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News Article | November 9, 2016
Site: www.sciencedaily.com

Tagging gold nanoparticles with a small dose of radiation has helped researchers trace the precious metal as it delivers a drug right into the heart of cancer cells, according to new laboratory research being presented at the 2016 National Cancer Research Institute (NCRI) Cancer conference. Researchers from the CRUK/MRC Oxford Institute for Radiation Oncology have been working on better ways to transport a drug directly into the control room of cancer cells, where the chromosomes are kept. This specific drug targets a molecule -- telomerase -- that builds up the protective caps at the end of chromosomes called telomeres. In most cells of the body, telomeres act like an in-built timer to ensure that the cell does not live past its expiry date. Telomeres shorten each time the cell divides. Once a critical length is reached, the cell can no longer divide and it dies. Cancer cells manage to get around this safety check by reactivating telomerase allowing them to continue to grow out of control. One of the biggest hurdles in treating cancer is getting effective drugs into cancer cells, particularly to where the chromosomes are stored. Gold nanoparticles have proven to be well suited to being absorbed into cells, safely delivering drugs that could otherwise be blocked. By engineering the gold nanoparticles and adding the radioactive tracer, the researchers were able to prove that their drug was reaching the desired target in skin cancer cells grown in the lab and was shutting telomerase down, halting cancer's growth. While the radioactive tracer was used to precisely follow the drug in this study, the same method can also be used to deliver a dose of radioactivity to cancer cells, helping to kill them. This second dose is especially powerful because inactivation of telomerase makes cancer cells more sensitive to radiation. Professor Kate Vallis, lead researcher based at the CRUK/MRC Oxford Institute for Radiation Oncology, said: "Gold is precious in more than one way. We have used tiny gold nanoparticles loaded with targeted drugs to kill cancer cells in the laboratory. Our long term goal is to design new treatments for cancer patients based on this promising approach." Sir Harpal Kumar, Cancer Research UK's chief executive, said: "Gold has been used in medicine for many years and this research adds further insight into its potential. Ensuring that treatment is accurately targeted at cancer and avoids healthy cells is the goal for much of cancer research, and this is an exciting step towards that." Dr Karen Kennedy, Director of the NCRI, said: "Research continues to shed light on how cancer cells behave and how to effectively deliver a lethal payload to the tumour. This exciting research offers that potential and needs further investigation to see how it would be used in patients. The future looks exciting with research such as this improving the way the disease is treated."


News Article | November 8, 2016
Site: www.biosciencetechnology.com

Tagging gold nanoparticles with a small dose of radiation has helped researchers trace the precious metal as it delivers a drug right into the heart of cancer cells, according to new laboratory research* being presented at the 2016 National Cancer Research Institute (NCRI) Cancer conference. Researchers from the CRUK/MRC Oxford Institute for Radiation Oncology have been working on better ways to transport a drug directly into the control room of cancer cells, where the chromosomes are kept. This specific drug targets a molecule - telomerase - that builds up the protective caps at the end of chromosomes called telomeres. In most cells of the body, telomeres act like an in-built timer to ensure that the cell does not live past its expiry date. Telomeres shorten each time the cell divides. Once a critical length is reached, the cell can no longer divide and it dies. Cancer cells manage to get around this safety check by reactivating telomerase allowing them to continue to grow out of control. One of the biggest hurdles in treating cancer is getting effective drugs into cancer cells, particularly to where the chromosomes are stored. Gold nanoparticles have proven to be well suited to being absorbed into cells, safely delivering drugs that could otherwise be blocked. By engineering the gold nanoparticles and adding the radioactive tracer, the researchers were able to prove that their drug was reaching the desired target in skin cancer cells grown in the lab and was shutting telomerase down, halting cancer's growth. While the radioactive tracer was used to precisely follow the drug in this study, the same method can also be used to deliver a dose of radioactivity to cancer cells, helping to kill them. This second dose is especially powerful because inactivation of telomerase makes cancer cells more sensitive to radiation. Professor Kate Vallis, lead researcher based at the CRUK/MRC Oxford Institute for Radiation Oncology, said: "Gold is precious in more than one way. We have used tiny gold nanoparticles loaded with targeted drugs to kill cancer cells in the laboratory. Our long term goal is to design new treatments for cancer patients based on this promising approach." Sir Harpal Kumar, Cancer Research UK's chief executive, said: "Gold has been used in medicine for many years and this research adds further insight into its potential. Ensuring that treatment is accurately targeted at cancer and avoids healthy cells is the goal for much of cancer research, and this is an exciting step towards that." Dr. Karen Kennedy, Director of the NCRI, said: "Research continues to shed light on how cancer cells behave and how to effectively deliver a lethal payload to the tumour. This exciting research offers that potential and needs further investigation to see how it would be used in patients. The future looks exciting with research such as this improving the way the disease is treated."


