NFCR Writer David Perry, Author at NFCR - Page 2 of 2

NFCR Writer David Perry

Forty Percent of American Cancer Cases Linked to Weight

In a report published by the U.S. Centers for Disease Control and Prevention, obesity and even being overweight are associated with at least 13 different types of cancer, comprising 40% of all cancer diagnoses. More than 630,000 people in the U.S. are annually diagnosed with a cancer associated with obesity and high weight.

“Around 55 percent of cancers in women and 24 percent of cancers in men were associated with overweight and obesity,” said Dr. Lisa Richardson, director of the CDC Division of Cancer Prevention and Control.

The 13 cancers are meningioma (cancer of the tissue covering the brain and spinal cord), thyroid and multiple myeloma (cancer of the blood cells), adenocarcinoma (esophagus), colorectal cancer, and cancers of the kidneys, uterus, ovaries, breast (post-menopausal), gallbladder, upper stomach, liver, and pancreas. In the period spanning 2005 to 2014, 12 of the cancers associated with weight rose seven percent, while rates of other cancers in the same period actually fell by 13%.

Also noted was the fact that most Americans do not know of the link between cancer and weight.

“Awareness of some cancers being associated with obesity and [being] overweight is not yet widespread,” said Dr. Anne Schuchat, the deputy director of the CDC.

And despite advances in colorectal cancer screenings and successful treatment, people who are overweight or obese are also about 30 percent more likely to develop that particular cancer than individuals with normal weight, according to the report. Women who are overweight or obese are about two to four times more likely to develop endometrial cancer, said Richardson.

“The obesity epidemic is a complex and major public health challenge that requires comprehensive efforts,” said Schuchat. “People can eat healthy, be physically active, and get recommended cancer screening.”

Not unsurprisingly, age is also a factor, with an uptick in the mentioned cancers occurring in people aged 50 to 74.


Anne Schuchat and Lisa Richardson, “Obesity and Cancer,” Vital Signs – October Teleconference Transcript, Oct. 3, 2017.

Cancer and Obesity, Oct. 3. Date accessed: Nov. 29.

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Lung Cancers Can Differ by Race

According to Clinical Cancer Research, a journal of the American Association for Cancer Research, recently discovered genetic differences in non-small cell lung cancers (NSCLCs) between some African-Americans and European-Americans suggest that there are racial differences in the biology of the disease. These findings could have a clinical impact on personalized cancer therapies in the future.

“We are entering the age of ‘precision medicine’ in which diagnosis and therapy decisions for each cancer patient will be based on detailed molecular and chemical fingerprints,” said researcher Bríd M. Ryan, a researcher at the National Cancer Institute’s Center for Cancer Research and the study’s author.

“Much of the revolutionary work that underpins precision medicine has been conducted on populations of European descent, with limited work in minority populations,” she added. “We want to make sure that all populations can benefit from this approach. Studying the biology of lung cancer in African-Americans is one step toward that goal.”

Dr. Ryan and her team analyzed normal and NSCLC tissue obtained from 64 African-Americans and 74 European-Americans. Tissue from 22 African-Americans and 19 European-Americans was analyzed for mRNA expression, which provides information about gene expression, and tissue from the remaining patients was analyzed for microRNA expression. These two different kinds of RNA have related, but different, roles inside the cell.

The researchers found that expression of 2,210 genes was more than two-fold increased or decreased in NSCLC from African-Americans compared with matched normal tissue. For European-American samples, 2,921 genes were differentially expressed by more than two-fold. Many of the genes were differentially expressed between NSCLC and normal tissue in both African-Americans and European-Americans, but 637 and 1,844 were differentially expressed only in African-Americans and European-Americans, respectively.

The genes differentially expressed only in the African-American NSCLC samples were enriched for those involved in stem cell biology and invasive behavior. The genes differentially expressed only in European-Americans were enriched for those involved in cell cycle, mitosis, and proliferation.

