Novel strategies for targeting leukemia stem cells: sounding the death knell for blood cancer

Abstract

Background Cancer stem cells (CSCs), also known as tumor-initiating cells (TICs), are characterized by high self-renewal and multi-lineage differentiation capacities. CSCs are thought to play indispensable roles in the initiation, progression and metastasis of many types of cancer. Leukemias are thought to be initiated and maintained by a specific sub-type of CSC, the leukemia stem cell (LSC). An important feature of LSCs is their resistance to standard therapy, which may lead to relapse. Increasing efforts are aimed at developing novel therapeutic strategies that selectively target LSCs, while sparing their normal counterparts and, thus, minimizing adverse treatment-associated side-effects. These LSC targeting therapies aim to eradicate LSCs through affecting mechanisms that control their survival, self-renewal, differentiation, proliferation and cell cycle progression. Some LSC targeting therapies have already been proven successful in pre-clinical studies and they are now being tested in clinical studies, mainly in combination with conventional treatment regimens. Conclusions A growing body of evidence indicates that the selective targeting of LSCs represents a promising approach to improve disease outcome. Beyond doubt, the CSC hypothesis has added a new dimension to the area of anticancer research, thereby paving the way for shaping a new trend in cancer therapy.

Involvement of mitochondrial dynamics in the antineoplastic activity of cisplatin in murine leukemia L1210 cells

“…Leukemia is also known as blood cancer and has a high mortality rate. It is pathologically characterized by the massive proliferation of abnormal hematopoietic stem cells (1,2). Although the precise pathogenesis of leukemia remains to be elucidated, various genetic mutations occurring in response to factors including genetic factors, immune deficiency, toxic agents and the leukosis virus in the process of leukocyte differentiation have been widely accepted as the main causes of leukemia (3).…”

Potential four‑miRNA signature associated with T�stage and prognosis of patients with pancreatic ductal adenocarcinoma identified by co‑expression analysis

“…The overexpression of miR-214 decreases the sensitivity of PDAC tumor cells to gemcitabine by inhibiting inhibitor of growth family member 4 (26). Furthermore, the association of certain aberrantly expressed miRNAs with the clinical outcomes of patients with PDAC has been reported in numerous previous studies (27–30). For example, elevated miR-21 expression levels are significantly correlated with worse overall survival and progression-free survival in patients with PDAC (31).…”

The short-term effect of histone deacetylase�inhibitors, chidamide and valproic acid, on�the�NF‑κB�pathway in multiple myeloma cells

“…Previous studies have revealed that chidamide and DNA damaging agents can synergistically promote apoptosis in relapsed and refractory acute myeloid leukemia cells and reduce tumor burden in patients ( 39 ), and that VPA and bortezomib cooperate to induce pancreatic cancer cell death ( 40 ). Although chidamide and VPA did not inhibit MM cell proliferation and promote apoptosis, as expected, in the short term (6 h), which may be associated with the complexity of cell proliferation and development mechanisms, the rapid inhibition of NF-κB may inhibit the continued growth of MM cells in the early stages.…”