For over 30 years, stem cells have been used in the replenishment of blood and immune systems damaged by the cancer cells or during treatment of cancer by chemotherapy or radiotherapy. Apart from their use in the immuno-reconstitution, the stem cells have been reported to contribute in the tissue regeneration and as delivery vehicles in the cancer treatments. The recent concept of 'cancer stem cells' has directed scientific communities towards a different wide new area of research field and possible potential future treatment modalities for the cancer. Aim of this review is primarily focus on the recent developments in the use of the stem cells in the cancer treatments, then to discuss the cancer stem cells, now considered as backbone in the development of the cancer; and their role in carcinogenesis and their implications in the development of possible new cancer treatment options in future.

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Role of stem cells in cancer therapy and cancer stem cells: a review

Background: Benefits of prophylactic hematopoietic colony-stimulating factors (CSFs) in adults and children receiving cancer chemotherapy or undergoing stem-cell transplantation (SCT) are unclear. Purpose: To determine whether prophylactic CSFs decrease mortality, infections, and febrile neutropenia more than does placebo or no therapy in patients with cancer and in patients undergoing SCT. Data Sources: Electronic searches of Ovid MEDLINE and EMBASE from inception until April 2007 and of the Cochrane Central Register of Controlled Trials until the second quarter of 2006. Study Selection: We selected 148 trials that were reported in any language that randomly assigned patients to CSFs or to either placebo or no therapy. Prophylactic CSFs were given concurrently with or after initiation of chemotherapy. Data Extraction: Two reviewers independently extracted data onto standardized forms. Data Synthesis: Short-term all-cause mortality appeared to be similar between the prophylactic CSF and the control groups (7.6% vs. 8.0%; relative risk, 0.95 [95% CI, 0.84 to 1.08]; absolute risk reduction, 0.4% [CI, 0.5% to 1.4%]). Risks for infection-related death with CSFs and placebo or no therapy were 3.1% and 3.8%, respectively (relative risk, 0.82 [CI, 0.66 to 1.02]; absolute risk reduction, 0.8% [CI, 0.0% to 1.5%]). Use of CSFs reduced the following more than did placebo or no therapy: documented infections (median rate, 38.9% vs. 43.1%; rate ratio, 0.85 [CI, 0.79 to 0.92]), microbiologically documented infections (median rate, 23.5% vs. 28.6%; rate ratio, 0.86 [CI, 0.77 to 0.96]), and episodes of febrile neutropenia (median rate, 25.3% vs. 44.2%; rate ratio, 0.71 [CI, 0.63 to 0.80]). Limitations: Trial designs, including assessments of infections, and participants were heterogeneous. Estimates of mortality effects were imprecise. Conclusions: Prophylactic CSFs may have little or no effect on mortality but do decrease rates of infection in patients receiving cancer chemotherapy or those undergoing SCT.

Meta-analysis: effect of prophylactic hematopoietic colony-stimulating factors on mortality and outcomes of infection.

After hematopoietic SCT (HSCT), G-CSF is commonly used to enhance stem cell engraftment to minimize the morbidity and mortality associated with prolonged neutropenia. However, there is no consensus on the optimal use of G-CSF after high-dose chemotherapy followed by HSCT. This review was performed to evaluate the evidence regarding the use of G-CSF after autologous and allogeneic HSCT. Studies investigating the use of G-CSF in comparison to control (observation or placebo), early vs delayed initiation of G-CSF, and other approaches driven by patient-specific parameters to identify optimal use of G-CSF have been reviewed. Various outcomes such as neutrophil and platelet engraftment, post-transplant length of hospital stay, post-transplant complications such as infection and GVHD, and survival have been assessed. Finally, we provide the level of evidence for each of the outcomes analyzed while evaluating strategies for using G-CSF in patients undergoing autologous or allogeneic HSCT.

Optimal use of G-CSF administration after hematopoietic SCT

Neuroblastoma is the most common extra-cranial solid tumor in children. It is a heterogeneous disease, consisting of neural crest-derived tumors with remarkably different clinical behaviors. It can present in a wide variety of ways, including lesions which have the potential to spontaneously regress, or as an extremely aggressive form of metastatic cancer which is resistant to all forms of modern therapy. They can arise anywhere along the sympathetic nervous system. The median age of presentation is approximately 18 months of age. Urinary catecholamines (HVA and VMA) are extremely sensitive and specific tumor markers and are used in diagnosis, treatment response assessment and post-treatment surveillance. The largest national treatment groups from North America, Europe and Japan have formed the International Neuroblastoma Risk Group Task Force (INRG) to identify prognostic factors, to understand the mechanisms of tumorigenesis in this rare disease and to develop multi-modality therapies to improve outcomes and decrease treatment-related toxicities. This international cooperation has resulted in a significant leap in our understanding of the molecular pathogenesis of neuroblastoma. Lower staged disease can be cured if the lesion is resectable. Treatment of unresectable disease (loco-regional and metastatic) is stratified depending on clinical features (age at presentation, staging investigations) and specific tumor biological markers that include histopathological analyses, chromosomal abnormalities and the quantification of expression of an oncogene (MYCN). Modern treatment of high-risk neuroblastoma is the paradigm for the evolution of therapy in pediatric oncology. Outcomes have improved substantially with multi-modality therapy, including chemotherapy, surgery, radiation therapy, myeloablative therapy with stem cell transplant, immunotherapy and differentiation therapy; these comprise the standard of care worldwide. In addition, newer targeted therapies are being tested in phase I/II trials. If successful these agents will be incorporated into mainstream treatment programs.

Neuroblastoma: the impact of biology and cooperation leading to personalized treatments.

Pegfilgrastim compared with Filgrastim after autologous hematopoietic peripheral blood stem cell transplantation

This randomised trial was designed to compare two groups treated with different G-CSF administration schedules with a third group receiving no G-CSF, after autologous peripheral blood stem cell transplantation (APBSCT). Children and adults with haematological malignancies or solid tumours were randomly assigned to receive either 150 microg/m2/day of Lenograstim starting on day 1 (G1) or on day 5 (G5) post APBSCT, or no Lenograstim (G0). Randomisation was stratified according to the conditioning regimen (Busulfan vs TBI vs no Busulfan and no TBI) and the graft CD 34+ cell count. A total of 240 patients were randomised; 239 were evaluable. All three patient groups were comparable. Median duration of neutropenia was 9 days (4-40), and 10 days (5-15) in the G1 and G5 groups, respectively, significantly shorter than in the G0 group, 13 days (7-36) (P < 0.0001). No difference was observed in the duration of thrombocytopenia, transfusion support and extra-haematological complications. The duration of post transplant hospitalisation was significantly shorter in adults who received G-CSF. Clinical and cost arguments favour the initiation of G-CSF on day 5 in adults. The same policy could be applied in children given that clinical management is easier and costs are similar.

Cost effectiveness of day 5 G-CSF (Lenograstim) administration after PBSC transplantation: results of a SFGM-TC randomised trial.

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Cost effectiveness of day 5 G-CSF (Lenograstim) administration after PBSC transplantation: results of a SFGM-TC randomised trial.