In addition, the genes differentially expressed only in African-Americans or European-Americans were analyzed using a drug-response prediction model. The two gene subsets predicted similar resistance/sensitivity for NSCLC from African-Americans and European-Americans to some drugs. For other drugs, the predictions varied by race, with NSCLC from African-Americans predicted to be resistant to 53 drugs to which NSCLC from European-Americans was sensitive. Among these drugs was irinotecan, used for treating certain types of cancer.

“This study helps close a gap in our knowledge of which genes are expressed in lung cancers from African-Americans, revealing clear differences in lung cancer biology between African- Americans and European-Americans,” said Mitchell. “By understanding these racial differences in gene expression, we can account for how they may contribute to disease progression and treatment response and, ultimately, help reduce some health outcome disparities.”

The study parallels a recent publication in Theranostics, one of whose authors is NFCR-sponsored scientist, Dr. Wei Zhang, of Wake Forest Baptist Medical Center. That team’s precision oncology study of racial differences in genetic alterations in smoking-related cancers revealed that African-Americans had a significantly increased mutation rate in the TP53 gene (tumor suppressor gene), and five genes were significantly amplified in this population. The researchers also found that a number of genes—including those that repair DNA damage—mutated at higher frequencies in African-American cancer patients versus European-Americans. 

Dr. Zhang stated, “These results provide strong evidence that genomic instability is a fundamental hallmark of cancer, and the events underlying the regulation of genome stability are centered on interactions with environmental factors and lifestyle, such as smoking.”

Too, the study points to genetic mutations common to African-Americans as a factor contributing to cancer outcome disparities. This latter discovery may lead to the development of novel diagnostic and improved therapeutic options for patients. 


Kytola V, Topaloglu U, Miller LD, Bitting RL, Goodman MM, D`Agostino RB Jr, Desnoyers RJ, Albright C, Yacoub G, Qasem SA, DeYoung B, Thorsson V, Shmulevich I, Yang M, Shcherban A, Pagni M, Liu L, Nykter M, Chen K, Hawkins GA, Grant SC, Petty WJ, Alistar AT, Levine EA, Staren ED, Langefeld CD, Miller V, Singal G, Petro RM, Robinson M, Blackstock W, Powell BL, Wagner LI, Foley KL, Abraham E, Pasche B, Zhang W. Mutational Landscapes of Smoking-Related Cancers in Caucasians and African Americans: Precision Oncology Perspectives at Wake Forest Baptist Comprehensive Cancer Center, Theranostics. 2017; 7(11):2914-2923. doi:10.7150/thno.20355

Ryan, Bríd  M. Comparative Transcriptome Profiling Reveals Coding and Noncoding RNA Differences in NSCLC from African Americans and European Americans, Clinical Cancer Research. (December 2017).




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Using Cancer to Fight Cancer

Researchers at the University of Michigan (U-M) devised a process to grow a series of honeycomb-like arrays of tiny, lab-grown cancers that could one day help doctors zero in on individualized treatments for ovarian cancer. The findings are detailed in a study in the journal, Clinical Cancer Research.

Led by Geeta Mehta, the Dow Corning Assistant Professor of Materials Science and Engineering at U-M and head of the research team that developed the technique, the process involves growing hundreds of cultured cell masses, called spheroids, from just a few tumor cells derived from a patient. Grown in a structure called a 384-hanging drop array, each spheroid is encased in a tiny droplet of a special culturing medium. This 3-D method yields cells that grow and multiply as they would inside the human body.

The researchers hope those spheroids can serve as a testing ground unique to each patient, and lead to personalized therapies. Doctors could quickly try out many different medications, finding the best combination for an individual patient and making adjustments as the disease evolves.

The hanging drop array’s hundreds of individual compartments make it possible to grow many spheroids at once and quickly gather data about multiple drugs. This is key, as chemotherapy treatment often requires complex cocktails of multiple drugs administered together. The cells could provide a way to test many such cocktails simultaneously.

“Today we’re limited to two-dimensional cells grown in bovine serum that’s derived from cows. Cells grown this way often don’t respond to medication the same way as ovarian cancer cells inside the body,” explains Mehta. “Three-dimensional cultured spheroids provide a much more predictive way to test many different medications, and a way to grow many cultured cells from just a few of the patient-derived cells.”

