Cancer Tips and Solutions!!!: July 2017

Wednesday, 26 July 2017

Immune cells the missing ingredient in new bladder cancer treatment

Source: University of British Columbia
Summary:: New research offers a possible explanation for why a new type of cancer treatment hasn't been working as expected against bladder cancer.

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New research offers a possible explanation for why a new type of cancer treatment hasn't been working as expected against bladder cancer.

The study finds that checkpoint immunotherapy, which is designed to activate the immune system, is not effective on some bladder cancers because there are no immune cells in the tumours. The finding explains what is happening at a cellular level to prevent the immune cells from getting into the tumour and points scientists in the right direction towards developing a combination therapy that could work.
"It's been a mystery for decades as to how tumours escape the immune system," said Mads Daugaard, an assistant professor of urologic science at UBC and a senior scientist at the Vancouver Prostate Centre and Vancouver Coastal Health Research Institute (VCHRI). "We've identified a cellular signaling pathway that regulates whether the body's immune cells are allowed to infiltrate the tumour."
Bladder cancer is the fifth most common cancer in Canada. There is only one line of chemotherapy available, cisplatin-based therapy, for invasive tumours. Once cancers become resistant, only checkpoint immunotherapy is approved as second-line treatment.
Atezolizumab is a checkpoint immunotherapy drug that strengthens the body's immune response and recently became the first new bladder cancer drug to be approved in more than twenty years. Initial results were very promising but subsequent clinical trials have shown that only one in five patients showed an objective response to treatment. The reason for that has puzzled researchers, until now.
In this study, Daugaard and his colleagues, Dr. Peter Black, an associate professor in urologic sciences at UBC and a senior scientist at the Vancouver Prostate Centre and VCHRI, and a team of scientists from H3 Biomedicine headed by Ping Zhu, found that some invasive bladder cancer tumours block the immune cells from accessing it by activating a cell signaling pathway called the peroxisome proliferator-activated receptor gamma (PPAR-γ) pathway.
"With this pathway, the tumours close the door to the immune system," said Daugaard. "Without immune cells in the tumour, checkpoint immunotherapy has little effect. Now we know what door the tumours are closing and we can therefore focus our efforts on breaking down that door and let the immune system back in."
Daugaard and his team have taken the first steps to develop a drug able to target the PPAR-γ pathway. The rationale is to use such a drug in combination with checkpoint immunotherapy treatment.
"The most efficient way to combat a cancer would be to have the immune system take care of it itself. This is ultimately what we want to achieve," he said.

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Weight in adolescence may affect colorectal cancer risk

Source: Wiley
Summary:: A new study has uncovered a link between being overweight or obese in adolescence and an increased risk of developing colon cancer in adulthood. Obesity was also associated with an elevated risk of developing rectal cancer.

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A new study has uncovered a link between being overweight or obese in adolescence and an increased risk of developing colon cancer in adulthood. Obesity was also associated with an elevated risk of developing rectal cancer. Published early online in CANCER, a peer-reviewed journal of the American Cancer Society, the findings come at a time of growing concern about the impact of adolescent overweight and obesity on chronic disease later in life.

Study results on a potential link between adolescent obesity and the risk of colorectal cancer are conflicting, and many of the studies' designs have been limited. To provide more clarity, Zohar Levi, MD, of the Rabin Medical Center and the Tel Aviv University in Israel, and his colleagues analyzed information on 1,087,358 Jewish males and 707,212 Jewish females who underwent health examinations, including measures of body mass index (BMI), at age 16 to 19 years (predominantly aged 17 years) between 1967 and 2002. Individuals were followed to 2012.
Over a median follow-up of 23 years, 2967 new cases of colorectal cancer were identified, including 1977 among men (1403 colon, 574 rectum) and 990 among women (764 colon, 226 rectum). Overweight and obesity were associated with 53% and 54% higher risks of colon cancer for men and women, respectively. Obesity was associated with a 71% increased risk of rectal cancer in men and more than a twofold increased risk in women.
"This is a huge cohort with a minimum follow up of 10 years, and all individuals had measured BMI, not just reported or recalled," said Prof. Levi. "This is the largest study ever, including both men and women, and it had the power to prove the importance of BMI at age 17 on events later in life."
The main limitation of the study is that the cohort was still young, with the median age at colorectal cancer diagnosis of 49.4 years. The study also lacked data on diet, physical activity, and smoking, which might affect risk estimates. Family history of colorectal cancer was also unknown.

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Saturday, 15 July 2017

How statins could be more effective in treatment of ovarian cancer

Source: Keele University
Summary:: Statins may be used as a potentially effective treatment against ovarian cancer, suggests evidence from a new study.

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A new study led by Keele University has shown how statins may be used as a potentially effective treatment against ovarian cancer.

Previous laboratory studies have largely been positive and shown statins to be active against cancer cells but, in contrast, when statins have been tested in real human patients with cancer, they have largely been ineffective. Published this week in Scientific Reports, the new research provides an explanation for this paradox and recommends the improved design for a new clinical trial.
              Dr Alan Richardson, who led the research at Keele and co-authored the paper, explained, "We believe we have found the answer to the paradox: for statins to be effective as a cancer therapy, the right statin needs to be used, it needs to be delivered at the right dose and interval, and diet needs to be controlled to reduce sources of geranylgeraniol, which can limit the statin's effect on cancer cells."
The researchers at Keele University identified that a particular statin called pitavastatin is uniquely suited to target ovarian cancer cells because it combines a suitably long metabolic half-life (allowing it to continually inhibit tumour growth) with a structure which makes it a potent inhibitor of tumour growth in mice. However, it was also found that diet can limit the effectiveness of pitavastatin. Retrospective clinical studies of human patients taking statins to reduce cholesterol have also shown some reduced risk of dying of cancer.
             Dr Richardson, whose work focuses on ovarian cancer, is the Therapeutics theme lead in the Institute of Science and Technology in Medicine and a Reader in Pharmacology in the School of Pharmacy at Keele University. He is also the author of the "Why do scientists do what scientists do?" website (http://whydoscientists.org/) which provides a lay explanation of how scientists design and interpret experiments. He explained, "Our research found that the tumour-inhibiting effects of pitavastatin in mice were limited when dietary geranylgeraniol was present. Statins work in cancer by preventing cancer cells making geranylgeraniol. However, geranylgeraniol is present in various foods including sunflower oil and some rice, so in future clinical trials, we need to carefully control diet to limit geranylgeraniol."
The next stage of research will be to conduct full clinical trials in humans -- something that Dr Richardson and his team are already planning.
             Dr Richardson commented, "The key message of our work is that clinical trials of pitavastatin can now be properly designed, and we are in the very early stages of developing trials with our colleagues at Keele University and Birmingham University. It is also noteworthy that pitavastatin is available in a generic form, potentially making this a relatively inexpensive treatment."

