Recent findings by scientists could help advance the fight against breast cancer (BC). A team at the University of Kentucky (UoK) Markey Cancer Center has identified a key molecular mechanism in BC that enables tumour cells to metastasise, while a separate study has uncovered five new regions of the genome that increase a woman's risk of developing the disease by between 6 and 16 per cent.
The work conducted by the UoK could lead to new lines of research aimed at developing treatments for metastatic BC (MBC). The research, published in the 13th April online issue of The EMBO Journal (10.1038/emboj.2010.63), focused on the process by which tumour cells stop clinging to other cells and become motile. The increased motility of tumour cells at the initial step of metastasis is similar to epithelial-mesenchymal transition (EMT). In all EMT processes, cells lose the expression of E-cadherin, which functions as a "molecular glue" that attaches cells to one another. The team explained that when E-cadherin is broken down, tumour cells start to migrate and spread throughout the body.
A protein called Snail acts as a master switch in the cell's nucleus to suppress E-cadherin expression and induce EMT in the cell. Agents that can disrupt the interaction of Snail are thought to have great therapeutic potential for treating MBC. Leading on from these findings, the scientists at the UoK are keen to develop drugs that can treat metastatic cancer.
Separately, a study funded by Cancer Research UK (CRUK) and the Wellcome Trust has found five new regions of the genome that increase a woman's risk of developing BC by between 6 and 16 per cent. As more of these low-risk sites are found, scientists believe that it may be possible to create tests for a combination of them that together significantly increase risk, which could ultimately help doctors to make decisions about prevention, diagnosis and treatment for women who are more likely to get BC.
The scientists scanned the entire genetic code of over 4,000 women with BC and a family history of the disease for genetic variations that appeared more often compared to healthy women. They then tested the most promising regions in over 12,000 women with BC and 12,000 women without the disease in an international collaboration. Although the results now take the total number of gene regions linked to the risk of BC to 18, scientists are still unsure which genes are causing this increased risk. Lead author, Professor Doug Easton, director of CRUK's Genetic Epidemiology Unit at the University of Cambridge, commented: "While each of these sites have a small impact on breast cancer risk, by finding more of these genes, we may be able to develop a test that can predict more reliably a woman's risk of developing breast cancer."
Alice Rossiter - Editor, Cancer Drug News
Showing posts with label Cancer Research UK. Show all posts
Showing posts with label Cancer Research UK. Show all posts
Friday, May 14, 2010
Friday, April 9, 2010
Skin cancer rates rapidly rising
In line with its launch of the 2010 SunSmart campaign, Cancer Research UK (CRUK) has revealed that people aged 60 to 79 years of age are now over five-times more likely to be diagnosed with malignant melanoma (MM) than their parents would have been 30 years ago.
Of all ages, this generation has seen the biggest increase in incidence rates of melanoma, rising from seven cases per 100,000 people in the mid-1970s to 36 cases per 100,000 today. This rise shows the impact that a shift in tanning behaviour has had on a whole generation of men and women who would have been in their 20s and 30s in the 1970s, when holidays in the sun became cheap and popular, and sunbeds arrived in the UK.
According to CRUK statistics, the most common kind of skin cancer is non-melanoma skin cancer. More than 75,000 cases are registered each year in the UK, but it is estimated that the actual number is at least 100,000. More than 10,400 cases of MM are diagnosed each year in the UK and more than 2,000 people a year die from the disease.
For men in their 60s and 70s, the rates of melanoma have risen most dramatically; they are over seven-times more likely to be diagnosed with the disease than in the 1970s. For men and women of all ages, melanoma incidence rates have quadrupled since the 1970s. This rise in incidence rates is expected to continue: by 2024, rates in people aged 60 to 79 are predicted to increase by one-third from current statistics. Caroline Cerny, SunSmart manager at CRUK, commented: "The battle against melanoma is far from won. Today, the problem threatens to get worse as teenagers continue to crave a tan on the beach and top it up cheaply on sunbeds."
CRUK also noted that there has been a large increase in the overall death rates. Over a similar period, they have more than doubled from 1.2 per 100,000 in 1971 to 2.6 per 100,000 in the UK in 2007. If melanoma death rates had stayed the same as they were in 1973, approximately 19,000 fewer people would have died from the disease.