A particularly pernicious cancer type, ovarian cancer’s deadly adaptability contributes to a 70% relapse rate among patients who had surgery to remove a tumor. Its free-floating spheroids shuttle cancer through the abdomen with the ability to form new tumors wherever they go—the liver, the intestines, the abdominal wall, etc. And the cells within those spheroids mutate often and unpredictably, quickly developing new strains that resist chemotherapy drugs.

“This is a really important step to expedite personalized medicine for cancer patients,” added Ronald Buckanovich, a professor of medicine at the University of Pittsburgh and a senior co-author of the study. “The ability to take patients’ samples, rapidly grow them in a more physiologic manner and study their response to therapy, without using mice, will be a faster, cheaper and more humane way to rapidly test a patient’s response to dozens of therapeutics.”

The National Foundation for Cancer Research (NFCR) too sponsors personalized medicine-based research and clinical initiatives for various cancer types. For example, Massachusetts General Hospital’s Dr. Alice Shaw focuses on targeted therapy and drug resistance in lung cancer and uses patient-derived lung cancer models to test for effective treatments. Dr. Wei Zhang of Wake Forest University’s School of Medicine utilizes data from next-generation sequencing of tumor DNA found in patients’ bloodstream to identify growth-promoting genes or drug resistant genes for guiding therapeutic approaches for breast, prostate, lung, colorectal, pancreatic and brain cancer. And Dr. Rakesh Jain, also of Massachusetts General Hospital, has been identifying molecular characteristics that cause resistance to anti-angiogenic therapy in patients with the deadliest form of brain cancer, glioblastoma multiforme (GBM); his research may allow oncologists to tailor anti-angiogenesis therapies for each patient.


Mehta, Geeta. (2017, November) Personalized medicine-based approach to model patterns of chemoresistance and tumor recurrence using ovarian cancer stem cell spheroids. Clinical Cancer Research, pp. 22-23.

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Parasite Killer Too Found to be Effective Cancer Treatment Candidate

Researchers have ascertained that the anti-tapeworm drug, nitazoxanide (NTZ), may also hold out hope as a precision therapy for various cancers.

Prostate and colon cancer cells contain high amounts of activated beta-catenin, which correlate to treatment-resistant cancer cells and other oncological parameters. In a study of the cancer-abetting potential of several non-cancer-designated drugs, a team led by Norwegian scientists discovered that NTZ, a well-known and approved anti-parasite drug, decomposed activated beta-catenin.

“We discovered that this specific substance is blocking the signaling pathway in the cancer cells… It is not often that researchers discover a substance that targets specific molecules as precisely as this one,” says University of Bergen Professor Karl-Henning Kalland, the leader of the team responsible for the finding

Speaking of the considerable advantages associated with repurposing drugs which have already undergone rigorous clinical trials and obtained a regulatory green-light, “the advantage of testing already approved drugs is that we know they work in the human body and have no serious side effects, which means that a future treatment may happen quicker,” Dr. Kalland explains.

Repurposed drugs are not uncommon. The erectile dysfunction treatment, Viagra, was initially intended as a high blood pressure medication. The drug, thalidomide, first conceived as a sedative before it was discovered to cause catastrophic birth defects, is now accepted as a treatment for leprosy and multiple myeloma

By hindering activated beta-catenin, NTZ also shows signs of stimulating central parts of the immune system. Immunotherapy, a particularly promising and rapidly developing field of medicine, seeks to enhance and enable patients’ own defenses to recognize and successfully attack cancers and other diseases. Such treatments can be particularly beneficial in battling ailments, not the least due to advantages associated with minimized to negligible side effects, and drug resistance being overcome

“At the moment, we are working on how to strengthen the body’s immune defense against prostate cancer by using the mechanisms we discovered (pertaining to) NTZ,” Dr. Kalland says.