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Genetically enhanced, cord-blood derived immune cells strike B-cell cancers

Engineered to hit CD19, boosted to persist, natural killer cells now in first-in-human clinical trial

Source: University of Texas M. D. Anderson Cancer Center
Summary:: Immune cells with a general knack for recognizing and killing many types of infected or abnormal cells also can be engineered to hunt down cells with specific targets on them to treat cancer, researchers report.

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Immune cells with a general knack for recognizing and killing many types of infected or abnormal cells also can be engineered to hunt down cells with specific targets on them to treat cancer, researchers at The University of Texas MD Anderson Cancer Center report in the journal Leukemia.

The team's preclinical research shows that natural killer cells derived from donated umbilical cords can be modified to seek and destroy some types of leukemia and lymphoma. Genetic engineering also boosts their persistence and embeds a suicide gene that allows the modified cells to be shut down if they cause a severe inflammatory response.
               A first-in-human phase I/II clinical trial of these cord-blood-derived, chimeric antigen receptor-equipped natural killer cells opened at MD Anderson in June for patients with relapsed or resistant chronic lymphocytic leukemia (CLL), acute lymphocytic leukemia (ALL), or non-Hodgkin lymphoma. All are cancers of the B cells, another white blood cell involved in immune response.
"Natural killer cells are the immune system's most potent killers, but they are short-lived and cancers manage to evade a patient's own NK cells to progress," said Katy Rezvani, M.D., Ph.D., professor of Stem Cell Transplantation and Cellular Therapy.
"Our cord-blood derived NK cells, genetically equipped with a receptor that focuses them on B-cell malignancies and with interleukin-15 to help them persist longer -- potentially for months instead of two or three weeks are designed to address these challenges," Rezvani said.
                                                                                                                                                                  Moon Shots Program funds project
             The clinical trial is funded by MD Anderson's Moon Shots Program™, designed to more rapidly develop life-saving advances based on scientific discoveries.
The chimeric antigen receptor (CAR), so-called because it's added to the cells, targets CD19, a surface protein found on B cells.
In cell lines and mouse models of lymphoma and CLL, CD19-targeted NK cells killed cancer cells and extended survival of animals compared to simply giving NK cells alone. Addition of IL-15 to the CD19 receptor was crucial for the longer persistence and enhanced activity of the NK cells against tumor cells.
NK cells are a different breed of killer from their more famous immune system cousins, the T cells. Both are white blood cells, but T cells are highly specialized hunters that look for invaders or abnormal cells that bear a specific antigen target, kill them and then remember the antigen target forever.
Natural killers have an array of inhibitory and activating receptors that work together to allow them to detect a wider variety of infected, stressed or abnormal cells.
          "By adding the CD19 CAR, we're also turning them into guided missiles," said Elizabeth Shpall, M.D., professor of Stem Cell Transplantation and Cell Therapy.
Using a viral vector, the researchers transduce NK cells taken from cord blood with the CD19 CAR, the IL-15 gene, and an inducible caspase-9-based suicide gene.
Cell line tests found the engineered NK cells to be more efficient killers of lymphoma and CLL cells, compared to unmodified NK cells, indicating the engineered cells' killing was not related to non-specific natural killer cell cytotoxicity.
           Another experiment showed the engineered cord blood NK cells killed CLL cells much more efficiently than NK cells taken from CLL patients and engineered, highlighting the need to transplant CAR-engineered NK cells from healthy cord blood rather than use a patient's own cells.
Suicide gene to counter cytokine release syndrome
Mouse model lymphoma experiments using a single infusion of low dose NK cells resulted in prolongation of survival. At a higher, double dose, none of the mice treated with the CD19/IL-15 NK cells died of lymphoma, with half surviving for 100 days and beyond. All mice treated with other types of NK cells died by day 41.
            A proportion of mice treated with the higher dose of engineered NK cells died of cytokine release syndrome, a severe inflammatory response that also occurs in people treated with CAR T cells.
To counteract this toxicity, the researchers incorporated a suicide gene (iC9) that can be activated to kill the NK cells by treatment with a small-molecule dimerizer. This combination worked to swiftly reduce the engineered NK cells in the mouse model.
Subsequent safety experiments were conducted in preparation for the clinical trial. Rezvani, the principal investigator of the clinical trial, says the protocol calls for vigilance for signs of cytokine release syndrome, treatment with steroids and tocilizumab for low-grade CRS with AP1903 added to activate the suicide gene for grade 3 or 4 CRS.
                                                                                                                                                               NK CARs available off the shelf
             T cells modified with chimeric antigen receptors against CD19 have shown efficacy in clinical trials. In these therapies, a patient's own T cells are modified, expanded, and given back to the patient, a process that takes weeks. Finding a matched donor for T cells would be a challenge, but would be necessary because unmatched T cells could attack the recipient's normal tissue -- graft vs. host disease.
Rezvani and Shpall have given patients cord-blood derived NK cells in a variety of clinical trials and found that they do not cause graft vs. host disease, therefore don't have to be matched. NK cells can be an off-the-shelf product, prepared in advance with the necessary receptor and given promptly to patients.
"CAR NK cells are scalable in a way that CAR T cells are not," Rezvani noted.
A strength of T cells is the development of memory cells that persist and repeatedly attack cells bearing the specific antigen that return. NK cells do not seem to have a memory function, but Rezvani says the experience of the longer-lived mice, which are now more than a year old, raises the possibility that a prolonged NK cell attack will suffice.
              Shpall, Rezvani and colleagues are developing cord blood NK CARs for other targets in a variety of blood cancers and solid tumors.
MD Anderson and the researchers have intellectual property related to the engineered NK cells, which is being managed in accordance with the institution's conflict-of-interest rules.
Shpall founded and directs MD Anderson's Cord Blood Bank, originally established to provide umbilical cord blood stem cells for patients who need them but cannot get a precise donor match. Donated by mothers who deliver babies at seven Houston hospitals and two others from California and Michigan, the bank now has 26,000 cords stored. MD Anderson researchers pioneered the extraction and expansion of NK cells from umbilical cords.