Although the incidence rates are predicted to rise, there are currently many promising drugs in development for MM. Of particular note, Pain Therapeutics (PT) recently reported encouraging clinical data with PTI-188, an early-stage drug for MM. Although efficacy was not a primary endpoint, PT and its clinical investigators were encouraged by the number of melanoma tumours that had either stabilised or decreased in size after a single dose of PTI-188. Further, Vical recently completed enrolment of the planned 375 subjects in its multi-national, Phase III trial of Allovectin-7 in patients with MM. Allovectin-7 is a novel gene-based immunotherapeutic with a unique mechanism of action that is fundamentally different from currently-approved treatments and has the potential to be the first new primary treatment approved for MM in nearly 20 years.
Alice Rossiter
Editor, Cancer Drug News
Of all ages, this generation has seen the biggest increase in incidence rates of melanoma, rising from seven cases per 100,000 people in the mid-1970s to 36 cases per 100,000 today. This rise shows the impact that a shift in tanning behaviour has had on a whole generation of men and women who would have been in their 20s and 30s in the 1970s, when holidays in the sun became cheap and popular, and sunbeds arrived in the UK.
According to CRUK statistics, the most common kind of skin cancer is non-melanoma skin cancer. More than 75,000 cases are registered each year in the UK, but it is estimated that the actual number is at least 100,000. More than 10,400 cases of MM are diagnosed each year in the UK and more than 2,000 people a year die from the disease.
For men in their 60s and 70s, the rates of melanoma have risen most dramatically; they are over seven-times more likely to be diagnosed with the disease than in the 1970s. For men and women of all ages, melanoma incidence rates have quadrupled since the 1970s. This rise in incidence rates is expected to continue: by 2024, rates in people aged 60 to 79 are predicted to increase by one-third from current statistics. Caroline Cerny, SunSmart manager at CRUK, commented: "The battle against melanoma is far from won. Today, the problem threatens to get worse as teenagers continue to crave a tan on the beach and top it up cheaply on sunbeds."
CRUK also noted that there has been a large increase in the overall death rates. Over a similar period, they have more than doubled from 1.2 per 100,000 in 1971 to 2.6 per 100,000 in the UK in 2007. If melanoma death rates had stayed the same as they were in 1973, approximately 19,000 fewer people would have died from the disease.
Although the incidence rates are predicted to rise, there are currently many promising drugs in development for MM. Of particular note, Pain Therapeutics (PT) recently reported encouraging clinical data with PTI-188, an early-stage drug for MM. Although efficacy was not a primary endpoint, PT and its clinical investigators were encouraged by the number of melanoma tumours that had either stabilised or decreased in size after a single dose of PTI-188. Further, Vical recently completed enrolment of the planned 375 subjects in its multi-national, Phase III trial of Allovectin-7 in patients with MM. Allovectin-7 is a novel gene-based immunotherapeutic with a unique mechanism of action that is fundamentally different from currently-approved treatments and has the potential to be the first new primary treatment approved for MM in nearly 20 years.
Alice Rossiter
Editor, Cancer Drug News
Monday, March 1, 2010
Scientists establish link between deprivation and poor prognosis for BC
Deprivation has long been known to play a role in the development of a wide range of diseases, and to a higher risk of recurrence or death for patients diagnosed with a number of cancers. Previously, the effect of material deprivation on cancer survival in England and Wales was measured by Cancer Research UK, and results showed that cancer survival for adults is generally lower among patients in more deprived groups, even after allowance is made for the higher mortality from all causes of death in these groups.
The reasons for survival rates differing between breast cancer (BC) sufferers from poorer areas and more affluent areas has never been fully understood. Now, researchers from the University of Dundee have established a link between deprivation and the p53 gene, which explains why women from poorer backgrounds are less likely to survive BC. The team identified, for the first time, that p53 mutation in BC is associated with socio-economic deprivation, and that this helps account for the poorer prognosis for women from deprived communities.
As detailed in the 26th January online edition of the British Journal of Cancer (10.1038/sj.bjc.6605540), the scientists found that women from deprived backgrounds were more likely to experience a mutation of p53, and that this linked to higher relapse and mortality rates. According to the team, there are two ways that p53 mutations can come about; one is as a result of genetic predisposition and the other is as a result of lifestyle. Smoking, drinking and poor diet can lead to p53 mutations, and are more common in women from lower socio-economic groups, who are also more likely to experience a recurrence of the disease and to die as a result of BC.
