Objectives Propolis is a honeybee product used extensively in traditional medicine for its antioxidant, anti-inflammatory, immunomodulatory and anticancer effects. Propolis exhibits a broad spectrum of biological activities because it is a complex mixture of natural substances. In this review, the antitumour effects of propolis extracts and its constituents (e.g. flavonoids, terpenes and caffeic acid phenethyl ester) are discussed. Key findings The effect of propolis on experimental carcinogenesis is discussed, as well as its possible mechanisms of action against tumours, involving apoptosis, cell cycle arrest and interference on metabolic pathways. Propolis seems to be efficient against different tumour cells both in vitro and in vivo, which suggests its potential in the development of new anticancer drugs. Summary Propolis extracts may be important economically and would allow a relatively inexpensive cancer treatment. Preclinical investigations are needed to further elucidate the benefits of propolis and its antitumour properties.

It is well known that the etiology of human breast cancer is significantly affected by environmental factors. Virus-associated cancer refers to a cancer where viral infection results in the malignant transformation of the host's infected cells. Human papillomaviruses (HPV), mouse mammary tumor virus (MMTV) and Epstein-Barr (EBV) virus are prime candidate viruses as agents of human breast cancer. The precise role that viruses play in tumorigenesis is not clear, but it seems that they are responsible for causing only one in a series of steps required for cancer development. The idea that a virus could cause breast cancer has been investigated for quite some time, even though breast cancer could be a hereditary disease; however, hereditary breast cancer is estimated to account for a small percentage of all breast cancer cases. Based on current research, this review present at moment, substantial, but not conclusive, evidence that HPV, EBV and MMTV may be involved in breast cancer.

Acute lymphoblastic leukemia (ALL) is the commonest childhood malignancy, accounting for approximately 80 % of leukemia in the pediatric group, and its etiology is unknown. This neoplasia is characterized by male predominance, high-risk features and poor outcome, mainly in recurrence patients and adults. In recent years, advances in the success of childhood ALL treatment were verified, and the rate of cure is over 80 % of individuals. However, there is a considerable scope for improving therapeutic outcome in this neoplasia. Improvements in ALL therapy might readily be achieved by developing additional biomarkers that can predict and refine prognosis in patients with ALL. In normal hematopoietic cells, cytokines provide the stimulus for proliferation, survival, self-renewal, differentiation and functional activation. Abnormalities of cytokines are characteristic in all forms of leukemia, including ALL. The stromal cell-derived factor-1 (SDF-1 or CXCL12) is a member of the CXC chemokine family that binds to CXC chemokine receptor 4 (CXCR4). The CXCL12/CXCR4 axis appears to play a role in dissemination of solid tumors and hematopoietic diseases. Understanding the mechanisms by which ALL cells are disseminated will provide additional information to expand therapeutic approach. Therefore, this review summarizes information relating to ALL cell biology, focusing specifically in a cytokine receptor important axis, CXCL12/CXCR4, that may have implications for novel treatment strategies to improve life expectancy of patients with this neoplasia.

The recognition of pathogens is assigned to an evolutionarily conserved family of receptors, the Toll-like receptors (TLRs). The investigation of RNA-based immunology has been reinvigorated with the observation that TLR3s interact with RNA (dsRNA of viral origin, poly (I:C) and endogenous RNA). Many RNAs, therefore, join the list of endogenous ligands for TLRs. The further finding that nucleoside modification alters RNA-mediated TLR signaling presents a mechanism for the long-observed differences in immunogenicity. The involvement of RNA modification in the pathogenesis of diseases, and its implications in the therapeutics, are still being studied, and will have important implications in the future.

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