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Tumor-targeting drug shows potential for treating bone cancer patients

Preclinical study shows BMTP-11 targets high-risk osteosarcoma

Source: University of Texas M. D. Anderson Cancer Center
Summary:: The treatment of osteosarcoma, the most common tumor of bone, is challenging. A new study found a drug known as bone metastasis-targeting peptidomimetic (BMTP-11) has potential as a new therapeutic strategy for this devastating illness.

FULL STORY

The treatment of osteosarcoma, the most common tumor of bone, is challenging. A study led by The University of Texas MD Anderson Cancer Center found a drug known as bone metastasis-targeting peptidomimetic (BMTP-11) has potential as a new therapeutic strategy for this devastating illness.

Results from the preclinical study, which looked at BMTP-11 alone and in combination with the chemotherapy agent gemcitabine, were published in the July 11, 2017, online issue of Proceedings of the National Academy of Sciences.
             Although osteosarcoma is a relatively rare cancer, it is a leading disease-related cause of death in children and young adults ages 10 to 20. However, over the last 25 years, the five-year survival rate has remained unchanged, and the treatment options for these patients are few. In addition, the side effects of available treatment options often are significant and cumulative, and may cause other health problems and damage to major organs.
              "What's novel about this treatment is that BMTP -11 targets the tumor and spares other organs," said Valerae O. Lewis, M.D., chair of Orthopaedic Oncology at MD Anderson. "We believe this study lays the groundwork for a clinical trial for the treatment of osteosarcoma without the cumulative and mortal side effects seen with the current treatment options."
             The study results identified IL-11Rα as an osteosarcoma cell surface receptor that correlated with tumor progression and poor prognosis in osteosarcoma patients. The team, which included co-authors Renata Pasqualini, Ph.D., and Wadih Arap, M.D., Ph.D., both of whom worked on the study while at MD Anderson and are now professors at the University of New Mexico Health Sciences Center (UNMSC) School of Medicine, also illustrated that IL-11Rα and IL-11 are up-regulated in human metastatic osteosarcoma cell lines, and this correlated with the development of lung metastases in mouse models of the disease. The metastatic potential of the osteosarcoma cell lines could be modulated by targeting IL-11Rα expression. Death from respiratory failure linked to metastasis to the lungs remains a significant problem among osteosarcoma patients.
              "We were able to document anti-tumor activity against osteosarcoma models," said Pasqualini. "Given that a first-in-human trial of BMTP-11 has recently been reported, one would hope that this proof-of-concept study might lead to early translational clinical trials in human osteosarcoma as a logical next step in the context of an unmet medical oncology need."
Arap added that "this work provides a preclinical foundation for the potential design and development of a second line combination therapy regimen composed of conventional chemotherapeutics plus the targeted candidate drug BMTP-11 for application in unfortunate patients with recalcitrant osteosarcoma."

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Blood test for early detection of pancreatic cancer headed to clinic

Source: Perelman School of Medicine at the University of Pennsylvania
Summary:: A newly identified biomarker panel could pave the way to earlier detection and better treatment for pancreatic cancer. Currently over 53,000 people in the United States are diagnosed with pancreatic cancer the fourth leading cause of cancer death every year. The blood biomarkers correctly detected pancreatic cancer in blood samples from patients at different stages of their disease.

FULL STORY

A pancreatic ductal adenocarcinoma.

Credit: The lab of Ken Zaret, Perelman School of Medicine, University of Pennsylvania

A newly identified biomarker panel could pave the way to earlier detection and better treatment for pancreatic cancer, according to new research from the Perelman School of Medicine at University of Pennsylvania. Currently over 53,000 people in the United States are diagnosed with pancreatic cancer the fourth leading cause of cancer death every year. The blood biomarkers, detailed today in Science Translational Medicine, correctly detected pancreatic cancer in blood samples from patients at different stages of their disease.

          The majority of pancreatic cancer patients are not diagnosed until an advanced stage, beyond the point at which their tumors can be surgically removed.
A team led by Ken Zaret, PhD, director of the Penn Institute for Regenerative Medicine and the Joseph Leidy Professor of Cell and Developmental Biology, and Gloria Petersen, PhD, from the Mayo Clinic, identified a pair of biomarkers that physicians could soon use to discover the disease earlier.
"Starting with our cell model that mimics human pancreatic cancer progression, we identified released proteins, then tested and validated a subset of these proteins as potential plasma biomarkers of this cancer," Zaret said. The authors anticipate that health care providers will use the early-detection biomarkers to test for their presence and levels in blood from pancreatic cancer patients and blood drawn from individuals with a high risk of developing pancreatic cancer, including those who have a first-degree relative with pancreatic cancer, are genetically predisposed to the disease, or who had a sudden onset of diabetes after the age of 50.
            "Early detection of cancer has had a critical influence on lessening the impact of many types of cancer, including breast, colon, and cervical cancer. A long standing concern has been that patients with pancreatic cancer are often not diagnosed until it is too late for the best chance at effective treatment," said Robert Vonderheide, MD, DPhil, director of the Abramson Cancer Center (ACC) at the University of Pennsylvania. "Having a biomarker test for this disease could dramatically alter the outlook for these patients."
              The biomarker panel, enabled by discovery work of first author Jungsun Kim, PhD, a postdoctoral fellow in Zaret's lab, builds on a first-of-its-kind human-cell model of pancreatic cancer progression the lab described in 2013. They used stem-cell technology to create a cell line from a patient with advanced pancreatic ductal adenocarcinoma. Genetically reprogramming late-stage human cancer cells to a stem-cell state enabled them to force the reprogrammed cells to progress to an early cancerous state, revealing secreted blood biomarkers of early-stage disease along the way.
              The best candidate biomarker, plasma thrombospondin-2 (THBS2), was screened against 746 cancer and control plasma samples using an inexpensive, commercially available protein-detection assay. The team found that blood levels of THBS2, combined with levels of a known later-stage biomarker called CA19-9, was reliable at detecting the presence of pancreatic cancer in patients.
The team refined the assay with independent investigations of plasma samples from patients with different stages of cancer, from individuals with benign pancreatic disease, and from healthy controls, all obtained from Petersen, who directs the biospecimen resource program for pancreas research at the Mayo Clinic.
             "Positive results for THBS2 or CA19-9 concentrations in the blood consistently and correctly identified all stages of the cancer," Zaret said. "Notably, THBS2 concentrations combined with CA19-9 identified early stages better than any other known method." The combination panel also improved the ability to distinguish cases of cancer from pancreatitis. The panel will next be validated in a set of samples from pancreatic cancer patients who provided a research blood sample prior to their diagnosis.