The survey looked at a total of 246 women who underwent treatment for BC between 1997 and 2001. Examining frozen tissue, tests were carried out to determine p53 mutation status. Using the patients' postcodes, a deprivation score was attributed to each and examined against the outcome (full recovery, relapse, death). The team found that patients in the lowest socio-economic group were significantly more likely to have a relapse and die compared to those in more affluent categories. They also demonstrated that the worse survival and shorter disease-free interval in BC for the most deprived patients is associated with tumour p53 mutation.
This research demonstrates a strong link between p53 and deprivation, and then between p53 mutation and recurrence and death. The social application of this work would suggest that if deprivation can be targeted, then the deprived population would be less likely to have problems with their p53 gene and go on to develop BC. In reality, this is unlikely to be achieved, however, there has been numerous work surrounding the p53 protein: Cyclacel Pharmaceuticals' seliciclib (CYC202) is a promising anticancer agent that promotes cancer cell death by downregulation of key proteins, such as p53 and Mcl-1, associated with survival of cancer cells; and new research by Dartmouth Medical School has shown that p53 limits the growth of cells with incorrect numbers of chromosomes and prevents their progression toward cancer.
Alice Rossiter
Editor, Cancer Drug News
The reasons for survival rates differing between breast cancer (BC) sufferers from poorer areas and more affluent areas has never been fully understood. Now, researchers from the University of Dundee have established a link between deprivation and the p53 gene, which explains why women from poorer backgrounds are less likely to survive BC. The team identified, for the first time, that p53 mutation in BC is associated with socio-economic deprivation, and that this helps account for the poorer prognosis for women from deprived communities.
As detailed in the 26th January online edition of the British Journal of Cancer (10.1038/sj.bjc.6605540), the scientists found that women from deprived backgrounds were more likely to experience a mutation of p53, and that this linked to higher relapse and mortality rates. According to the team, there are two ways that p53 mutations can come about; one is as a result of genetic predisposition and the other is as a result of lifestyle. Smoking, drinking and poor diet can lead to p53 mutations, and are more common in women from lower socio-economic groups, who are also more likely to experience a recurrence of the disease and to die as a result of BC.
The survey looked at a total of 246 women who underwent treatment for BC between 1997 and 2001. Examining frozen tissue, tests were carried out to determine p53 mutation status. Using the patients' postcodes, a deprivation score was attributed to each and examined against the outcome (full recovery, relapse, death). The team found that patients in the lowest socio-economic group were significantly more likely to have a relapse and die compared to those in more affluent categories. They also demonstrated that the worse survival and shorter disease-free interval in BC for the most deprived patients is associated with tumour p53 mutation.
This research demonstrates a strong link between p53 and deprivation, and then between p53 mutation and recurrence and death. The social application of this work would suggest that if deprivation can be targeted, then the deprived population would be less likely to have problems with their p53 gene and go on to develop BC. In reality, this is unlikely to be achieved, however, there has been numerous work surrounding the p53 protein: Cyclacel Pharmaceuticals' seliciclib (CYC202) is a promising anticancer agent that promotes cancer cell death by downregulation of key proteins, such as p53 and Mcl-1, associated with survival of cancer cells; and new research by Dartmouth Medical School has shown that p53 limits the growth of cells with incorrect numbers of chromosomes and prevents their progression toward cancer.
Alice Rossiter
Editor, Cancer Drug News
Thursday, October 15, 2009
Vaccination and testing for HPV could eradicate CC
According to a cervical cancer (CC) screening expert, Professor Jack Cuzick, from Cancer Research UK, the disease could be eradicated within the next 50 years if countries implement national screening programmes based on the detection of the human papillomavirus (HPV). Cuzick told the recent joint 15th ECCO and 34th ESMO Congress that while the current HPV vaccines protect against two cancer-causing strains of the HPV virus, soon there would be vaccines available that protect against nine types. If vaccination were to be combined with HPV screening, which is much more sensitive than the currently used Pap smear test, then eventually the cancer would disappear in those countries that had successfully implemented national programmes. However, this would require political will and effort at both national and European levels.
The current vaccine holds the promise of eradicating approximately 70 to 75 per cent of CC (caused by HPV types 16 and 18), and there appears to be some additional cross protection amongst types that are closely related to 16 or 18, in particular 31, 45 and a part of 33. There are new vaccines being planned that will vaccinate against nine types; if they are successful, there should be no need to screen women that have been vaccinated at all.
