Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Developing chemotherapeutic regimens that can be given at the optimal dose and schedule continues to be one of the greatest challenges in clinical oncology. Simon and Norton discuss how they used guiding principles to derive the Norton–Simon hypothesis, and describe how this has improved clinical trial design and helped to achieve the goal of more effective and less toxic chemotherapeutic regimens.
The incidence of male breast cancer is rising, and the treatment of this disease has been extrapolated from the knowledge of female breast cancer despite multiple differences in the pathogenesis, biology and genetics of these two disease entities. Although there have been major advances in hormonal manipulation for the treatment of breast cancer, an improved understanding of the potential differences between male and female breast cancer is essential to providing new opportunities for therapeutic intervention and likely improved outcome, as discussed in this review.
As more aggressive cytotoxic agents and targeted therapies become the standard treatment approach in oncology, tumor lysis syndrome (TLS) will be more frequently encountered. Not only should the metabolic abnormalities of acute TLS and its complications be treated, but it is critical for prevention that patients at risk are identified as early as possible. This review discusses the symptoms and clinical features of this syndrome and the authors highlight the issues related to appropriate monitoring of treatment and the use of prophylaxis.
The oncogene addition concept was established to explain how some cancers that contain multiple genetic, epigenetic, and chromosomal abnormalities are dependent on or are “addicted” to one or more genes for both maintenance of the malignant phenotype and cell survival. Weinstein and Joe summarize current experimental and clinical evidence of this concept and describe some of the molecular mechanisms of this phenomenon. The use of molecular targeted agents in combination with cytotoxic agents, and the advances in systems biology and network theory can help to facilitate an optimal treatment approach.