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Spread of breast cancer reduced by targeting acid metabolite

Source: Medical College of Georgia at Augusta University
Summary:: It's a metabolite found in essentially all our cells that, like so many things, cancer over expresses. Now scientists have shown that when they inhibit 20-HETE, it reduces both the size of a breast cancer tumor and its ability to spread to the lungs.

FULL STORY

(From left are) Drs. B.R. Achyut; Thaiz F. Borin, postdoctoral fellow and a corresponding author; and Ali S. Arbab.

Credit: Phil Jones

It's a metabolite found in essentially all our cells that, like so many things, cancer over expresses. Now scientists have shown that when they inhibit 20-HETE, it reduces both the size of a breast cancer tumor and its ability to spread to the lungs.

"The drug is reducing the ability of cancer cells to create a distant micro-environment where they can thrive," said Dr. Ali S. Arbab, leader of the Tumor Angiogenesis Initiative at the Georgia Cancer Center and a professor in the Department of Biochemistry and Molecular Biology at the Medical College of Georgia at Augusta University.
           Arbab notes that cancer cells are constantly doing test runs, sending cells out into the bloodstream to see if they will take hold. About 30 percent of patients with breast cancer experience spread, or metastasis, of the disease. The most common sites are the lymph nodes, liver, bones and brain, as well as the lungs.
For the preclinical studies by postdoctoral fellow, Dr. Thaiz F. Borin, published in the journal PLOS ONE, the scientists used the drug HET0016, a 20-HETE inhibitor developed to learn more about the metabolite's many functions.
           While not ready to say that the drug has potential use in humans, Arbab says the work points toward a new and logical target for reducing tumor spread. He notes that there are already drugs out there, including some over-the-counter anti-inflammatory drugs, which may also inhibit this overexpressed and now destructive pathway.
20-HETE 20-Hydroxyeicosatetraenoic acid is a metabolite of arachidonic acid, a fatty acid we make and constantly use for a wide variety of functions like helping make lipids for our cell membranes. 20-HETE also has a wide range of normal functions, including helping regulate blood pressure and blood flow. It's also a known mediator of inflammation, which under healthy conditions can help us fight infection and protect us from cancer and other invaders.
"There is normal function and there is tumor-associated function," says Dr. B.R. Achyut, cancer biologist, assistant professor in the MCG Department of Biochemistry and Molecular Biology and a study coauthor. "Tumors highjack our system and use that molecule against us."
            In fact, Arbab's research team has shown that the high production of 20-HETE that occurs in cancer becomes an unwitting provider of almost everything cancer needs to prepare a place to comfortably spread.
Scientists call it the "seed and soil" hypothesis. To spread, cancer cells must detach from the primary site, in this case breast tissue, get aggressive enough to survive travel, gather supporting tissue and blood vessels where they land, take seed and eventually colonize the distant site, in this case, the lungs.
Arbab and his team have shown 20-HETE appears to help prepare this distant site by activating things like protein kinases that can change the function of proteins, their location and what cells they associate with, as well as growth factors that can make cells grow in size, proliferate and differentiate. It can even help make blood vessels, which a tumor will need once it reaches a certain size. 20-HETE also activates signaling kinases that enable cell division. It encourages inflammation-promoting factors like tumor necrosis factor alpha and several of the interleukins, another class of proteins that help regulate the immune response. In this scenario, they are turning up inflammation, which is a hallmark of cancer and other diseases.
"We are going after that tumor microenvironment," says Arbab.
              For their studies, they put human breast cancer cells and mouse mammary tumor cells in the mammary fat pad of mice, waited for the cancer to take hold and begin to spread, then intravenously gave mice HET0016 five days per week for three weeks.
They found HET0016 reduced the migration and invasion of tumor cells: 48 hours after the drug was given, cancer cells were less able to move about in small test tubes. The drug also reduced levels of metalloproteinases in the lungs, enzymes that can destroy existing protein structures, so that, in this case, cancer cells can penetrate the area and new blood vessels can grow. It also reduced levels of other key inhabitants of a tumor microenvironment like growth factors as well as myeloid-derived suppressor cells that can help shield cancer from the immune system. "It gets rid of one of the natural protections tumors use, and tumor growth in the lung goes down," Arbab notes.
             He, Achyut and their colleague Dr. Meenu Jain, assistant research scientist, reported earlier this year in the journal Scientific Reports that the drug also reduced tumor growth and prolonged survival in an animal model of the highly lethal, rapidly growing and vascular brain tumor, glioblastoma. That finding and related work got the scientists wondering if the research drug -- or something similar -- could one day help control the typically deadly spread of cancer.
Now they are looking at exosomes, traveling packages all cells send out as a way to communicate and swap substances. In the case of cancer cells, exosomes appear to be packed with items needed to build the supportive environment for their new distant location in the lungs or elsewhere. Once exosomes establish a niche, they send back a signal to the primary site for cancer cells to join them. The scientists want to further pursue the ability of HET0016 to block these cancer-derived packages.
20-HETE's co-opting by cancer has it emerging as a focal point for cancer treatment, says Arbab who has published more than half of the 20-HETE-related studies on the rapidly emerging topic.

Hormone replacement therapies help breast cancer grow, spread

Hormone replacement therapies could cause specialized cancer cells to induce growth, metastasis

Source: University of Missouri-Columbia
Summary:: Women who take hormone replacement therapies have a higher incidence of breast cancer, research shows. Now, researchers have linked natural and synthetic progestins to the body's production of specialized cancer cells that act like stem cells in humans. Findings could help scientists target these rare cells that proliferate in breast cancers and metastasize elsewhere, and may help clinicians identify immunotherapies to combat the spread of the disease.

FULL STORY

Hormone replacement therapies, or medications containing female hormones, may help cancer to spread.

Credit: © Ivelin Radkov / Fotolia

Hormone replacement therapies, or medications containing female hormones that substitute those no longer produced by the body, often are prescribed to reduce the effects of menopausal symptoms in women. Research has indicated that women who take hormone replacement therapies have a higher incidence of breast cancer. Now, researchers at the University of Missouri have linked natural and synthetic progestins to the body's production of specialized cancer cells that act like stem cells in humans. Findings could help scientists target these rare cells that proliferate in breast cancers and metastasize elsewhere, and may help clinicians identify immunotherapies to combat the spread of the disease.

