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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.