News Article | November 7, 2016
Site: www.eurekalert.org

Substantial weight gain over many years increases the risk of obesity-related cancers in men by 50 per cent and in women by almost 20 per cent, according to new research* presented at the National Cancer Research Institute's (NCRI) Cancer Conference in Liverpool, today (Monday). Researchers at The University of Manchester and The Health eResearch Centre, looked at weight gain over many years and assessed the risk of developing obesity-related cancers. This is a new way of looking at the long-term impact of being obese throughout a person's life and the link to developing cancer. In the study of approximately 300,000 people in America, including around 177,500 men and 111,500 women, researchers categorised the population into five different lifetime weight trajectories**. They looked at changes in BMI between the ages of 18 and 65. Some people gained a little weight between the ages of 18 and 65 years, while others became morbidly obese. The population was then followed up for an average of 15 years to see who went on to develop obesity-related cancers. It found that men who went from a BMI of around 22 to 27*** had a 50 per cent increased risk of developing obesity-related cancer compared to a man who stayed within a healthy weight range. And in men who went from being overweight to morbidly obese, the risk went up by 53 per cent compared to the same group. Women who went from a BMI of 23 to around 32, had a 17 per cent increased risk in comparison to women whose weight started off in the healthy bracket and remained stable. Of the 300,000 people in the study, there were around 9,400 women and 5,500 men who were diagnosed with obesity-related cancers after the age of 65. Being overweight or obese is the second biggest preventable cause of cancer in the UK after smoking and contributes to around 18,100**** cases of cancer every year. It is linked to a range of cancer types including bowel, breast, and pancreatic. Several of the obesity-related cancer types can only affect women - for example, womb cancer and ovarian cancer. Dr Hannah Lennon, lead author and researcher at The University of Manchester, said: "This research shows how important it is to look at weight gain over a person's lifetime - to give a clearer picture of cancer risk through life compared to assessing someone's BMI at a single point. "This study could also be really useful in public health. It could help identify people who would benefit the most from taking action to control their weight before any health problems arise - including a cancer diagnosis." Sir Harpal Kumar, Cancer Research UK's chief executive said: "This is a really interesting way to look at lifetime risk of obesity-related cancers and helps us understand the effects of weight gain over time. "It's important that people are informed about ways to reduce their risk of cancer. And while there are no guarantees against the disease, keeping a healthy weight can help you stack the odds in your favour and has lots of other benefits too. Making small changes in eating, drinking and taking exercise that you can stick with in the long term is a good way to get to a healthy weight - and stay there." Dr Karen Kennedy, Director of the NCRI, said: "This study provides a deeper understanding of the health implications caused by the obesity epidemic. It helps paint the picture of how risk could accumulate over time for different people, and could provide health professionals with a means to asses an individual's risk." This work is funded by Cancer Research UK as part of the National Awareness and Early Diagnosis Initiative (NAEDI). Supported by the Farr Institute and linked with the new NIHR Manchester BRC Cancer Prevention and Early Detection theme. For media enquiries contact Stephanie McClellan in the NCRI press office on 0203 469 5314 or, out of hours, on 07050 264 059. * NCRI abstract: Lifetime BMI trajectories and obesity-related cancer risk in a US retrospective cohort study http://abstracts. *** A BMI of between 18.5 and 25 kg/m^2 is considered a healthy weight; between 25-30 is overweight; over 30 is obese. For men, this is equivalent to an extra 2.5 stone increase for the average height man of 177cm between the ages of 18 and 65, because even the 'normal/reference' trajectories allows for a little weight gain as we age. This is the lean marked category compared to lean moderate category. For women example, this is the lean marked category compared to lean stable category. **** Calculated by the Statistical Information Team at Cancer Research UK, the estimated population attributable fractions overweight and obesity for cancer cases (ICD10 C00-C97, excl. C44) in the UK in 2011 using Parkin, D. M. & Boyd, L. Overweight and obesity-attributable cancer burden in the UK in 2010. Br J Cancer 2011;105 (S2):S6-S13.


