Nature reviews. Cancer (NAT REV CANCER)

Publications in this journal

• Article: Bose Antik Kiron, Das Nirmalendu, Dewan Ivy Sankar, Purification, peptide sequencing and modeling of ostreolysin from Pleurotus ostreatus strain Plo5 : Formation of a modified ostreolysin with cytolytic effect only on cancer cell l

  Bose Antik Kiron, Das Nirmalendu, Dewan Ivy Sankar
  Nature reviews. Cancer 01/2011;
• Article: Opinion: PARP inhibition: PARP1 and beyond

  Mich|[egrave]|le Rouleau, Anand Patel, Michael J. Hendzel, Scott H. Kaufmann, Guy G. Poirier
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  ABSTRACT: Recent findings have thrust poly(ADP-ribose) polymerases (PARPs) into the limelight as potential chemotherapeutic targets. To provide a framework for understanding these recent observations, we review what is known about the structures and functions of the family of PARP enzymes, and then outline a series of questions that should be addressed to guide the rational development of PARP inhibitors as anticancer agents.
  Nature reviews. Cancer 03/2010; 10(4):293-301.
• Article: Stem cells: Insights into breast cancer heterogeneity

  Skinner, Mhairi
  Nature reviews. Cancer 03/2010; 10:163.
• Article: Tumorigenesis: Cone cells set the stage

  Skinner, Mhairi
  Nature reviews. Cancer 08/2009; 9:534.
• Article: Angiogenesis: How Down's syndrome protects

  Skinner, Mhairi
  Nature reviews. Cancer 06/2009; 9:456.
• Article: Opinion: H2AX and cancer

  William M. Bonner, Christophe E. Redon, Jennifer S. Dickey, Asako J. Nakamura, Olga A. Sedelnikova, St|[eacute]|phanie Solier, Yves Pommier
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  ABSTRACT: Histone H2AX phosphorylation on a serine four residues from the carboxyl terminus (producing H2AX) is a sensitive marker for DNA double-strand breaks (DSBs). DSBs may lead to cancer but, paradoxically, are also used to kill cancer cells. Using H2AX detection to determine the extent of DSB induction may help to detect precancerous cells, to stage cancers, to monitor the effectiveness of cancer therapies and to develop novel anticancer drugs.
  Nature reviews. Cancer 11/2008; 8(12):957-967.
• Article: Biomarkers: Finding the needle in the haystack

  Safia Ali Danovi
  Nature reviews. Cancer 08/2008; 8(9):659-659.
• Article: Diet and cancer prevention: the roles of observation and experimentation

  Mar|[iacute]|a Elena Mart|[iacute]|nez, James R. Marshall, Edward Giovannucci
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  ABSTRACT: Observational epidemiology and experimentation by randomized controlled trials (RCTs) have been used to evaluate dietary factors in cancer prevention; however, consistency in findings has been elusive. In several circles, RCTs are viewed as more credible than observational studies. As the testing of dietary epidemiological findings in RCTs has been more common for colorectal cancer than for other cancers, we use experience with this malignancy to critically appraise the reasons for discrepancies between results of observational and experimental studies.
  Nature reviews. Cancer 08/2008; 8(9):694-703.
• Article: Opinion: The interplay between MYC and HIF in cancer

  Chi V. Dang, Jung-whan Kim, Ping Gao, Jason Yustein
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  ABSTRACT: The interaction of MYC and hypoxia inducible factors (HIFs) under physiological, non-tumorigenic conditions provides insights into normal homeostatic cellular responses to low oxygen levels (hypoxia). Many tumours contain genetic alterations, such as MYC activation, that can collaborate with HIF to confer metabolic advantages to tumour cells, which tend to exist in a hypoxic microenvironment. This Perspective emphasizes the differences between the transcriptional network that operates under normal homeostatic conditions and the network in a tumorigenic milieu.
  Nature reviews. Cancer 12/2007; 8(1):51-56.
• Article: Opinion: Role of autophagy in cancer

  Robin Mathew, Vassiliki Karantza-Wadsworth, Eileen White
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  ABSTRACT: Autophagy is a cellular degradation pathway for the clearance of damaged or superfluous proteins and organelles. The recycling of these intracellular constituents also serves as an alternative energy source during periods of metabolic stress to maintain homeostasis and viability. In tumour cells with defects in apoptosis, autophagy allows prolonged survival. Paradoxically, autophagy defects are associated with increased tumorigenesis, but the mechanism behind this has not been determined. Recent evidence suggests that autophagy provides a protective function to limit tumour necrosis and inflammation, and to mitigate genome damage in tumour cells in response to metabolic stress.
  Nature reviews. Cancer 11/2007; 7(12):961-967.
• Article: Tumorigenesis: Size is everything

  Nicola McCarthy
  Nature reviews. Cancer 10/2007; 7(11):815-815.
• Article: Are oncoantigens suitable targets for anti-tumour therapy?

  Federica Cavallo, Raffaele Adolfo Calogero, Guido Forni
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  ABSTRACT: When a vaccine-elicited immune response is directed against oncoantigens--proteins required for the neoplastic process--the chance that the tumour will evade the vaccine should be reduced. But how can these causal oncoantigens be identified? One approach is to find tumour-associated and microenvironment-associated oncoantigens required for progression from one tumour stage to the next by comparing gene signatures isolated from the different stages of tumour progression in cancer-prone transgenic mice. Mouse oncoantigens subsequently shown to be involved in human cancer can then be validated in mouse vaccination experiments. This provides the groundwork for the rational design of cancer vaccines for clinical trials.
  Nature reviews. Cancer 10/2007; 7(9):707-13.
• Source

  Available from: unibs.it

  Article: Maximizing mouse cancer models.