The Pap test relies on subjective assessments by people examining the cells in the smear with a microscope and therefore is open to human error. Cuzick believes that such errors will increase as the proportions of smears with affected cells decline due to increasing numbers of women having been vaccinated. In contrast, the HPV test is almost completely automated, is designed to detect the virus in the smear rather than relying on visual examination and therefore is much less likely to be affected by human error. Cuzick commented: "there's overwhelming evidence that HPV screening is more effective than the Pap smear test, which misses about a third to a half of all high-grade lesions". However, Cuzick warned that the EU and national governments should take the initiative in discussions on implementing screening and vaccination programmes, rather than leaving it to pharmaceutical companies to lead the debate.
During the last fortnight, much data have been reported in relation to CC drug and vaccine trials. Of particular note, results from the PATRICIA (PApilloma TRIal Cervical cancer In young Adults or HPV 008) study showed that GlaxoSmithKline's Cervarix is highly effective at protecting against the two most common CC-causing HPV types, 16 and 18. Furthermore, Cervarix demonstrated efficacy against cervical intraepithelial neoplasia 2+ lesions associated with 12 additional HPV types beyond 16 and 18, including HPV 31, 33 and 45.
In addition, Phase I trial results of ADXS11-001 have shown 36-month survival in three of the 13 evaluable patients treated with Advaxis' therapeutic cancer vaccine, which treats women who have already developed CC as a result of HPV infection, indicating the possibility of persistent immune protection. Further, interim safety and immunogenicity data from a Phase I trial of Inovio Biomedical's VGX-3100 showed that the therapeutic CC vaccine was generally safe and well tolerated, plus it achieved significant cellular and humoral immune responses at the lowest dose administered. VGX-3100 is a DNA vaccine targeting the E6 and E7 proteins of HPV types 16 and 18.
Alice Rossiter - Cancer Drug News Editor
The current vaccine holds the promise of eradicating approximately 70 to 75 per cent of CC (caused by HPV types 16 and 18), and there appears to be some additional cross protection amongst types that are closely related to 16 or 18, in particular 31, 45 and a part of 33. There are new vaccines being planned that will vaccinate against nine types; if they are successful, there should be no need to screen women that have been vaccinated at all.
The Pap test relies on subjective assessments by people examining the cells in the smear with a microscope and therefore is open to human error. Cuzick believes that such errors will increase as the proportions of smears with affected cells decline due to increasing numbers of women having been vaccinated. In contrast, the HPV test is almost completely automated, is designed to detect the virus in the smear rather than relying on visual examination and therefore is much less likely to be affected by human error. Cuzick commented: "there's overwhelming evidence that HPV screening is more effective than the Pap smear test, which misses about a third to a half of all high-grade lesions". However, Cuzick warned that the EU and national governments should take the initiative in discussions on implementing screening and vaccination programmes, rather than leaving it to pharmaceutical companies to lead the debate.
During the last fortnight, much data have been reported in relation to CC drug and vaccine trials. Of particular note, results from the PATRICIA (PApilloma TRIal Cervical cancer In young Adults or HPV 008) study showed that GlaxoSmithKline's Cervarix is highly effective at protecting against the two most common CC-causing HPV types, 16 and 18. Furthermore, Cervarix demonstrated efficacy against cervical intraepithelial neoplasia 2+ lesions associated with 12 additional HPV types beyond 16 and 18, including HPV 31, 33 and 45.
In addition, Phase I trial results of ADXS11-001 have shown 36-month survival in three of the 13 evaluable patients treated with Advaxis' therapeutic cancer vaccine, which treats women who have already developed CC as a result of HPV infection, indicating the possibility of persistent immune protection. Further, interim safety and immunogenicity data from a Phase I trial of Inovio Biomedical's VGX-3100 showed that the therapeutic CC vaccine was generally safe and well tolerated, plus it achieved significant cellular and humoral immune responses at the lowest dose administered. VGX-3100 is a DNA vaccine targeting the E6 and E7 proteins of HPV types 16 and 18.
Alice Rossiter - Cancer Drug News Editor
Thursday, November 20, 2008
Targeted drugs reduce attrition rates
The results of a new study published in the 14th November online edition of Nature Reviews Drug Discovery (10.1038/nrd2758) suggest that advances in drug development have led to an increase in the number of drugs reaching cancer patients. Scientists from Cancer Research Technology (CRT; Cancer Research UK [CRUK]) obtained data on 974 cancer drugs in clinical development, and calculated that there was a probability that 18 per cent of those entering the clinic would make it to market. Previously it was estimated that in some studies only 5 per cent of cancer drugs in the pipeline become standard treatments for the disease.