SOUTH SAN FRANCISCO, Calif.--(BUSINESS WIRE)--Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY), today announced data from the positive, pivotal Phase III GALLIUM study that compared Gazyva® (obinutuzumab) plus chemotherapy followed by Gazyva alone head-to-head against Rituxan® (rituximab) plus chemotherapy followed by Rituxan alone for people with previously untreated follicular lymphoma. At a pre-planned interim analysis in May 2016, an independent data monitoring committee determined that the study met its primary endpoint early. The results showed Gazyva-based treatment reduced the risk of disease worsening or death (progression-free survival; PFS, as assessed by investigator) by 34 percent compared to Rituxan-based treatment (HR=0.66; 95% CI 0.51-0.85, p=0.0012). Median PFS was not yet reached. Adverse events with either Gazyva or Rituxan were consistent with those seen in previous studies. “Follicular lymphoma, the most common slow-growing form of non-Hodgkin’s lymphoma, is an incurable blood cancer characterized by cycles of remission and disease progression, and becomes harder to treat with every relapse,” said Sandra Horning, M.D., chief medical officer and head of Global Product Development. “This study of Gazyva-based treatment is the first and only Phase III trial to date to show superior progression-free survival compared to Rituxan-based treatment, the current standard of care, in previously untreated follicular lymphoma.” The primary results from the GALLIUM study (Abstract #6) will be presented during the Plenary Scientific Session of the 58th American Society of Hematology (ASH) Annual Meeting in San Diego by Dr. Robert Marcus, King’s College Hospital, London and the National Cancer Research Institute (NCRI), on Sunday, December 4 at 2:00 P.M. PST. Additionally, an analysis of minimal residual disease (MRD) status in the GALLIUM study (Abstract #613) will be presented in a separate oral session by Dr. Christiane Pott, University Hospital Schleswig-Holstein, Kiel, Germany, and the German Low Grade Lymphoma Study Group (GLSG) on Monday, December 5 at 7:00 A.M. PST. GALLIUM is the third positive Phase III study for Gazyva, following the CLL11 study in patients with previously untreated chronic lymphocytic leukemia (CLL) and the GADOLIN study in patients with indolent (slow-growing) non-Hodgkin’s lymphoma whose disease progressed during or within six months of prior Rituxan-based therapy. The results of the GALLIUM study will be submitted to health authorities around the world for approval consideration. GALLIUM (NCT01332968) is a global Phase III open-label, multicenter, randomized two-arm study examining the efficacy and safety of Gazyva plus chemotherapy followed by Gazyva alone for up to two years, as compared head-to-head against Rituxan plus chemotherapy followed by Rituxan alone for up to two years. Chemotherapies used were CHOP, CVP or bendamustine and were selected by each participating study site prior to beginning enrollment. GALLIUM included 1401 patients with previously untreated indolent non-Hodgkin’s lymphoma (iNHL), of which 1202 patients had follicular lymphoma. The primary endpoint of the study was investigator-assessed PFS in patients with follicular lymphoma, with secondary endpoints including PFS assessed by independent review committee (IRC), PFS in the overall study population (iNHL), response rate (overall response, ORR; and complete response, CR), overall survival (OS) and safety. The GALLIUM study is being conducted in cooperation with the GLSG (Germany), the East German Study Group Hematology and Oncology (OSHO; Germany) and the NCRI (United Kingdom). A summary of the GALLIUM study results presented at ASH is included below. 1 Primary endpoint is PFS as assessed by investigator; median follow-up of 34.5 months 2 Measured by computerized tomography (CT) scans 3 MRD-negativity means no cancer can be detected in the blood or bone marrow using a specific highly sensitive test 4 Defined as any AE occurring during or within 24 hours of infusion of Gazyva or Rituxan and considered drug-related Follicular lymphoma is the most common indolent (slow-growing) form of non-Hodgkin’s lymphoma (NHL), accounting for about one in five cases of NHL. It is considered incurable and relapse is common. In the United States, it is estimated that more than 14,000 new cases of follicular lymphoma will be diagnosed in 2016. Gazyva is an engineered monoclonal antibody designed to attach to CD20, a protein found on certain types of B-cells. It is thought to work by attacking targeted cells both directly and together with the body's immune system. Gazyva was discovered by Roche Glycart AG, a wholly owned, independent research unit of Roche. In the United States, Gazyva is part of a collaboration between Genentech and Biogen. Combination studies investigating Gazyva with other approved or investigational medicines, including cancer immunotherapies and small molecule inhibitors, are planned or underway across a range of blood cancers. Patients must tell their doctor right away about any side effects they experience. Gazyva can cause side effects that can become serious or life threatening, including: Hepatitis B Virus (HBV): Hepatitis B can cause liver failure and death. If a patient has had history of hepatitis B infection, Gazyva could cause it to return. Patients should not receive Gazyva if they have active hepatitis B liver disease. The patient’s doctor or healthcare team will need to screen for hepatitis B before, and