Unrelated to the Norwegian team’s work, but too exemplifying other exciting developments in the field of oncological immunotherapy, efforts at Virginia Commonwealth University led by National Foundation for Cancer Research-sponsored scientist, Paul B. Fisher, are underway. There, a team is exploring a viral-based immunotherapy for cancer patients who have few other choices of treatment. Dr. Fisher is exploring a potentially paradigm-shifting technique whereby a genetically engineered virus seeks out, finds and delivers a gene for an immune system response yielding cancer cell suicide (apoptosis), bypassing non-cancerous and healthy cells. Studied indications include prostate, brain and pancreatic cancers, and a primary protein molecule associated with Dr. Fisher’s research has been shown to be safe in a Phase I clinical trial.

Kalland, Karl-Henning. (2017,October). Small molecule promotes ᵝ-catenin citrullination and inhibits Wnt signaling in cancer. Nature Chemical Biology. University of Bergen, Norway.

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“System Mistrust” Interferes With Post-Surgery Breast Cancer Treatments

BALTIMORE — A study led by a Johns Hopkins Bloomberg School of Public Health researcher indicates nearly one-third of breast cancer surgery patients went against their doctor’s advice, choosing to not begin or complete adjuvant anti-cancer therapy. The primary factor: a general mistrust of the American healthcare system.

Adjuvant therapy for breast cancer, usually chemotherapy, hormone therapy or radiation treatment, is a post-surgery procedure meant to kill any cancer cells not eliminated by the initial operation. It is widely regarded as necessary, and research has shown that adjuvant therapy on average reduces the likelihood of breast cancer’s recurrence and increases patients’ chances of long-term survival.

A survey asked participants about their trust in their doctors and in the healthcare system in general, with researchers using the patients’ responses to place them into high and low categories of general health care system distrust. A subsequent analysis found that those in the “high-distrust” category, compared to those in the lower-distrust category, were about 22 percent more likely to report not having followed their doctor’s full set of recommended treatments. Published in Cancer Epidemiology, Biomarkers & Prevention, this study is by far the largest evaluation of this issue.

The survey included 2,754 breast cancer patients in Florida and Pennsylvania during a two-year period. Sixty-nine percent of patients were white, 27 percent were black/African-American and four percent identified as another race or ethnicity. The key finding is that “treatment discordance” (not following a doctor’s recommended treatment plan in its entirety) was more likely among patients in the survey who reported distrust of medical institutions and insurers. The patients’ trust or distrust of their own doctors did not seem to be a factor.

 “If we want more women with breast cancer to complete their treatment, we’ll need to deal with their beliefs about the healthcare system, and I do think we can modify those beliefs,” says Lorraine T. Dean, ScD, assistant professor in the Bloomberg School’s Department of Epidemiology and the study’s lead author.

“Improving health care system distrust may require strategies that are not solely focused on boosting physician trust,” Dean says. “If ordinary businesses can learn to increase trust in their brands, why not the same with healthcare institutions?”


  • Dean, Lorraine T., et al.  (2017, November)  Healthcare System Distrust, Physician Trust, and Patient Discordance with Adjuvant Breast Cancer Treatment Recommendations.  Baltimore, MD: Johns Hopkins Bloomberg School of Public Health
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Novel Cancer Genes Discovered Via New Statistical Model

LONDON — A new statistical model developed by scientists at the Francis Crick Institute
revealed 27 novel genes thought to prevent cancer from forming, in an analysis of over 2000
tumors across 12 human cancer types. The findings could help create new cancer treatments that
target these genes, and open up other avenues of cancer research. Novel genes are generally
duplicated genes that develop new (thus, “novel”) functions.

“Using this powerful toolkit, we’ve uncovered rare tumor suppressor genes that when lost in
mutated cells, cause cancer” says researcher Jonas Demeulemeester. “This could pave the way
for the development of personalized cancer treatments.”

Mutation is a necessary component of evolution, but not all mutations are benevolent. To combat
virulent mutations that can lead to tumors, each individual human cell has two copies of tumor
suppressor genes to prevent it from turning cancerous. If one of these genes is lost, the other can
pick up the slack, but if both genes are lost, tumor formation is free to occur and the body may not
see it as harmful.

