant. This work investigated, for the first time, the role of IL-23 in CRC resection and chemotherapy, showing no correlation with the severity of disease, tumor removal, and chemotherapeutic treatment. However, other works are needed to better clarify if IL-23 could be considered a key-molecule in human CRC and a target for tumor treatment.

[Acute typhlitis associated with taxane-based chemotherapy]. / Tiflite acuta dopo trattamento chemioterapico con taxani.

A rare case of acute typhlitis is reported. The patient had undergone chemotherapy for a breast cancer. Clinical and diagnostic tools as well as general and topical care are examined.