monitor the patient for hepatitis during and after, treatment with Gazyva. Sometimes this will require treatment for hepatitis B. Symptoms of hepatitis include: worsening of fatigue and yellow discoloration of skin or eyes. Progressive Multifocal Leukoencephalopathy (PML): PML is a rare and serious brain infection caused by a virus. PML can be fatal. A patient’s weakened immune system could put the patient at risk. The patient’s doctor will watch for symptoms. Symptoms of PML include: confusion, difficulty talking or walking, dizziness or loss of balance, and vision problems. Additional possible serious side effects of Gazyva: Patients must tell their doctor right away about any side effects they experience. Gazyva can cause side effects that may become severe or life threatening, including: The most common side effects of Gazyva in CLL are infusion reactions, low white blood cell counts, low platelet counts, low red blood cell counts, fever, cough, nausea, and diarrhea. The safety of Gazyva was evaluated based on 392 patients with indolent NHL (iNHL) of whom 81 percent had follicular lymphoma. In patients with follicular lymphoma, the most common side effects that were seen were consistent with the overall population who had iNHL. The most common side effects of Gazyva are infusion reactions, low white blood cell counts, nausea, fatigue, cough, diarrhea, constipation, fever, low platelet counts, vomiting, upper respiratory tract infection, decreased appetite, joint or muscle pain, sinusitis, low red blood cell counts, general weakness, and urinary tract infection. Before receiving Gazyva, patients should talk to their doctor about: Immunizations: Before receiving Gazyva therapy, the patient should tell the patient’s healthcare provider if the patient has recently received or is scheduled to receive a vaccine. Patients who are treated with Gazyva should not receive live vaccines. Pregnancy: A patient should tell the doctor if the patient is pregnant, plans to become pregnant, or is breastfeeding. Gazyva may harm the unborn baby. Mothers who have been exposed to Gazyva during pregnancy should discuss the safety and timing of live virus vaccinations for their infants with their child’s healthcare providers. It is not known if Gazyva may pass into the patient’s breast milk. The patient should speak to the doctor about using Gazyva if the patient is breastfeeding. Patients must tell their doctor about any side effects. These are not all of the possible side effects of Gazyva. For more information, patients should ask their doctor or pharmacist. Gazyva is available by prescription only. Report side effects to the FDA at (800) FDA-1088, or http://www.fda.gov/medwatch. Report side effects to Genentech at (888) 835-2555. Please visit http://www.Gazyva.com for the Gazyva full Prescribing Information, including Boxed WARNINGS, for additional Important Safety Information. Rituxan® (rituximab) is indicated for the treatment of patients with: People with serious infections should not receive Rituxan. It is not known if Rituxan is safe or effective in children. Patients must tell their doctor right away about any side effects they experience. Rituxan can cause serious side effects that can lead to death, including: What are the additional possible serious side effects of Rituxan? Patients must tell their doctor right away about any side effects they experience. Rituxan can cause serious side effects that can lead to death, including: The most common side effects of Rituxan are infusion reactions, chills, infections, body aches, tiredness and low white blood cells. Patients must tell their doctor if they are pregnant, plan to become pregnant or are breastfeeding. It is not known if Rituxan may harm the patient’s unborn baby or pass into the patient’s breast milk. Women should use birth control while using Rituxan and for 12 months after treatment. Patients must tell their doctor about any side effect that bothers them or that does not go away. These are not all of the possible side effects of Rituxan. For more information, patients should ask their doctor or pharmacist. Report side effects to the FDA at (800) FDA-1088 or http://www.fda.gov/medwatch. Report side effects to Genentech at (888) 835-2555. Please visit http://www.Rituxan.com for the Rituxan full Prescribing Information, including Boxed WARNINGS and Medication Guide, for additional Important Safety Information. For more than 20 years, Genentech has been developing medicines with the goal to redefine treatment in hematology. Today, we’re investing more than ever in our effort to bring innovative treatment options to people with diseases of the blood. In addition to approved medicines, Genentech’s pipeline of investigational hematology medicines includes an anti-CD79b antibody drug conjugate (polatuzumab vedotin/RG7596) and a small molecule antagonist of MDM2 (idasanutlin/RG7388). Genentech’s dedication to developing novel medicines for blood diseases expands beyond oncology, with the development of the investigational hemophilia A treatment emicizumab (ACE910). For more information visit http://www.gene.com/hematology. Founded 40 years ago, Genentech is a leading biotechnology company that discovers, develops, manufactures and commercializes medicines to treat patients with serious or life-threatening medical conditions. The company, a member of the Roche Group, has headquarters in South San Francisco, California. For additional information about the company, please visit http://www.gene.com.


