No abstract

The emerging approach to cancer treatment known as targeted therapies offers hope in improving the treatment of therapy-resistant cancers. Recent understanding of the molecular pathogenesis of cancer has led to the development of targeted novel drugs such as monoclonal antibodies, small molecule inhibitors, mimetics, antisense and small interference RNA-based strategies, among others. These compounds act on specific targets that are believed to contribute to the development and progression of cancers and resistance of tumors to conventional therapies. Delivered individually or combined with chemo- and/or radiotherapy, such novel drugs have produced significant responses in certain types of cancer. Among the most successful novel compounds are those which target tyrosine kinases (imatinib, trastuzumab, sinutinib, cetuximab). However, these compounds can cause severe side-effects as they inhibit pathways such as epidermal growth factor receptor (EGFR) or platelet-derived growth factor receptor, which are also important for normal functions in non-transformed cells. Recently, a number of proteins have been identified which show a remarkable tumor-specific cytotoxic activity. This toxicity is independent of tumor type or specific genetic changes such as p53, pRB or EGFR aberrations. These tumor-specific killer proteins are either derived from common human and animal viruses such as E1A, E4ORF4 and VP3 (apoptin) or of cellular origin, such as TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) and MDA-7 (melanoma differentiation associated-7). This review aims to present a current overview of a selection of these proteins with preferential toxicity among cancer cells and will provide an insight into the possible mechanism of action, tumor specificity and their potential as novel tumor-specific cancer therapeutics.

No abstract

No abstract

No abstract

The use of prophylactic antibiotics in the context of septorhinoplasty (SRP) is a frequently debated topic among plastic surgeons. Most surgeons routinely use antibiotics to prevent the dreaded physical and psychological morbidity of post-operative infections, although this practice is controversial. With antimicrobial resistance becoming a global threat, however, optimising antibiotic prescribing is essential. The current evidence would suggest that the rate of post-operative infection is low and routine antibiotic use is unnecessary in SRP surgery. Rates range from 0.5% to 2% in simple SRP surgery, majority of which are minor nasal infections which respond to oral antibiotics and do not require hospital admission. In cases of complex SRP, defined as revision cases or where grafts or implants have been utilised, infection rates can be much higher with an incidence of 7-11%, and as such utilisation of antibiotics is reasonable. When considering the regime to be utilised, a single preoperative dose of intravenous antibiotics has the same efficacy in reducing the incident of post-operative infection as a postoperative 7-day course of oral antibiotics. In the authors practice, all patients receive a single intravenous dose of antibiotics on induction, and in the case of utilisation of a graft from a non-nasal site, this is complimented with an oral course of post-operative antibiotics. With this approach, infections rates are at the lowest range of available published literature.

No abstract

No abstract