Hot off the presses! Jun 01 Nat Rev Can

The Jun 01 issue of the Nat Rev Can is now up on Pubget (About Nat Rev Can): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

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  - Nat Rev Can 11(6):309 (2011)
  
• Leukaemia: Notch has commitment issues | PDF (240 KB)
  - Nat Rev Can 11(6):385 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Prostate cancer: Studying the classics | PDF (286 KB)
  - Nat Rev Can 11(6):386 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Ovarian cancer: Model building | PDF (225 KB)
  - Nat Rev Can 11(6):386 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Conversion on the road... | PDF (79 KB)
  - Nat Rev Can 11(6):386 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Signalling | Oncogenes | Therapy | Hypoxia | PDF (88 KB)
  - Nat Rev Can 11(6):387 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Leukaemia: Now get out of that... | PDF (189 KB)
  - Nat Rev Can 11(6):388 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Tumour suppression: Unpicking a Gordian knot | PDF (231 KB)
  - Nat Rev Can 11(6):388 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Senescence: Double or quit? | PDF (190 KB)
  - Nat Rev Can 11(6):389 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Pathology: Two of a kind | PDF (228 KB)
  - Nat Rev Can 11(6):390 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Molecular profiling: A double agent | PDF (264 KB)
  - Nat Rev Can 11(6):390 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Gist natural killers | PDF (98 KB)
  - Nat Rev Can 11(6):390 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Hypoxia: HIF switch | PDF (432 KB)
  - Nat Rev Can 11(6):391 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.
• Targeting hypoxia in cancer therapy
  - Nat Rev Can 11(6):393 (2011)
  Hypoxia is a feature of most tumours, albeit with variable incidence and severity within a given patient population. It is a negative prognostic and predictive factor owing to its multiple contributions to chemoresistance, radioresistance, angiogenesis, vasculogenesis, invasiveness, metastasis, resistance to cell death, altered metabolism and genomic instability. Given its central role in tumour progression and resistance to therapy, tumour hypoxia might well be considered the best validated target that has yet to be exploited in oncology. However, despite an explosion of information on hypoxia, there are still major questions to be addressed if the long-standing goal of exploiting tumour hypoxia is to be realized. Here, we review the two main approaches, namely bioreductive prodrugs and inhibitors of molecular targets upon which hypoxic cell survival depends. We address the particular challenges and opportunities these overlapping strategies present, and discuss the c! entral importance of emerging diagnostic tools for patient stratification in targeting hypoxia.
• Cancer to bone: a fatal attraction
  - Nat Rev Can 11(6):411 (2011)
  Hypoxia is a feature of most tumours, albeit with variable incidence and severity within a given patient population. It is a negative prognostic and predictive factor owing to its multiple contributions to chemoresistance, radioresistance, angiogenesis, vasculogenesis, invasiveness, metastasis, resistance to cell death, altered metabolism and genomic instability. Given its central role in tumour progression and resistance to therapy, tumour hypoxia might well be considered the best validated target that has yet to be exploited in oncology. However, despite an explosion of information on hypoxia, there are still major questions to be addressed if the long-standing goal of exploiting tumour hypoxia is to be realized. Here, we review the two main approaches, namely bioreductive prodrugs and inhibitors of molecular targets upon which hypoxic cell survival depends. We address the particular challenges and opportunities these overlapping strategies present, and discuss the c! entral importance of emerging diagnostic tools for patient stratification in targeting hypoxia.
• Cell-free nucleic acids as biomarkers in cancer patients
  - Nat Rev Can 11(6):426 (2011)
  Hypoxia is a feature of most tumours, albeit with variable incidence and severity within a given patient population. It is a negative prognostic and predictive factor owing to its multiple contributions to chemoresistance, radioresistance, angiogenesis, vasculogenesis, invasiveness, metastasis, resistance to cell death, altered metabolism and genomic instability. Given its central role in tumour progression and resistance to therapy, tumour hypoxia might well be considered the best validated target that has yet to be exploited in oncology. However, despite an explosion of information on hypoxia, there are still major questions to be addressed if the long-standing goal of exploiting tumour hypoxia is to be realized. Here, we review the two main approaches, namely bioreductive prodrugs and inhibitors of molecular targets upon which hypoxic cell survival depends. We address the particular challenges and opportunities these overlapping strategies present, and discuss the c! entral importance of emerging diagnostic tools for patient stratification in targeting hypoxia.
• Assessing the risk of second malignancies after modern radiotherapy
  - Nat Rev Can 11(6):438 (2011)
  Hypoxia is a feature of most tumours, albeit with variable incidence and severity within a given patient population. It is a negative prognostic and predictive factor owing to its multiple contributions to chemoresistance, radioresistance, angiogenesis, vasculogenesis, invasiveness, metastasis, resistance to cell death, altered metabolism and genomic instability. Given its central role in tumour progression and resistance to therapy, tumour hypoxia might well be considered the best validated target that has yet to be exploited in oncology. However, despite an explosion of information on hypoxia, there are still major questions to be addressed if the long-standing goal of exploiting tumour hypoxia is to be realized. Here, we review the two main approaches, namely bioreductive prodrugs and inhibitors of molecular targets upon which hypoxic cell survival depends. We address the particular challenges and opportunities these overlapping strategies present, and discuss the c! entral importance of emerging diagnostic tools for patient stratification in targeting hypoxia.
• Targeting hypoxia in cancer therapy
  - Nat Rev Can 11(6):450 (2011)
  Hypoxia is a feature of most tumours, albeit with variable incidence and severity within a given patient population. It is a negative prognostic and predictive factor owing to its multiple contributions to chemoresistance, radioresistance, angiogenesis, vasculogenesis, invasiveness, metastasis, resistance to cell death, altered metabolism and genomic instability. Given its central role in tumour progression and resistance to therapy, tumour hypoxia might well be considered the best validated target that has yet to be exploited in oncology. However, despite an explosion of information on hypoxia, there are still major questions to be addressed if the long-standing goal of exploiting tumour hypoxia is to be realized. Here, we review the two main approaches, namely bioreductive prodrugs and inhibitors of molecular targets upon which hypoxic cell survival depends. We address the particular challenges and opportunities these overlapping strategies present, and discuss the c! entral importance of emerging diagnostic tools for patient stratification in targeting hypoxia.
• Leukaemia: Notch has commitment issues
  - Nat Rev Can 11(6):458 (2011)
  Notch signalling is normally considered oncogenic in the haematopoietic system. However, Klinakis, Lobry and colleagues now show that inactivation of the Notch pathway is associated with a subset of patients with chronic myelomonocytic leukaemia (CMML), which suggests that Notch signalling can be both oncogenic and tumour suppressive in haematological malignancies, as is the case for solid tumours.