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Hepatocellular carcinoma (HCC) is highly lethal and has a high incidence worldwide. However, at present there is only a basic understanding of the genetic, cellular and environmental mechanisms that drive HCC pathogenesis. What is known, and what are the challenges and opportunities?
Progress in molecular radiobiology has improved the understanding of the pathogenesis of side effects that develop months or years after radiotherapy has been completed. This knowledge will help to improve the therapeutic efficacy of radiotherapy and the quality of life of long-term cancer survivors.
Several small-molecule inhibitors and monoclonal antibodies are now approved for the therapy of various cancers. Focusing on the example of the epidermal growth factor receptor inhibitors, this Review compares and contrasts these two classes of agents.
Multiple mutations and alterations in the cancer genome lead to the deregulation of various cell-signalling pathways that control cell function. Can molecular-profiling studies be used to fully understand this complexity and provide an opportunity to link pathway deregulation with potential therapeutic strategies?
The ARF tumour suppressor can activate p53-dependent transcriptional pathways by inhibiting the ubiquitin ligase MDM2. However, ARF has been reported to have p53-independent activities. How important are these activities in tumorigenesis? This Review critically appraises the current data.
Drugs that target mTOR (mammalian target of rapamycin) have entered clinical trials for cancer treatment. However, current mTOR inhibitors have an unexpectedly complex mechanism of action. Can our emerging knowledge of this pathway be used to develop more effective mTOR-targeted therapies?
Polymers can be conjugated to anticancer drugs and proteins to improve their therapeutic index. Some such conjugates are in routine clinical use and there are exciting advances in development, such as polymer-based combination therapies.
The role of cancer registries has expanded from the description of incidence trends to calculating survival and individual care management. Now, 21% of the world’s population is covered by registries, and this review surveys the global situation.
Drug distribution within solid tumours is an often-neglected area of research in chemotherapeutic resistance. This Review summarizes the evidence that many chemotherapeutic drugs do not completely penetrate tumours, and suggests strategies to circumvent this problem.
Recent advances in the understanding of tumour–host interactions have revealed some key effectors of tumoral immune escape that limit the successful use of treatments that rely on boosting immune function. Can some of these effectors be targeted by small-molecule inhibitors?
Recent findings have indicated that the tyrosine-kinase receptor MET is a sensor of adverse microenvironmental conditions (such as hypoxia), and can drive cell invasion and metastasis through the transcriptional activation of a set of genes that control blood coagulation.
Microarray analyses have enabled tumours to be grouped on the basis of their genomic alterations rather than their tissue of origin. But does the identification of lineage-survival genes implicate lineage dependency (or lineage addiction) as a mechanism that is also affected by tumour genetic alterations?
Biomarkers used in determining the response to cytotoxic agents are not optimal for predicting benefit from anti-angiogenic drugs. Which anti-angiogenic biomarkers might prove useful for identifying initial drug choice, appropriate dosing, early clinical benefit, emerging resistance and second-line treatments?
What are the challenges in bringing cancer biomarkers to market? Steven Gutman and Larry Kessler, both of whom work at the US Food and Drugs Administration, share their views and expertise.
Nucleophosmin (encoded byNPM1) is frequently overexpressed, mutated, rearranged and deleted in human cancer. NPM has many functions, so how does either the gain or loss of function of NPM activity contribute to tumorigenesis?
The effectiveness of anticancer therapies depends on other medications, food and/or herbal supplements being taken by the patient. This is because of interactions that occur at various stages of drug processing, through pharmacokinetic or pharmacodynamic mechanisms.
Immunotoxins are potent bacterial toxins fused to antibodies that bind tumour-specific antigens, and can dramatically improve the clinical utility of some anti-tumour antibodies. This review describes the construction and efficacy of several recombinant immunotoxins, using results from recent clinical trials.
Nitric oxide (NO) and nitric oxide synthases are ubiquitous in malignant tumours, and have both pro- and anti-tumour effects. This review summarizes the current understanding of the function of NO in tumour progression and discusses potential NO-based strategies for cancer treatment.
Transforming growth factor-β (TGFβ) can function either within the tumour cell or through host–tumour cell interactions. The complex nature of TGFβ signalling and crosstalk in the tumour microenvironment presents unique challenges and opportunities to develop therapeutic intervention strategies.
Photodynamic therapy (PDT) kills tumour cells by apoptosis and/or necrosis, and is thought to stimulate an anti-tumour immune response. How important is this inflammatory response to the efficacy of PDT?