The identified double gene copy deletions can provide clues for tumor suppressor genes in
cancer. However, cancer samples normally contain both healthy cells and cancerous cells in
unknown proportions, making it difficult to work out if just a single copy or both copies of the gene
have been lost in the cancer cells.

In addition, cancer is not a single, straightforward mutation; it can be difficult to distinguish
between harmful deletions of tumor suppressor genes and non-harmful deletions of other genes
at fragile sites along the genome. Just as not all mutations are benevolent, not all are virulent, or
even effectual. Scientists can investigate the new candidate tumor suppressor genes identified in
this study to understand their mechanism of action, and try to find drug targets.

The Frick team developed computational tools to analyze 2,218 tumors from 12 cancer types
including breast, lung, and bowel cancers. By determining the relative proportions of cancerous
and healthy cells in each sample, they could work out the number of copies of each gene in the
cancer cells. This analysis revealed 96 regions of the human genome that are frequently lost
during tumor development.

The analysis also revealed that harmful tumor suppressor gene deletions have a different “DNA
footprint” to non-harmful deletions. This enabled the researchers to categorize deletions,
revealing 16 previously known tumor suppressor genes, and 27 new ones. Some of these had
previously been suspected to contribute to cancer development, while others were completely

“Cancer genomics is a growing area of research,” says Peter Van Loo, group leader at the
Francis Crick Institute, “and the computational tools we use are a powerful way to find new genes
involved in cancer.”

The research, published in Nature Communications, was led by scientists at the Francis Crick
Institute and the University of Leuven, in collaboration with the University of Chicago and the
University of Oslo.

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Genetic Marker Can Help Focus Prostate Cancer Therapies

CLEVELAND, OH — Two studies conducted by the Cleveland Clinic revealed how a testosterone-related genetic abnormality can help predict individual patient responses to specific prostate cancer therapies. The studies, published in the October 12 issue of JAMA Oncology, suggest that men who inherit this variant would benefit from a personalized treatment plan that targets specific hormonal pathways.

In the first study, Nima Sharifi, M.D., of the Cleveland Clinic Lerner Research Institute, and his team studied the role of the gene variant known to science as “HSD3B1(1245C)” in two different prostate cancer patient populations, after those patients received androgen deprivation therapy (ADT). ADT works by blocking prostate cancer’s supply of male hormones in the testes, and is the go-to treatment for the recurrent form of the disease. However, ADT is notorious for suddenly losing its effectiveness. This allows the cancer to grow and metastasize.

Dr. Sharifi discovered that prostate cancer cells with the HSD3B1(1245C) abnormality survive ADT by producing their own androgens.

In the first study, 213 prostate cancer patients whose tumor recurred after radiation treatment were then treated with ADT. Dr. Sharifi found that patients with the HSD3B variant developed metastatic cancer and it developed more rapidly than those without the variant. He and his team showed that the genetic variant was predictive of the time to develop metastasis.

The second study examined a group of 90 men with metastatic prostate cancer that had become resistant to ADT. These patients were subsequently treated with the drug ketoconazole, which blocks the production of androgens outside of the testes, such as those developed by prostate cancer cells evading treatment.

Surprisingly, men with the genetic anomaly fared better on ketoconazole than men without the variant. This finding raises the possibility that targeting the variant tumors’ backup androgen supply could be a successful strategy when ADT fails.

“We hypothesized that HSD3B1(1245C) variant tumors become resistant to ADT because they have a backup supply of androgens,” said Dr. Sharifi. “However, relying on these extra-gonadal androgens makesthem more sensitive to ketoconazole.”

Unfortunately, with the current state of prostate cancer treatments as they are, the outlook of men with this particular gene variant remains poor; in 2017, Sharifi received a Top Ten Clinical Research Achievement award from the Clinical Research Forum for his landmark discovery that men who carry the HSD3B1(1245C) variant are more likely to die from their disease. However, his most recent studies in the identification of HSD3B1(1245C) in patients sets up the gene as a predictive biomarker to help in the diagnosis and treatment of their prostate cancer. It also helps with the ongoing research and development of next-generation androgen inhibitors, such as abiraterone and enzalutamide.