             "In previous studies, we have shown that both natural and synthetic progestins accelerate the development of breast cancer and increase their metastasis to lymph nodes," said Salman Hyder, the Zalk Endowed Professor in Tumor Angiogenesis and professor of biomedical sciences in the College of Veterinary Medicine and the Dalton Cardiovascular Research Center. "Our laboratory is committed to identifying the cell mechanisms that bring about increased breast cancer risks. Recently, our research focused on special cells which are called 'cancer stem cell-like cells' -- that induce aggressive tumor growth, metastasis and cancer recurrence."
             In a series of tests, the team used hormone-responsive human breast cancer cells to examine the effects of progestin on the cell markers typically found in breast cancers. Both natural and synthetic progestins significantly increased protein expression of CD44, a molecule involved in cell proliferation, cell communication and migration. Additionally, the presence of progestins caused these components to behave like cancer stem cell-like cells.
            These rare cells are a small population of cells that -- acting like normal stem cells are self-renewing, create identical copies of themselves and proliferate exponentially. Further testing showed that the rare subset of cancer cells actually were enriched by progestin.
"The findings show that exposure to natural and synthetic progestins leads to the development of these cancer stem-cell like cells," Hyder said. "These cells greatly increase the likelihood of resistance to therapies and the risk for metastasis. Our findings also suggest that clinicians may be able to combat the progestin-dependent tumor growth through immunotherapy."

Wednesday, 12 July 2017

Experimental 'enhancer' drug may boost conventional therapies for deadly pediatric brain cancers

Test tube and mouse studies show TAK228 enhances the tumor-killing effects of radiation and chemotherapy

Source:: Johns Hopkins Medicine
Summary:: Laboratory studies suggest that an experimental drug already in early clinical trials for a variety of adult cancers might enhance radiation and chemotherapy for two childhood brain cancers that currently are virtually always fatal.

FULL STORY

Laboratory studies suggest that an experimental drug already in early clinical trials for a variety of adult cancers might enhance radiation and chemotherapy for two childhood brain cancers that currently are virtually always fatal.

In a report on two studies conducted by Johns Hopkins Kimmel Cancer Center researchers, the drug, known as TAK228, suppressed the growth of human cancer cells cultured in the laboratory and significantly extended the lives of mice implanted with cells from the two cancers, diffuse intrinsic pontine glioma (DIPG) and atypical teratoid/rhabdoid tumors (AT/RTs).
DIPG a cancer in the brainstem affecting about 3,000 children worldwide each year -- is universally fatal even with currently available treatments including surgery, chemotherapy and radiation. AT/RTs, the most common brain cancer in infants, have a similarly poor prognosis, with most patients surviving between six and 11 months after diagnosis.
             Hoping to help beat these odds, Johns Hopkins researchers and their colleagues, led by Eric H. Raabe, M.D., Ph.D., assistant professor of oncology and instructor of pathology at the Johns Hopkins Kimmel Cancer Center, focused their attention on TAK228. Previous research showed the drug (also known as MLN0128) can cross the blood-brain barrier and reduces the production of a protein called mTOR, which appears to sustain cancer by combining with other proteins to signal the cells to grow, invade tissues and survive therapy. Both pediatric cancer types typically have genetic alterations that lead to increases in mTOR activity, thus Raabe and his team's hypothesis that TAK228 could be an effective treatment for these cancers.
            In one set of experiments, Raabe and his colleagues applied the drug to cells of each cancer type isolated from human patients. Results showed that TAK228 reduced proliferation of DIPG cells cancer cells by about 30 percent compared with control (untreated) cells and killed about 6 percent of the cells.
However, when combined with radiation -- currently the most effective treatment for extending life in children with DIPG nearly double the number of cells were killed compared with radiation alone, suggesting that TAK228 might sensitize cells to make radiation more effective, Raabe says.
When the team tested TAK228 on AT/RT cells, they found similar reductions in tumor cell proliferation and increases in cancer cell death. Further, when they gave a combination of TAK228 and cisplatin, a chemotherapy commonly used to treat AT/RTs, to mice bearing implanted human AT/RT tumors, the mice receiving the combined treatment lived approximately 30 days longer than those that received either treatment alone. Some 40 percent of the combination-treated mice were long-term survivors (living more than 60 days after tumor injection), while none of the mice treated with either chemotherapy or TAK228 alone lived longer than 25 days.
             A report of the experiments in DIPG is published online April 25 in Cancer Letters, and the AT/RT report is published June 3 in Neuro-Oncology. Together, Raabe says, these results suggest that TAK228 could hold promise for human patients.
"Both of these papers set the stage for clinical trials for TAK228," he says. "Our experiments show that TAK228 can make traditional chemotherapy and radiation more effective, which may offer hope to patients for whom current therapy doesn't work very well."
The team is currently investigating further how the drug works with radiation and chemotherapy, and if other drugs might be able to heighten this synergistic effect.

Drinking coffee could lead to a longer life, scientist says

Whether it's caffeinated or decaffeinated, coffee is associated with lower mortality, which suggests the association is not tied to caffeine

Source: University of Southern California
Summary:: Scientists have found that people who drink coffee appear to live longer. Drinking coffee was associated with lower risk of death due to heart disease, cancer, stroke, diabetes, and kidney disease. People who consumed a cup of coffee a day were 12 percent less likely to die compared to those who didn't drink coffee. This association was even stronger for those who drank two to three cups a day 18 percent reduced chance of death.

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People who drink coffee live longer, new research suggests.

Here's another reason to start the day with a cup of joe: Scientists have found that people who drink coffee appear to live longer.