News Article | November 11, 2016
Site: www.techtimes.com

About 17 percent of women diagnosed with breast cancer experience symptoms other than breast lump, a most common symptom of breast cancer, reports a recent research. According to the study presented at 2016 National Cancer Research Institute (NCRI) Cancer conference in Liverpool, about one in six women diagnosed with non-lump breast cancer experiences symptoms like breast pain, shape abnormalities, ulceration, inflamed or infected breast and skin abnormalities. For the purpose of the study, the researchers reviewed data of over 2,300 women diagnosed with breast cancer in Britain between 2009 and 2010. Despite the fact that most women got medical attention quickly, women with non-lump breast cancer delayed seeking medical help when compared to those that had breast lumps. Notably, women who had breast lump along with non-lump symptoms were also found to have delayed seeking medical attention. It was also observed that women who experienced symptoms like infection or inflammation in breast, breast ulceration, pain or swelling in the arm or armpit and nipple abnormalities delayed for more than three months to seek medical aid. Monica Koo, who presented the study, said that one in six women delay getting help for non-lump breast cancer. Women should be aware of the fact that lump in breast is not the only symptom of cancer. Women should visit a physician as soon as they start experiencing any abnormality in breast. Koo added that diagnosing cancer as early as possible will help in increasing the patient's survival rate. Women should be made aware of all the symptoms of breast cancer through campaigns like Be Clear on Cancer for early intervention. Dr Karen Kennedy, NCRI's director, said that the research reveals that women are not much aware of the fact that breast cancer could exhibit various symptoms other than just the lump. "Awareness campaigns need to raise awareness of all of the potential symptoms of breast cancer so that people know how to spot the signs and when to go to a doctor," said Kennedy in press release. The symptoms of breast cancer include pain in nipple, nipple turning inward, nipple discharge other than breast milk, lump in underarms, breast pain, dimpling or skin irritation, swelling of breast and scaliness, redness or thickening of breast skin or nipples, reports Breast Cancer.Org. While the above symptoms could indicate the presence of breast cancer, they can also be due to various non-cancerous problems like infection or cyst. However, women should seek medical aid as soon as the symptoms are felt in order to severe consequences in later stages. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.