  Kristopher K Frese, David A Tuveson
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  ABSTRACT: Animal models of cancer provide an alternative means to determine the causes of and treatments for malignancy, thus representing a resource of immense potential for cancer medicine. The sophistication of modelling cancer in mice has increased to the extent that investigators can both observe and manipulate a complex disease process in a manner impossible to perform in patients. However, owing to limitations in model design and technology development, and the surprising underuse of existing models, only now are we realising the full potential of mouse models of cancer and what new approaches are needed to derive the maximum value for cancer patients from this investment.
  Nature reviews. Cancer 10/2007; 7(9):645-58.
• Article: Oestrogen-receptor-mediated transcription and the influence of co-factors and chromatin state.

  Kelly A Green, Jason S Carroll
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  ABSTRACT: Oestrogen receptor-alpha (ERalpha)-regulated transcription in breast cancer cells involves protein co-factors that contribute to the regulation of chromatin structure. These include co-factors with the potential to regulate histone modifications such as acetylation or methylation, and therefore the transcriptional state of target genes. Although much of the information regarding the interaction of specific co-factors with ER has been generated by studying specific promoter regions, we now have an improved understanding of the nature of these interactions and are better placed to relate these with ER activity and potentially with the activity of breast cancer drugs, including tamoxifen.
  Nature reviews. Cancer 10/2007; 7(9):713-22.
• Article: Vitamin D signalling pathways in cancer: potential for anticancer therapeutics.

  Kristin K Deeb, Donald L Trump, Candace S Johnson
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  ABSTRACT: Epidemiological studies indicate that vitamin D insufficiency could have an aetiological role in various human cancers. Preclinical research indicates that the active metabolite of vitamin D, 1alpha,25(OH)2D3, also known as calcitriol, or vitamin D analogues might have potential as anticancer agents because their administration has antiproliferative effects, can activate apoptotic pathways and inhibit angiogenesis. In addition, 1alpha,25(OH)2D3 potentiates the anticancer effects of many cytotoxic and antiproliferative anticancer agents. Here, we outline the epidemiological, preclinical and clinical studies that support the development of 1alpha,25(OH)2D3 and vitamin D analogues as preventative and therapeutic anticancer agents.
  Nature reviews. Cancer 10/2007; 7(9):684-700.
• Article: Role of JAK2 in the pathogenesis and therapy of myeloproliferative disorders.

  Ross L Levine, Animesh Pardanani, Ayalew Tefferi, D Gary Gilliland
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  ABSTRACT: The myeloproliferative disorders polycythaemia vera (PV), essential thombocythaemia (ET), and primary myelofibrosis (PMF) are clonal disorders of multipotent haematopoietic progenitors. The genetic cause of these diseases was not known until 2005, when several independent groups demonstrated that most patients with PV, ET and PMF acquire a single point mutation in the cytoplasmic tyrosine kinase JAK2 (JAK2V617F). These discoveries have changed the landscape for diagnosis and classification of PV, ET and PMF, and show the ability of genomic technologies to identify new molecular targets in human malignancies with pathogenetic, diagnostic and therapeutic significance.
  Nature reviews. Cancer 10/2007; 7(9):673-83.
• Article: Building better magic bullets--improving unconjugated monoclonal antibody therapy for cancer.

  Louis M Weiner
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  ABSTRACT: The potential of monoclonal antibodies to effectively treat cancer is beginning to be widely acknowledged. Advances in antibody engineering make it possible to produce various recombinant proteins that exploit the specificity of the antibody-combining site to manipulate tumour-related signalling, and to stimulate anti-tumour immune responses. Future advances in the field will rely on the improved identification of functional antibody targets to perturb cancer-relevant signalling, and by the improved selection of tumours that can be effectively treated. These advances will be complemented by the use of antibodies that induce clinically meaningful host-protective immune responses. But, can we afford this progress?
  Nature reviews. Cancer 10/2007; 7(9):701-6.
• Article: Molecular mechanisms of alcohol-mediated carcinogenesis.

  Helmut K Seitz, Felix Stickel
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  ABSTRACT: Approximately 3.6% of cancers worldwide derive from chronic alcohol drinking, including those of the upper aerodigestive tract, the liver, the colorectum and the breast. Although the mechanisms for alcohol-associated carcinogenesis are not completely understood, most recent research has focused on acetaldehyde, the first and most toxic ethanol metabolite, as a cancer-causing agent. Ethanol may also stimulate carcinogenesis by inhibiting DNA methylation and by interacting with retinoid metabolism. Alcohol-related carcinogenesis may interact with other factors such as smoking, diet and comorbidities, and depends on genetic susceptibility.
  Nature reviews. Cancer 09/2007; 7(8):599-612.
• Source

  Available from: oralcancerfoundation.org

  Article: The resurgence of platinum-based cancer chemotherapy.

  Lloyd Kelland
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  ABSTRACT: The accidental discovery of the anticancer properties of cisplatin and its clinical introduction in the 1970s represent a major landmark in the history of successful anticancer drugs. Although carboplatin--a second-generation analogue that is safer but shows a similar spectrum of activity to cisplatin--was introduced in the 1980s, the pace of further improvements slowed for many years. However, in the past several years interest in platinum drugs has increased. Key developments include the elucidation of mechanisms of tumour resistance to these drugs, the introduction of new platinum-based agents (oxaliplatin, satraplatin and picoplatin), and clinical combination studies using platinum drugs with resistance modulators or new molecularly targeted drugs.
  Nature reviews. Cancer 09/2007; 7(8):573-84.