These discoveries are part of an existing trend in medical science to individualize the treatment of a cancer patient, treating each body as a unique environment and where cancer treatment is no longer considered a formulaic, one-size-fits-all formula.

“We are hopeful that these findings will lead to more personalized and effective treatments for prostate cancer,” said Dr. Sharifi. He continues, “If men carry a specific testosterone-related genetic abnormality, we may be able to personalize their therapy and treat specific patients more aggressively.”

In addition, National Foundation for Cancer Research (NFCR) sponsored scientist Dr. Paul B. Fisher at Virginia Commonwealth University and his team are developing new viral-based treatments for patients with metastatic prostate cancer that are unresponsive to ADT and other treatments and who have no other choices. The gene therapy involves an immune system cytokine, either Interferon gamma (IFNγ) or MDA-7/IL- 24 — the latter discovered by Dr. Fisher and works by inducing metastatic cells to commit cell suicide (apoptosis). Prostate cancer spreads to bone in 73% of patients with metastatic prostate cancer and MDA-7/IL- 24 also has anti-bone metastatic properties. MDA-7/IL- 24 has been shown to be safe from results in a Phase I clinical trial which should allow this potential new treatment for advanced prostate cancer to enter clinical trials easily upon completion of this pre-clinical research.

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New Compound Targets Metastatic Cancer Cells

TEL-AVIV​ ​—​ ​Scientists​ ​at​ ​Bar-Ilan​ ​University​ ​in​ ​Israel​ ​successfully​ ​targeted​ ​and​ ​rendered​ ​inert​ ​the​ ​enzyme that metastatic​ ​cancer​ ​cells​ ​need​ ​to​ ​survive​ ​in​ ​the​ ​body​ ​once​ ​they​ ​have​ ​left​ ​their​ ​host​ ​tumor.​ ​The​ ​findings​ ​of Professor​ ​Uri​ ​Nir,​ ​of​ ​the​ ​Mina​ ​and​ ​Everard​ ​Goodman​ ​Faculty​ ​of​ ​Life​ ​Sciences​ ​at​ ​Bar-Ilan​ ​University,​ ​and​ ​his team​ ​could​ ​pave​ ​the​ ​way​ ​to​ ​therapies​ ​that prevent metastasis, or the spreading of​ ​cancer​ ​cells from their point of origin. 

Nir​ ​and​ ​his​ ​team​ ​discovered​ ​the​ ​existence​ ​of​ ​an​ ​enzyme,​ ​FerT,​ ​in​ ​the​ ​mitochondria​ ​of​ ​cancer​ ​cells​ ​that is not​ ​present in those​ ​of​ ​normal​ ​cells​ ​(mitochondria​ ​are​ ​the​ ​“power​ ​generators”​ ​of​ ​a​ ​cell).​  ​Once​ ​free​ ​within​ ​the​ ​body, metastatic​ ​cancer​ ​cells​ ​face​ ​an​ ​environment​ ​short​ ​on​ ​the​ ​nutrients,​ ​such​ ​as​ ​glucose,​ ​needed​ ​to​ ​survive and grow;​ ​FerT kicks​ ​ ​the​ ​cancer’s​ ​mitochondria​ ​ into​ ​high​ ​gear​ to​ ​produce​ ​energy​ ​when​ ​the​ ​given​ ​environment​ ​lacks​ ​the necessary​ ​metabolic​ ​components​ ​for​ ​survival.​ ​Basically,​ ​it​ ​makes​ ​mitochondria​ ​do​ ​more​ ​with​ ​less. Interestingly,​ ​this​ ​is​ ​what​ ​FerT​ ​does​ ​in​ ​another​ ​cell​ ​that​ ​must​ ​survive​ ​outside​ ​its​ ​origin:​ ​sperm. 