The data search was limited to agents which entered Phase I trials after January 1995 and before September 2007, of which 137 are the molecularly-targeted drug class, kinase inhibitors. The research showed that kinase inhibitors were almost three-times more likely to reach patients than other types of anticancer drug. The investigators believe that a better understanding of the basic biology of cancer has enabled the development of this type of new drug, which includes Herceptin (trastuzumab) for breast cancer and Glivec/Gleevec (imatinib) for leukaemia.
The study highlights the fact that understanding more about the basic biology of cancer is making a real difference to the success rate of new anticancer drug development. Additionally, improved drug-discovery processes and advances in medicinal chemistry have also contributed to better success rates of drugs in development. Furthermore, better understanding of a patient's genetic make-up and how they will respond to certain drugs has led to improvements in clinical trial design.As drug development continues to advance, minimising the number of drugs which fail to make it to market will remain key as the cost of discovery and development of those drugs which do not reach market is borne by those that do. The true cost of a drug reaching the market has recently been estimated to be US$0.8 billion to US$1.0 billion.
According to one of the study authors, Professor Herbie Newell, Director of Translational Research at CRUK: "We strongly believe that both industry and academia must improve the availability of data related to failed as well as successful drug development programmes. The sharing of such information can only be beneficial for clinical, scientific and commercial reasons, and will help measure our progress as well as pinpoint areas for improvement."
Historically, the oncology pipeline has been largely made up of small-molecule cytotoxic drugs, which have a low therapeutic index and can fail in clinical trials due to toxicity or efficacy reasons. The recent explosion of information coming from work into understanding the molecular basis of cancer has led to an increase of drugs targeting specific pathways, drugs that are specifically designed to treat cancer, rather than randomly killing proliferating cells. As more information becomes available and newer drugs that are better targeted move into the pipeline, the attrition rate for cancer drugs may reach levels seen with other therapy areas, such as cardiovascular disease where 20 per cent of agents in development reach the market.
Matthew Dennis - Editor, Cancer Drug News
The data search was limited to agents which entered Phase I trials after January 1995 and before September 2007, of which 137 are the molecularly-targeted drug class, kinase inhibitors. The research showed that kinase inhibitors were almost three-times more likely to reach patients than other types of anticancer drug. The investigators believe that a better understanding of the basic biology of cancer has enabled the development of this type of new drug, which includes Herceptin (trastuzumab) for breast cancer and Glivec/Gleevec (imatinib) for leukaemia.
The study highlights the fact that understanding more about the basic biology of cancer is making a real difference to the success rate of new anticancer drug development. Additionally, improved drug-discovery processes and advances in medicinal chemistry have also contributed to better success rates of drugs in development. Furthermore, better understanding of a patient's genetic make-up and how they will respond to certain drugs has led to improvements in clinical trial design.As drug development continues to advance, minimising the number of drugs which fail to make it to market will remain key as the cost of discovery and development of those drugs which do not reach market is borne by those that do. The true cost of a drug reaching the market has recently been estimated to be US$0.8 billion to US$1.0 billion.
According to one of the study authors, Professor Herbie Newell, Director of Translational Research at CRUK: "We strongly believe that both industry and academia must improve the availability of data related to failed as well as successful drug development programmes. The sharing of such information can only be beneficial for clinical, scientific and commercial reasons, and will help measure our progress as well as pinpoint areas for improvement."
Historically, the oncology pipeline has been largely made up of small-molecule cytotoxic drugs, which have a low therapeutic index and can fail in clinical trials due to toxicity or efficacy reasons. The recent explosion of information coming from work into understanding the molecular basis of cancer has led to an increase of drugs targeting specific pathways, drugs that are specifically designed to treat cancer, rather than randomly killing proliferating cells. As more information becomes available and newer drugs that are better targeted move into the pipeline, the attrition rate for cancer drugs may reach levels seen with other therapy areas, such as cardiovascular disease where 20 per cent of agents in development reach the market.
Matthew Dennis - Editor, Cancer Drug News
Wednesday, August 13, 2008
Draft NICE guidance denies RCC drugs
The UK's National Institute for Health and Clinical Excellence (NICE) has issued preliminary recommendations for the treatment of renal cell carcinoma (RCC), concluding that Roche/Genentech's Avastin (bevacizumab), Bayer/Onyx Pharmaceuticals' Nexavar (sorafenib), Pfizer's Sutent (sunitinib) and Wyeth Pharmaceuticals' Torisel (temsirolimus) are not recommended as treatment options for advanced and/or metastatic disease. Although the drugs were shown to be clinically effective and extend life for RCC patients, they were deemed to not be a cost-effective use of NHS resources. NICE is expected to issue final guidance in January 2009.