             Drinking coffee was associated with a lower risk of death due to heart disease, cancer, stroke, diabetes, and respiratory and kidney disease for African-Americans, Japanese-Americans, Latinos and whites.
People who consumed a cup of coffee a day were 12 percent less likely to die compared to those who didn't drink coffee. This association was even stronger for those who drank two to three cups a day 18 percent reduced chance of death.
Lower mortality was present regardless of whether people drank regular or decaffeinated coffee, suggesting the association is not tied to caffeine, said Veronica W. Setiawan, lead author of the study and an associate professor of preventive medicine at the Keck School of Medicine of USC.
           "We cannot say drinking coffee will prolong your life, but we see an association," Setiawan said. "If you like to drink coffee, drink up! If you're not a coffee drinker, then you need to consider if you should start."
The study, which will be published in the July 11 issue of Annals of Internal Medicine, used data from the Multiethnic Cohort Study, a collaborative effort between the University of Hawaii Cancer Center and the Keck School of Medicine.
The ongoing Multiethnic Cohort Study has more than 215,000 participants and bills itself as the most ethnically diverse study examining lifestyle risk factors that may lead to cancer.
         "Until now, few data have been available on the association between coffee consumption and mortality in nonwhites in the United States and elsewhere," the study stated. "Such investigations are important because lifestyle patterns and disease risks can vary substantially across racial and ethnic backgrounds, and findings in one group may not necessarily apply to others."
Since the association was seen in four different ethnicities, Setiawan said it is safe to say the results apply to other groups.
"This study is the largest of its kind and includes minorities who have very different lifestyles," Setiawan said. "Seeing a similar pattern across different populations gives stronger biological backing to the argument that coffee is good for you whether you are white, African-American, Latino or Asian."
                                                                                                                                                                Benefits of drinking coffee
            Previous research by USC and others have indicated that drinking coffee is associated with reduced risk of several types of cancer, diabetes, liver disease, Parkinson's disease, Type 2 diabetes and other chronic diseases.
Setiawan, who drinks one to two cups of coffee daily, said any positive effects from drinking coffee are far-reaching because of the number of people who enjoy or rely on the beverage every day.
"Coffee contains a lot of antioxidants and phenolic compounds that play an important role in cancer prevention," Setiawan said. "Although this study does not show causation or point to what chemicals in coffee may have this 'elixir effect,' it is clear that coffee can be incorporated into a healthy diet and lifestyle."
About 62 percent of Americans drink coffee daily, a 5 percent increase from 2016 numbers, reported the National Coffee Association.
         As a research institution, USC has scientists from across disciplines working to find a cure for cancer and better ways for people to manage the disease.
The Keck School of Medicine and USC Norris Comprehensive Cancer Center manage a state-mandated database called the Los Angeles Cancer Surveillance Program, which provides scientists with essential statistics on cancer for a diverse population.
Researchers from the USC Norris Comprehensive Cancer Center have found that drinking coffee lowers the risk of colorectal cancer.
But drinking piping hot coffee or beverages probably causes cancer in the esophagus, according to a World Health Organization panel of scientists that included Mariana Stern from the Keck School of Medicine.
                                                                                                                                                              Hearing from the WHO
             In some respects, coffee is regaining its honor for wellness benefits. After 25 years of labeling coffee a carcinogen linked to bladder cancer, the World Health Organization last year announced that drinking coffee reduces the risk for liver and uterine cancer.
"Some people worry drinking coffee can be bad for you because it might increase the risk of heart disease, stunt growth or lead to stomach ulcers and heartburn," Setiawan said. "But research on coffee have mostly shown no harm to people's health."
                                                                                                                                                            Coffee by the numbers
             Setiawan and her colleagues examined the data of 185,855 African-Americans (17 percent), Native Hawaiians (7 percent), Japanese-Americans (29 percent), Latinos (22 percent) and whites (25 percent) ages 45 to 75 at recruitment. Participants answered questionnaires about diet, lifestyle, and family and personal medical history.
They reported their coffee drinking habits when they entered the study and updated them about every five years, checking one of nine boxes that ranged from "never or hardly ever" to "4 or more cups daily." They also reported whether they drank caffeinated or decaffeinated coffee. The average follow-up period was 16 years.
              Sixteen percent of participants reported that they did not drink coffee, 31 percent drank one cup per day, 25 percent drank two to three cups per day and 7 percent drank four or more cups per day. The remaining 21 percent had irregular coffee consumption habits.
Over the course of the study, 58,397 participants about 31 percent died. Cardiovascular disease (36 percent) and cancer (31 percent) were the leading killers.
The data was adjusted for age, sex, ethnicity, smoking habits, education, preexisting disease, vigorous physical exercise and alcohol consumption.
Setiawan's previous research found that coffee reduces the risk of liver cancer and chronic liver disease. She is currently examining how coffee is associated with the risk of developing specific cancers.
Researchers from the University of Hawaii Cancer Center and the National Cancer Institute contributed to this study. The study used data from the Multiethnic Cohort Study, which is supported by a $19,008,359 grant from the National Cancer Institute of the National Institutes of Health.

Chronic liver inflammation linked to Western diet

Food, antibiotics, and gender are just some of the factors that can throw off the balance between the gut and liver, according to a new report in The American Journal of Pathology

Source: Elsevier
Summary:: A new study reports that mice fed a Western diet, which is high in fat and sugar, resulted in hepatic inflammation, especially in males. Moreover, liver inflammation was most pronounced in Western diet-fed male mice that also lacked farnesoid x receptor (FXR), a bile acid receptor.

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(A) Histology of control diet (CD) and Western diet (WD)-fed wild-type (WT) and FXR knockout (KO) mice of both genders. (B) Histology of antibiotic-treated male mice. Abx is a cocktail of antibiotics that provides broad-spectrum coverage. Vancomycin (Vcm) and polymyxin B (PolyB) cover Gram-positive and negative bacteria, respectively. (C) Relative abundance of cecal microbiota of CD and WD-fed WT as well as FXR KO mice of both genders. (D) Relative abundance of cecal microbiota of antibiotic-treated CD- and WD-fed FXR KO male mice. (Mean values are shown)

Credit: The American Journal of Pathology

A new study in The American Journal of Pathology reports that mice fed a Western diet, which is high in fat and sugar, resulted in hepatic inflammation, especially in males. Moreover, liver inflammation was most pronounced in Western diet-fed male mice that also lacked farnesoid x receptor (FXR), a bile acid receptor.