 “Like​ ​metastatic​ ​cells,​ ​sperm​ ​cells​ ​are​ ​unique​ ​in​ ​that​ ​they​ ​can​ ​also​ ​generate​ ​energy​ ​under​ ​very​ ​harsh conditions.​ ​Once​ ​they​ ​have​ ​entered​ ​the​ ​female​ ​birth​ ​canal,​ ​where​ ​there​ ​is​ ​no​ ​blood​ ​supply​ ​for​ ​them,​ ​they produce​ ​and​ ​expend​ ​enormous​ ​amounts​ ​of​ ​energy​ ​under​ ​very​ ​extreme​ ​or​ ​abnormal​ ​conditions,”​ ​explains Nir.​ ​“We​ ​found​ ​that​ ​very​ ​aggressive​ ​metastatic​ ​cancer​ ​cells​ ​looked​ ​for​ ​and​ ​identified​ ​this​ ​sperm-specific protein,​ ​learned​ ​how​ ​to​ ​produce​ ​it,​ ​and​ ​harnessed​ ​it​ ​in​ ​order​ ​to​ ​potentiate​ ​their​ ​mitochondria​ ​and​ ​produce energy​ ​under​ ​very​ ​harsh​ ​conditions.” 

With​ ​this​ ​information,​ ​Nir​ ​developed​ ​a​ ​compound​ ​dubbed​ ​E260.​ ​When​ ​applied​ ​to​ ​metastatic​ ​cells​ ​in​ ​culture or​ ​mice​ ​with​ ​metastatic​ ​tumors,​ ​E260​ ​enters​ ​the​ ​metastatic​ ​cells​ ​and​ ​then​ ​​ ​the​ ​mitochondria,​ ​whereupon it​ ​binds​ ​to​ ​FerT,​ ​distorting​ ​its​ ​energy-generating​ ​activity​ ​to​ ​such​ ​a​ ​degree​ ​the​ ​mitochondria​ ​effectively​ ​shuts down.​ ​Metastatic​ ​cells​ ​are​ ​notoriously​ ​tenacious;​ ​they​ ​can​ ​detect​ ​damage​ ​to​ ​their​ ​mitochondria​ ​and​ ​even​ ​take steps​ ​to​ ​repair​ ​them.​  ​ Nir found that E260-applied​ ​cells​ ​did not have ​the​ ​energy​ ​necessary to​ ​both​ ​repair​ ​mitochondrial function​ ​and​ ​maintain​ ​other​ ​cell​ ​processes​ ​at​ ​the​ ​same​ ​time.​ ​The​ ​result: cell death. 

More​ ​promisingly,​ ​“We​ ​have​ ​treated​ ​mice​ ​with​ ​metastatic​ ​cancer​ ​and​ ​this​ ​compound​ ​completely​ ​cured them​ ​with​ ​no​ ​adverse​ ​or​ ​toxic​ ​effect​ ​that​ ​we​ ​can​ ​see.​ ​We​ ​have​ ​also​ ​checked​ ​several​ ​normal​ ​cells​ ​and​ ​they are​ ​not​ ​affected,”​ ​says​ ​Nir.

E260​ ​came​ ​about​ ​from​ ​the​ ​fact​ ​that​ ​cancer​ ​can​ ​most​ ​often​ ​be​ ​successfully​ ​treated​ ​in​ ​its​ ​early​ ​stages​ ​when confined​ ​to​ ​one​ ​organ. ​ ​While​ ​standing​ ​immunotherapy​ ​can​ ​be​ ​effective​ ​in​ ​treating​ ​the metastatic​ ​phase​ ​of​ ​the​ ​disease,​ ​only​ ​a​ ​limited​ ​number​ ​of​ ​patients​ ​fit​ ​the​ ​criteria​ ​for​ ​such.​ ​Generally speaking,​ ​once​ ​a​ ​cancer​ ​metastasizes,​ ​treatment​ ​becomes​ ​more​ ​difficult​ ​and​ ​mortality​ ​much​ ​higher. 

Nir​ ​and​ ​his​ ​team​ ​hope​ ​to​ ​pursue​ ​Phase​ ​1​ ​clinical​ ​trials​ ​within​ ​a​ ​year-and-a-half.​ ​The​ ​research​ ​was published​ ​this​ ​month​ ​in​ ​the​ ​journal​ ​​Nature​ ​Communications.

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