The past week has seen a mixture of positive and negative developments in Europe and the UK for chronic lymphocytic leukaemia (CLL), hepatocellular carcinoma (HCC) and non-small cell lung cancer (NSCLC).
Of particular interest, the UK's National Institute for Health and Clinical Excellence (NICE) has issued a recommendation for the use of Roche's MabThera (rituximab) in CLL. NICE's final guidance recommends rituximab in combination with fludarabine and cyclophosphamide chemotherapy (CT) as an option for previously-untreated patients with CLL. Professor John Gribben, Consultant Haematologist and Medical Oncologist, Barts and The London NHS Trust, commented: "the ability to add rituximab to chemotherapy is a major advance in the way we can treat CLL. Where previously our goal was just to improve symptoms, for the first time we now have a treatment combination that is capable of producing much higher remission rates and more durable responses."
Further, the EMEA's CHMP has issued a positive recommendation for the use of MabThera in patients with relapsed or refractory CLL. Physicians will soon be able to prescribe MabThera in combination with CT to patients in Europe who have been treated for the disease, but whose cancer has returned or have not appropriately responded to therapy.
Separately, the anticipated decision from NICE on the Final Appraisal Determination for Bayer HealthCare/Onyx Pharmaceuticals' Nexavar (sorafenib), for the treatment of advanced HCC, has been delayed to allow consideration of the patient access scheme, Bayer Schering Pharma has agreed with the Department of Health. The company hopes that NICE will take this opportunity to evaluate and fully understand the benefit of its proposed patient access scheme, and to listen to leading healthcare professionals in the field who were unanimous in their condemnation of the initial negative proposal.
Finally, the CHMP has adopted a negative opinion for the use of Erbitux (cetuximab) in combination with platinum-based CT for the treatment of patients with EGFr-expressing, advanced or metastatic NSCLC. Merck KGaA is evaluating potential appeal options requesting that the CHMP re-examines data demonstrating clinically-relevant benefits to patients. This has come as a huge blow to Merck, with its shares plummeting 12 per cent following the decision.
Alice Rossiter - Cancer Drug News Editor
Tuesday, July 28, 2009
Tuesday, July 21, 2009
Progress made in identifying genetic causes of melanoma
Researchers have identified various genes that cause melanoma and also novel epigenetic markers of the disease that may herald new treatments for patients.
Two studies, published online in Nature Genetics (10.1038/ng.410 and 10.1038/ng.411), and conducted by investigators at Queensland Institute of Medical Research in Australia, King's College London and the University of Leeds, have revealed novel genes implicated in the development of melanoma. One study found that specific changes in two genes, MTAP and PLA2G6, were found to make people more susceptible to developing nevi. In a further 4,000 people, the researchers went on to show that these genes increased the risk of developing melanoma; specifically, those who carry one of the two SNPs have a 25 per cent increased chance of developing melanoma, while for individuals carrying both variants, the risk is doubled.
The second study identified five loci with genotyped or imputed SNPs reaching very high significance. The analysis showed that the genes, MC1R and TYR, are associated with pigmentation, freckling and cutaneous sun sensitivity.
Separately, researchers from Yale University have mapped chemical modifications of DNA in the melanoma genome, finding new markers that will help to develop more effective treatment strategies to fight this disease. In this work, published online in Genome Research (10.1101/gr.091447.109), scientists found 76 promoters with altered methylation patterns in melanomas, most of these showing increased methylation compared to normal. The team focused on five genes in particular, three of which had not been implicated in melanoma until now. The scientists are hopeful that these epigenetic markers may provide a better method for determining the aggressiveness of the disease and for setting a course of treatment.
The incidence of melanoma has been increasing over the past decades. Currently, approximately 132,000 melanoma skin cancers occur globally each year and around 48,000 people worldwide die of melanoma annually. One in every three cancers diagnosed is a skin cancer and, according to Skin Cancer Foundation Statistics, one in every five Americans will develop skin cancer in their lifetime. Melanoma is diagnosed in more than 50,000 new patients in the US annually.
While the rate of incidences continues to rise, survival rate has not improved and the race is on to find the genetic and cellular changes driving melanoma and to devise new means of detection and treatment.
Alice Rossiter - Cancer Drug News Editor
Two studies, published online in Nature Genetics (10.1038/ng.410 and 10.1038/ng.411), and conducted by investigators at Queensland Institute of Medical Research in Australia, King's College London and the University of Leeds, have revealed novel genes implicated in the development of melanoma. One study found that specific changes in two genes, MTAP and PLA2G6, were found to make people more susceptible to developing nevi. In a further 4,000 people, the researchers went on to show that these genes increased the risk of developing melanoma; specifically, those who carry one of the two SNPs have a 25 per cent increased chance of developing melanoma, while for individuals carrying both variants, the risk is doubled.
The second study identified five loci with genotyped or imputed SNPs reaching very high significance. The analysis showed that the genes, MC1R and TYR, are associated with pigmentation, freckling and cutaneous sun sensitivity.