Following the decision, Cancer Research UK (CRUK) has called for NICE to alter the way that it appraises the value of drugs for rare diseases, such as metastatic RCC, where clinical benefit is proven but evidence is limited due to the small number of available patients. Professor Peter Johnson, CRUK's chief clinician, stated: "We are disappointed at NICE's view that although these drugs are clinically effective, their high price means that they are not considered to be value for money for the NHS. These drugs have shown a small but definite improvement in an illness where there are few alternative treatments. If this decision stands it will be very frustrating for cancer patients and their clinicians."
The charity put forward that possible solutions include looking at the way that pharmaceutical companies are charging the NHS for drugs, and whether appropriate allowances are being made by NICE to compensate for the lack of large-scale trials in these areas. However, it turns out that proposals were submitted by two of the manufacturers relating to drug acquisition costs. But these were not considered by the Department of Health as they had not been agreed before the appraisal.
The preliminary guidance raises questions as to how NICE evaluates cancer drugs, particularly for cancers that only affect a relatively small number of people. The gold-standard method of testing whether a treatment works and is safe is through the use of clinical trials. The larger the number of patients enrolled in a study, and the longer it lasts, the more sure researchers can be about its results. This works for diseases that affect large numbers of people, such as breast and lung cancer, but only around 2,000 people every year are diagnosed with metastatic RCC. Further, only one in ten people diagnosed with this stage of the disease is alive five years later. This means that for relatively rare diseases like this, it can take a long time to conduct large enough studies to gather the evidence needed to gain approval from regulatory agencies.
Even if these studies do demonstrate benefit, as those for the four drugs did, there is still the cost-effectiveness hurdle to overcome. When NICE analysed the data from the trials with its models, it found that the drugs were expensive (around £20,000 to £35,000 per patient per year) compared to the benefit they brought patients. However, concerns have also been raised about these models, which are designed to examine giving drugs to large numbers of people. Are they equally valid for looking at relatively uncommon diseases, such as metastatic RCC? Hopefully NICE will be able to answer these questions when its final guidance is published.
Matthew Dennis - Editor, Cancer Drug News
Following the decision, Cancer Research UK (CRUK) has called for NICE to alter the way that it appraises the value of drugs for rare diseases, such as metastatic RCC, where clinical benefit is proven but evidence is limited due to the small number of available patients. Professor Peter Johnson, CRUK's chief clinician, stated: "We are disappointed at NICE's view that although these drugs are clinically effective, their high price means that they are not considered to be value for money for the NHS. These drugs have shown a small but definite improvement in an illness where there are few alternative treatments. If this decision stands it will be very frustrating for cancer patients and their clinicians."
The charity put forward that possible solutions include looking at the way that pharmaceutical companies are charging the NHS for drugs, and whether appropriate allowances are being made by NICE to compensate for the lack of large-scale trials in these areas. However, it turns out that proposals were submitted by two of the manufacturers relating to drug acquisition costs. But these were not considered by the Department of Health as they had not been agreed before the appraisal.
The preliminary guidance raises questions as to how NICE evaluates cancer drugs, particularly for cancers that only affect a relatively small number of people. The gold-standard method of testing whether a treatment works and is safe is through the use of clinical trials. The larger the number of patients enrolled in a study, and the longer it lasts, the more sure researchers can be about its results. This works for diseases that affect large numbers of people, such as breast and lung cancer, but only around 2,000 people every year are diagnosed with metastatic RCC. Further, only one in ten people diagnosed with this stage of the disease is alive five years later. This means that for relatively rare diseases like this, it can take a long time to conduct large enough studies to gather the evidence needed to gain approval from regulatory agencies.
Even if these studies do demonstrate benefit, as those for the four drugs did, there is still the cost-effectiveness hurdle to overcome. When NICE analysed the data from the trials with its models, it found that the drugs were expensive (around £20,000 to £35,000 per patient per year) compared to the benefit they brought patients. However, concerns have also been raised about these models, which are designed to examine giving drugs to large numbers of people. Are they equally valid for looking at relatively uncommon diseases, such as metastatic RCC? Hopefully NICE will be able to answer these questions when its final guidance is published.
Matthew Dennis - Editor, Cancer Drug News
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