The study is important because it links diet to changes in the gut microbiota as well as bile acid profile, opening the possibility that probiotics and bile acid receptor agonists may be useful for the prevention and treatment of hepatic inflammation and progression into advanced liver diseases such as cancer.
"We know the transition from steatosis, or fatty liver, to steatohepatitis (inflammation in the fatty liver) plays a crucial role in liver injury and carcinogenesis. Because the liver receives 70% of its blood supply from the intestine, it is important to understand how the gut contributes to liver disease development," explained lead investigator Yu-Jui Yvonne Wan, PhD, Professor and Vice Chair of the Department of Pathology and Laboratory Medicine at UC Davis Health. "Our data show that diet, gender, and different antibiotic treatments alter the gut microbiota as well as bile acid profile and have different effects on liver inflammation."
           Dr. Wan and her team used an FXR-deficient mouse model (FXR KO), which has become an important tool to better understand the role of diet and inflammation in the development of liver diseases including cancer because patients with cirrhosis or liver cancer also have low FXR levels.
Other published data have already shown that FXR-deficient mice spontaneously develop steatohepatitis and liver tumors even when they are fed a normal rodent diet. In this study, wild-type and FXR-deficient mice were fed either a Western diet or a matching control diet for 10 months. They found similarities between Western diet intake and FXR deficiency. For instance, both Western diet-fed wild-type mice and control diet-fed FXR KO mice developed steatosis, which also was more severe in males than females. Interestingly, however, only the FXR-deficient male mice had massive lymphocyte and neutrophil infiltration in the liver, and only Western diet-fed male FXR KO mice had fatty adenomas.
"These studies show that a Western diet intake and FXR inactivation also increased hepatic inflammatory signaling, with a combined enhanced effect," Dr. Wan said. "Introducing antibiotics to reduce inflammation also had different effects based on the diets the mice received."
           Depending on what type of diet was provided, broad-spectrum antibiotics, which eliminated most gut bacteria, affected hepatic inflammation differently in FXR-deficient mice. In control diet-fed mice, a cocktail of ampicillin, neomycin, metronidazole, and vancomycin completely blocked hepatic neutrophil and lymphocyte infiltration. However, this cocktail of antibiotics (Abx) was not able to eliminate hepatic inflammation in Western diet-fed FXR KO mice. Additional analysis showed that many inflammatory genes had higher expression levels in Western diet than control diet-fed FXR KO mice after Abx treatment.
Analyzing the composition of the gut microbiota, investigators found that Proteobacteria and Bacteroidetes persisted after the broad-spectrum antibiotic treatment in the Western diet-fed FXR KO mice. In contrast, Gram-negative coverage antibiotic, i.e., polymyxin B, increased Firmicutes and decreased Proteobacteria as well as hepatic inflammation in Western diet-fed FXR KO male mice. They suggest that the adverse effects of Western diet on the liver may be explained in part by the persistence of pro-inflammatory Proteobacteria as well as the reduction of anti-inflammatory Firmicutes in the gut.
         Primary and secondary bile acids are synthesized by liver cells and gut bacteria, respectively. Bile acids are signaling molecules for lipid and sugar homeostasis as well as inflammatory response. The data generated from this group revealed that the reduced hepatic inflammation by antibiotics was accompanied by decreased free and conjugated secondary bile acids in a gender-dependent manner.
"Gut and liver health are linked. It is clear that microbial imbalance and dysregulated bile acid synthesis are inseparable, and they jointly contribute to hepatic inflammation via the gut-liver axis. In addition, gut microbiota and bile acid profiles may explain gender difference in liver disease as liver cancer incidence is much higher in men than women. Moreover, in antibiotic-treated mice, the change in the profile of bile acids can also be primary as well as secondary to the alterations in gut microbiota because antibiotics can directly eliminate bile acid-generating bacteria, which in turn causes additional changes in the bile acid composition," noted Dr. Wan. "Our results suggest that probiotics and FXR agonists hold promise for the prevention and treatment of hepatic inflammation and progression into advanced liver diseases such as cancer."

Monday, 10 July 2017

Nurse-led intervention helps carers' manage medication and cancer pain

Source: SAGE
Summary:: The potential benefits of a new nurse-led intervention in supporting carers to manage pain medication in people with terminal cancer have been revealed in a new article.

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A study funded by Marie Curie and Dimbleby Cancer Care published today shows the potential benefits of a new nurse-led intervention in supporting carers to manage pain medication in people with terminal cancer.1

Researchers from the University of Southampton, Cardiff University and University of Leeds have developed a nurse-led intervention to help carers with medication management, and evaluated its use in routine practice.
The Cancer Carers' Medicines Management (CCMM) intervention addresses carers' beliefs, knowledge and skills and promotes self-evaluation of competence. It centres on a structured conversational process between a nurse and carer.
It is the first time that a study has attempted to integrate an intervention developed using input from carers and nurses into routine palliative care.
             The research showed that the CCMM intervention compared favourably with current practice as it offered a more systematic and comprehensive approach to supporting carer management of pain medicines.
Researchers noted that nurses particularly valued the toolkit resource -- which included information about opioids and simple charts for documenting pain and medication, because they were of immediate practical value to carers.
The findings also identified some positive changes in medicines management, such as increased acceptance of the need for opiates, and behavioural changes, responding more readily to patients' request for pain relief and improved systems in place for giving and recording medicines.
Many people with advanced cancer experience persistent pain and are typically prescribed analgesics, including opioids. Carers often help patients to manage pain medicines, especially near the end of life, but often do not receive the support they need.
Professor Sue Latter, the lead researcher from the University of Southampton, said: "Despite the heavy burden placed on carers to help manage pain medication at home, there is a real lack of reliable research on effective methods of supporting carers with medicines management.
            "Medication management requires knowledge and practical skill, and involves carers in monitoring and interpreting symptoms, as well as selecting, administering and evaluating the effectiveness of medicines. Often, carers will not have trainingfor their role and will have preconceived views about pain and analgesics, particularly opioids."
Professor Jane Hopkinson from Cardiff University, and co-author, said: "Cancer Carers' Medicines Management made clinical sense to nurses, who recognised the challenges faced by carers managing analgesics at the end of life and saw potential benefits in improving education and support."
Most studies conclude that healthcare professionals need to provide carers with more information, training and continuing support.
            Dee Sissons, Director of Nursing at Marie Curie, said: "The responsibility of taking on a caring role for someone who is terminally ill can be immensely rewarding, but also daunting. Family carers play a critical role in supporting people with a terminal illness so they can be cared for and die at home when this is their wish.
This new study shows that nurses and carers can work together to better manage pain medication at home and enable carers to respond more readily to their loved ones request for pain relief with greater confidence."
The nurses who participated in the study also provided feedback on how to use the intervention more widely in palliative care nursing practice. Their suggestions included: involving patients with other terminal illnesses, including other 'end of life care' medication and introducing it earlier in the course of a patient's illness, which could increase benefits to carers.
The study results have informed further NIHR funded research on nurses supporting self-management of medicines at the end of life.

New epigenomic strategies in the clinical management of cancer of unknown primary

Source: IDIBELL-Bellvitge Biomedical Research Institute
Summary:: The invention of the EPICUP epigenetic test and its impact in the clinical management of Cancer of Unknown Primary is discussed in a new article.

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This is a microphotography of a tumor of unknown primary identified as lung cancer the EPICUP(R) test.

Credit: IDIBELL

The invention of the EPICUP® epigenetic test last year allowed physicians to elucidate what type of primary tumor had metastasized in patients with Cancer of Unknown Primary (CUP). Today, an article published in Nature Reviews Clinical Oncology by Dr. Manel Esteller, coordinator of the Epigenetics and Cancer Biology Program of the Bellvitge Biomedical Research Institute (IDIBELL), ICREA Researcher and Professor of Genetics at the University of Barcelona, explains how this test is being transferred to the clinical practice and the new advances that can develop from it.