Separately, researchers from Yale University have mapped chemical modifications of DNA in the melanoma genome, finding new markers that will help to develop more effective treatment strategies to fight this disease. In this work, published online in Genome Research (10.1101/gr.091447.109), scientists found 76 promoters with altered methylation patterns in melanomas, most of these showing increased methylation compared to normal. The team focused on five genes in particular, three of which had not been implicated in melanoma until now. The scientists are hopeful that these epigenetic markers may provide a better method for determining the aggressiveness of the disease and for setting a course of treatment.
The incidence of melanoma has been increasing over the past decades. Currently, approximately 132,000 melanoma skin cancers occur globally each year and around 48,000 people worldwide die of melanoma annually. One in every three cancers diagnosed is a skin cancer and, according to Skin Cancer Foundation Statistics, one in every five Americans will develop skin cancer in their lifetime. Melanoma is diagnosed in more than 50,000 new patients in the US annually.
While the rate of incidences continues to rise, survival rate has not improved and the race is on to find the genetic and cellular changes driving melanoma and to devise new means of detection and treatment.
Alice Rossiter - Cancer Drug News Editor
Thursday, July 2, 2009
CSCs set to improve cancer treatment
Research into cancer treatment is currently focusing on cancer stem cells (CSCs), which are responsible for some instances of the disease. Indeed, a University of Rochester Medical Center researcher has resolved the controversy and promise around a dangerous subtype of CSCs, which seem capable of resisting many modern treatments. The research, published in the 26th June edition of Science (2009;324:1670-1673), proposes that this subpopulation of malignant cells may one day provide an important avenue for controlling cancer, especially if new treatments that target the CSC are developed and combined with traditional chemotherapy and/or radiation.
Research from the past ten years suggests that because CSCs may be the root of cancer, they might also provide a new opportunity for a treatment. A group of collaborators, for example, are testing a new drug compound based on the feverfew plant that demonstrates great potential in the laboratory for causing leukaemia CSCs to self destruct.
Further, it was recently reported that researchers at the University of California, Los Angeles Jonsson Comprehensive Cancer Center, on a quest to find lung cancer (LC) SCs, have developed a unique model to allow further investigation into the cells that many believe may be at the root of all LCs. Since CSCs are known to possess unique properties and a predisposition to metastasise, the study's lead author proposed to extract candidate CSCs directly from clinical specimens based on the markers they express and then validate these cells functionally. As detailed in PLoS ONE (10.1371/journal.pone.0005884), in an effort to find LC SCs, the team collected specimens from patients with malignant pleural effusions, and created a microenvironment in which the tumour cells would remain heterogeneous and enable researchers to more easily identify candidate CSCs.
Separately, a study from the University of Michigan (UM) Comprehensive Cancer Center recently indicated that a gene well known to stop or suppress cancer plays a role in CSCs. The researchers found that several pathways linked to the gene, PTEN, also affected the growth of breast cancer SCs. Further, by using a drug that interferes with that pathway, the scientists produced an up to 90 per cent decrease in the number of CSCs within a tumour. As detailed in PLoS Biology (10.1371/journal.pbio.1000121), the UM researchers deleted PTEN in tumours grown in cell cultures and mice, and found an increase in the number of SCs. They also looked at pathways associated with PTEN and reported that the pathway, PI3-K/Akt, regulated the CSC population by activating another SC pathway, Wnt, which is also implicated in multiple cancer types. Thus, new and recent developments seem to reiterate the important role of CSC research in future treatment.
Alice Rossiter
Cancer Drug News - Editor
Research from the past ten years suggests that because CSCs may be the root of cancer, they might also provide a new opportunity for a treatment. A group of collaborators, for example, are testing a new drug compound based on the feverfew plant that demonstrates great potential in the laboratory for causing leukaemia CSCs to self destruct.
Further, it was recently reported that researchers at the University of California, Los Angeles Jonsson Comprehensive Cancer Center, on a quest to find lung cancer (LC) SCs, have developed a unique model to allow further investigation into the cells that many believe may be at the root of all LCs. Since CSCs are known to possess unique properties and a predisposition to metastasise, the study's lead author proposed to extract candidate CSCs directly from clinical specimens based on the markers they express and then validate these cells functionally. As detailed in PLoS ONE (10.1371/journal.pone.0005884), in an effort to find LC SCs, the team collected specimens from patients with malignant pleural effusions, and created a microenvironment in which the tumour cells would remain heterogeneous and enable researchers to more easily identify candidate CSCs.
Separately, a study from the University of Michigan (UM) Comprehensive Cancer Center recently indicated that a gene well known to stop or suppress cancer plays a role in CSCs. The researchers found that several pathways linked to the gene, PTEN, also affected the growth of breast cancer SCs. Further, by using a drug that interferes with that pathway, the scientists produced an up to 90 per cent decrease in the number of CSCs within a tumour. As detailed in PLoS Biology (10.1371/journal.pbio.1000121), the UM researchers deleted PTEN in tumours grown in cell cultures and mice, and found an increase in the number of SCs. They also looked at pathways associated with PTEN and reported that the pathway, PI3-K/Akt, regulated the CSC population by activating another SC pathway, Wnt, which is also implicated in multiple cancer types. Thus, new and recent developments seem to reiterate the important role of CSC research in future treatment.
Alice Rossiter
Cancer Drug News - Editor
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