Colorectal cancer (CRC) is the second most common cancer in women and the third most common in men. Adenocarcinoma accounts for 90% of CRC cases. There has been accumulating evidence in support of the cancer stem cell (CSC) concept of cancer which proposes that CSCs are central in the initiation of cancer. CSCs have been the focus of study in a range of cancers, including CRC. This has led to the identification and understanding of genes involved in the induction and maintenance of pluripotency of stem cells, and markers for CSCs, including those investigated specifically in CRC. Knowledge of the expression pattern of CSCs in CRC has been increasing in recent years, revealing a heterogeneous population of cells within CRC ranging from pluripotent to differentiated cells, with overlapping and sometimes unique combinations of markers. This review summarises current literature on the understanding of CSCs in CRC, including evidence of the presence of CSC subpopulations, and the stem cell markers currently used to identify and localise these CSC subpopulations. Future research into this field may lead to improved methods for early detection of CRC, novel therapy and monitoring of treatment for CRC and other cancer types.

Aim: To document the prevalence and to evaluate the management strategies of haemorrhagic complications following pancreaticoduodenectomy (PD). Methods: All patients who underwent PD from 1/2000 to 10/2005 and experienced at least one episode of haemorrhage during the 30 first days postoperatively were recorded. Etiology of haemorrhage, treatment strategy and mortality rate were recorded and analyzed. Results: A total of 362 patients underwent PD during this period and 32 (8.8%) had haemorrhage postoperatively of whom 15 died (47% mortality rate). Primary intraluminal haemorrhage was recorded in 13 patients, primary intra-abdominal haemorrhage in 5 patients and secondary haemorrhage in 14 patients. Successful management of haemorrhage with angioembilization occurred in 2 patients in the study group. Statistical analysis revealed sepsis and sentinel bleed as risk factors for post-PD haemorrhage and pancreatic leak and sentinel bleed as risk factors for secondary haemorrhage (p < 0.05). Conclusions: Haemorrhage after PD is a life-threatening complication. Sepsis, pancreatic leak, and sentinel bleed are statistical significant factors predicting post-PD haemorrhage. Sentinel bleed is not statistically significant associated with postoperative mortality, but with the onset of secondary haemorrhage. The effectiveness of therapeutic angioembolization was not demonstrated in our study.

Cancer stem cells (CSCs) are proposed to be the cells that initiate tumorigenesis and maintain tumor development due to their self-renewal and multipotency properties. CSCs have been identified in many cancer types and are thought to be responsible for treatment resistance, metastasis, and recurrence. As such, targeting CSCs specifically should result in durable cancer treatment. One potential option for targeting CSCs is by manipulation of the renin-angiotensin system (RAS) and pathways that converge on the RAS with numerous inexpensive medications currently in common clinical use. In addition to its crucial role in cardiovascular and body fluid homeostasis, the RAS is vital for stem cell maintenance and differentiation and plays a role in tumorigenesis and cancer prevention, suggesting that these roles may converge and result in modulation of CSC function by the RAS. In support of this, components of the RAS have been shown to be expressed in many cancer types and have been more recently localized to the CSCs in some tumors. Given these roles of the RAS in tumor development, clinical trials using RAS inhibitors either singly or in combination with other therapies are underway in different cancer types. This review outlines the roles of the RAS, with respect to CSCs, and suggests that the presence of components of the RAS in CSCs could offer an avenue for therapeutic targeting using RAS modulators. Due to the nature of the RAS and its crosstalk with numerous other signaling pathways, a systems approach using traditional RAS inhibitors in combination with inhibitors of bypass loops of the RAS and other signaling pathways that converge on the RAS may offer a novel therapeutic approach to cancer treatment.