" Traditional methods can only detect the primary tumor in 30% of cases of metastases of unknown origin. Some molecular methods could increase this percentage, but they are often expensive and use the RNA molecule (ribonucleic acid), which is very fragile and is often easily broken down in the samples available in the pathological anatomy services of hospitals," Dr. Manel Esteller explains.
"The EPICUP® test, on the other hand, is based on the DNA molecule, which is very stable, so it can be sent from the hospital where the patient is to the analysis laboratory in a simpler way. The results can be obtained in a week " adds the researcher.
Cancer of Unknown Primary (CUP) represents 10% of those human tumors in which metastasis is detected, but the primary tumor cannot be located despite several exploratory tests. Since the tumor type is not known, the survival of these patients is very low; the implementation of the EPICUP® test will lead to the development of more specific treatments in the future, according to the results presented in Nature Reviews Clinical Oncology: "Prospective trials are now needed to determine how these CUP patients, now correctly diagnosed, can benefit from more specific and less aggressive treatments for their disease" Dr. Esteller concludes.

Thursday, 6 July 2017

Bowel cancer diagnosis delayed by other illness

Source: University of Exeter
Summary:: A new study revealed that additional serious long-term health conditions, such as heart disease, can push a bowel cancer diagnosis back by up to twenty six days. The latest figures suggest that around 70% of people have at least one of these potentially serious long-term health conditions at the time they are diagnosed with cancer.

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The researchers from the University of Exeter analysed clinical data from over 4,500 patients across the UK who were later diagnosed with bowel cancer. In a study published in the British Journal of Cancer, they looked at whether pre-existing illness affected the time it took them to get a cancer diagnosis, making it one of the first studies to investigate this.

They found that if you have a single serious illness or mental health issue unrelated to cancer, such as depression or heart disease, your bowel cancer is diagnosed on average 10 days later than usual , a 13% increase from the usual time taken for a diagnosis. This could go up to over one month when patients had multiple illnesses. These illnesses may take up a lot of time in visits to the GP and leave not enough time available to investigate symptoms or signs linked to cancer.
           A bowel cancer sign or symptom which can be explained by a pre-existing condition, such as stomach pains, delayed cancer diagnosis by 9 days on average, a 12% increase from the usual time taken for a diagnosis. These cancer signs and symptom can be explained by the additional illness that the patient has so doctors are 'led astray', making it more difficult to arrive at a cancer diagnosis.
They also found that if you have Inflammatory Bowel Disease (IBD), it can delay a bowel cancer diagnosis by 26 days.
            Professor Jose Valderas, one of the lead researchers from the University of Exeter Medical School, said: "When you're trying to diagnose cancer, other illnesses can be a distraction either because they also require attention or because they can mask what would otherwise be flagged as a possible sign of cancer.
"It's vital that doctors realise that existing illnesses make a diagnosis of cancer more difficult and stay alert to recognize signs and symptoms of cancer as such. It's also important that patients flag symptoms with their doctor as early as possible, whether it's unexplained weight loss or changes to your bowel habits."
Professor Willie Hamilton, one of the lead researchers from the University of Exeter, said: "A ten day delay may not sound much but it may be the difference between a well-planned admission and an emergency admission with a complication. This really matters -- as the complications may kill."
The study, 'Comorbid conditions delay diagnosis of colorectal cancer: a cohort study using electronic primary care records' is published in the British Journal of Cancer. Authors are Luke TA Mounce, Sarah Price, Jose M Valderas, and Willie Hamilton.
           Commenting on the study, Deborah Alsina MBE, Chief Executive of Bowel Cancer UK, said: "As symptoms of bowel cancer can relate to later stage of disease it is important that delays in diagnosis are minimised. While the delays highlighted in this study are relatively small, if they add onto delays in patients presenting to their GP with symptoms, or in a diagnostic appointment, they become more serious. Currently around 20% of people are diagnosed with bowel cancer as an emergency when outcomes are generally poorer and almost 50% in later stages of the disease when it is harder to treat. "This interesting study highlights another aspect of the complexity of diagnosing bowel cancer as the majority of patients have multiple conditions. Therefore finding quicker, more effective ways to identify and diagnose these patients is crucial to help GPs and other clinicians identify or rule out bowel cancer quickly to give people the very best opportunity for successful treatment. Bowel cancer is after all, treatable and curable especially if diagnosed early."

Mapping genes could improve cancer diagnosis

Source: Babraham Institute,
Summary:: Large-scale changes to the structure of the genome are often seen in cancer cells. Scientists have found a way to detect these changes, which could enhance cancer diagnosis and aid the use of targeted treatments.

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Large-scale changes to the structure of the genome are often seen in cancer cells. Scientists at the Babraham Institute in Cambridge, UK, have found a way to detect these changes, which could enhance cancer diagnosis and aid the use of targeted treatments.

The report, in the journal Genome Biology, outlines a new application of a technique called Hi-C, which allows scientists to map how genetic material is arranged inside cells. By analysing this information, researchers can reliably identify major genetic changes that other methods may miss. This all comes at a lower cost than standard DNA sequencing methods.
         Hi-C can detect chromosome rearrangements where large sections of DNA are exchanged or moved between pieces of the genome called chromosomes and also copy number variation -- where genetic material gets copied or deleted. Both of these changes can have drastic effects on how the cell behaves.
First author on the paper, Dr Louise Harewood, said: "Chromosomal rearrangements are seen both in the general population and in the majority of cancers. Detection of chromosome rearrangements in patients can be troublesome and many can be missed. This can be detrimental, particularly in oncology where rearrangements can play both diagnostic and prognostic roles."
        The scientists, led by Professor Peter Fraser, used Hi-C to examine the genome of cancer cells from six people with brain tumours. They were able to identify major genome changes, often with pinpoint accuracy. Uniquely, this approach allows doctors and scientists to study genetic changes in the wider context of the whole genome. Hi-C could become a powerful tool for understanding the complex genetic changes found in many cancers.
        Professor Fraser, said: "Hi-C could play a pivotal role in the detection of chromosomal abnormalities and may aid the discovery of new fusion genes. The technique works with much lower quality samples than current techniques and has the additional advantage of being able to provide copy number information from the same data. This all comes at a significantly lower cost than standard methods that use DNA sequencing."