News Article | November 9, 2016
Site: www.eurekalert.org

BLOCKING a molecule could bypass bowel cancer's defence against the drug cetuximab, according to new research* presented at the National Cancer Research Institute (NCRI) Cancer Conference in Liverpool. Cetuximab is used to treat advanced bowel cancer, and just under half of bowel cancer patients are given the drug. While it helps many patients, there are some for whom it doesn't work at all and for others it loses effectiveness. To understand why this happens, scientists at Queen's University Belfast treated bowel cancer cells in the lab with cetuximab. They found that some cells survived the treatment by increasing the activity of a protein called ADAM17. But if they gave a drug that blocked the protein ADAM17 at the same time as cetuximab the cancer cells died. For other cancer cells, cetuximab treatment alone stopped them growing initially, but over time they became resistant and started growing again. In these cases, the cancer cells were finding a different way to outmanoeuvre the treatment that didn't involve ADAM17. Cetuximab works by blocking a molecule known as epidermal growth factor receptor (EGFR), which tells cells to grow. There are around 41,000 cases of bowel cancer diagnosed in the UK each year. And each year around 16,000 die of the disease. Dr Sandra Van Schaeybroeck, the lead researcher based at Queen's University Belfast, said: "While some bowel cancer patients respond well to cetuximab treatment, many will relapse, or not benefit from the drug. Our work shows that combining this treatment with an ADAM17 inhibitor could be a promising avenue of therapy for patients who don't respond to cetuximab by itself. "More work is needed before we can safely test this combination in patients, but the prospect of cutting off cancer's path to resistance is very exciting." Professor Peter Johnson, Cancer Research UK's chief clinician, said: "This work shows how some bowel cancer cells are able to avoid damage from a particular drug, and offers a way to prevent it. The next step is to find out whether this could work in patients." Professor Richard Wilson, Chair of the NCRI's Colorectal Cancer Clinical Studies Group, said: "Bowel cancer is the fourth most common cancer in the UK, and it's the second biggest cancer killer - so it's vital that we find ways to break through the disease's resistance to treatment." "A big issue facing bowel cancer patients is the prospect of their cancer coming back. Understanding the mechanisms that bowel cancer cells use to evade treatment with cetuximab will help us find ways to delay or prevent it recurring. This will help more people with bowel cancer live longer and with better quality of life." This research was funded by Cancer Research UK.


News Article | November 10, 2016
Site: www.sciencedaily.com

Blocking a molecule could bypass bowel cancer's defence against the drug cetuximab, according to new research presented at the National Cancer Research Institute (NCRI) Cancer Conference in Liverpool. Cetuximab is used to treat advanced bowel cancer, and just under half of bowel cancer patients are given the drug. While it helps many patients, there are some for whom it doesn't work at all and for others it loses effectiveness. To understand why this happens, scientists at Queen's University Belfast treated bowel cancer cells in the lab with cetuximab. They found that some cells survived the treatment by increasing the activity of a protein called ADAM17. But if they gave a drug that blocked the protein ADAM17 at the same time as cetuximab the cancer cells died. For other cancer cells, cetuximab treatment alone stopped them growing initially, but over time they became resistant and started growing again. In these cases, the cancer cells were finding a different way to outmanoeuvre the treatment that didn't involve ADAM17. Cetuximab works by blocking a molecule known as epidermal growth factor receptor (EGFR), which tells cells to grow. There are around 41,000 cases of bowel cancer diagnosed in the UK each year. And each year around 16,000 die of the disease. Dr Sandra Van Schaeybroeck, the lead researcher based at Queen's University Belfast, said: "While some bowel cancer patients respond well to cetuximab treatment, many will relapse, or not benefit from the drug. Our work shows that combining this treatment with an ADAM17 inhibitor could be a promising avenue of therapy for patients who don't respond to cetuximab by itself. "More work is needed before we can safely test this combination in patients, but the prospect of cutting off cancer's path to resistance is very exciting." Professor Peter Johnson, Cancer Research UK's chief clinician, said: "This work shows how some bowel cancer cells are able to avoid damage from a particular drug, and offers a way to prevent it. The next step is to find out whether this could work in patients." Professor Richard Wilson, Chair of the NCRI's Colorectal Cancer Clinical Studies Group, said: "Bowel cancer is the fourth most common cancer in the UK, and it's the second biggest cancer killer -- so it's vital that we find ways to break through the disease's resistance to treatment." "A big issue facing bowel cancer patients is the prospect of their cancer coming back. Understanding the mechanisms that bowel cancer cells use to evade treatment with cetuximab will help us find ways to delay or prevent it recurring. This will help more people with bowel cancer live longer and with better quality of life." See more at: http://abstracts.ncri.org.uk/abstract/adam17-a-potential-regulator-of-resistance-to-egfr-targeted-therapies-in-ras-wild-type-colorectal-cancer/


News Article | November 7, 2016
Site: www.sciencedaily.com

Patients with malignant melanoma -- whose disease has spread -- are more likely to respond to immunotherapy treatment if they had greater diversity in their gut bacteria, according to new research presented at the National Cancer Research Institute's (NCRI) Cancer Conference in Liverpool. Scientists at the University of Texas MD Anderson Cancer Centre studied over 200 mouth and over 100 gut microbiome samples from people who had advanced melanoma. They discovered that people whose cancer responded to immunotherapy treatment had more diversity in the types of bacteria found in their gut. They also found significant differences in the type of bacteria found in the gut of people whose cancer responded versus those who didn't. There was no difference in the type of mouth bacteria between patients. Early studies in mice have shown that changing the type of bacteria that live in the gut can improve the response to immunotherapy, but this is one of the first studies to look at the link in patients. Immunotherapy, which harness the body's immune system to target cancer cells, are an exciting avenue of cancer treatment. However, not all patients respond to these treatments, and researchers are trying to understand why. This research suggests that adapting people's gut bacteria, such as giving antibiotics, probiotics, or a faecal transplant before immunotherapy, could increase the benefits already achieved with new immunotherapy drugs now being used to treat several different types of cancer. However, this needs to be tested clinical trials. Melanoma is the fifth most common cancer in the UK with about 14,600 people being diagnosed each year. And each year about 2,300 die from the disease. Dr Jennifer Wargo, lead researcher at the University of Texas, said: "Our research shows a really interesting link that may mean the immune system is aided by gut bacteria when responding to these drugs. Not all patients respond to immunotherapy drugs and it's hard to know who will benefit from the treatment prior to it being given. "The gut microbiome can be changed through a number of different strategies, so there is real potential here to modify the gut microbiome to boost an immunotherapy response." Dr Pippa Corrie, Chair of the NCRI's Skin Cancer Clinical Studies Group, said: "There is growing evidence that gut bacteria play a vital role in warding off disease, absorbing nutrients from the food we eat, and maintaining normal function of our immune systems. "Gut microbes have been shown to influence the role of conventional chemotherapy, so it's probably not surprising that they impact on response to new immunotherapies being used in the clinic. Manipulating the gut flora may be a new strategy to enhance activity of immunotherapy drugs, as well as to manage problematic toxicity in the future."


News Article | November 10, 2016
Site: www.sciencedaily.com

Researchers have discovered that a marker found on aggressive prostate cancer cells could also be used as a way to guide treatments to the cancer, according to new research presented at the National Cancer Research Institute (NCRI) Cancer Conference in Liverpool. The molecule, called NAALADL2, is already measured to see if prostate cancer is likely to return, but the new study has shown that it can also help direct treatment to the cancer. The team, based at UCL, had already found that prostate cancer cells have more of the NAALADL2 molecule on their surface compared to cells from healthy tissue. Prostate cancer patients whose tumour cells have high levels of this molecule are more than twice as likely to see their disease return following surgery. In the new study, the researchers attached the drug saporin to an antibody targeted against NAALADL2 to destroy prostate cancer cells in the lab. Dr Hayley Luxton, lead researcher from the Molecular Diagnostics and Therapeutics Laboratory at University College London, said: "Using antibodies mounted with a toxic payload, we can exploit the fact that aggressive prostate cancer cells have more NAALADL2. "The next step is to further develop this for use in patients, which we hope can be done in a relatively short timeframe." Around 46,500 men are diagnosed with prostate cancer in the UK each year. And around 11,000 men will die from the disease each year. The study was funded by The Urology Foundation, John Black Charitable Trust and Cancer Research UK. Louise de Winter, CEO of The Urology Foundation, said: "This research was attractive to us as something that could potentially distinguish those so-called 'pussy cat' cancers from the 'tigers'. We're very excited by the potential shown and look forward to further findings." Dr Chris Parker, Chair of the NCRI's Prostate Cancer Clinical Studies Group, said: "When it comes to aggressiveness, prostate cancer can either be slow-growing or much faster to grow and spread. And there is an urgent need to find better treatments for the more aggressive version of the disease. "Interestingly, this study shows that the very marker that indicates a prostate tumour may be more aggressive, could also be the key to its downfall." See more at: http://abstracts.ncri.org.uk/abstract/can-we-use-n-acetyl-l-aspartyl-l-glutamate-peptidase-like-2-to-target-drugs-to-cancer-cells-2/


News Article | November 9, 2016
Site: www.biosciencetechnology.com

Researchers have discovered that a marker found on aggressive prostate cancer cells could also be used as a way to guide treatments to the cancer, according to new research presented at the National Cancer Research Institute (NCRI) Cancer Conference in Liverpool. The molecule, called NAALADL2, is already measured to see if prostate cancer is likely to return, but the new study has shown that it can also help direct treatment to the cancer. The team, based at UCL, had already found that prostate cancer cells have more of the NAALADL2 molecule on their surface compared to cells from healthy tissue. Prostate cancer patients whose tumour cells have high levels of this molecule are more than twice as likely to see their disease return following surgery. In the new study, the researchers attached the drug saporin to an antibody targeted against NAALADL2 to destroy prostate cancer cells in the lab. Dr. Hayley Luxton, lead researcher from the Molecular Diagnostics and Therapeutics Laboratory at University College London, said: "Using antibodies mounted with a toxic payload, we can exploit the fact that aggressive prostate cancer cells have more NAALADL2. "The next step is to further develop this for use in patients, which we hope can be done in a relatively short timeframe." Around 46,500 men are diagnosed with prostate cancer in the UK each year. And around 11,000 men will die from the disease each year. The study was funded by The Urology Foundation, John Black Charitable Trust and Cancer Research UK. Louise de Winter, CEO of The Urology Foundation, said: "This research was attractive to us as something that could potentially distinguish those so-called 'pussy cat' cancers from the 'tigers'. We're very excited by the potential shown and look forward to further findings." Dr. Chris Parker, Chair of the NCRI's Prostate Cancer Clinical Studies Group, said: "When it comes to aggressiveness, prostate cancer can either be slow-growing or much faster to grow and spread. And there is an urgent need to find better treatments for the more aggressive version of the disease. "Interestingly, this study shows that the very marker that indicates a prostate tumour may be more aggressive, could also be the key to its downfall."

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