Category Archives: Cancer

Gene thought to suppress cancer may actually promote spread of colorectal cancer

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Original Source Here Via EurekAlert!

UNIVERSITY OF MISSOURI-COLUMBIA

COLUMBIA, Mo. (Jan. 4, 2016) – A gene that is known to suppress the growth and spread of many types of cancer has the opposite effect in some forms of colorectal cancer, University of Missouri School of Medicine researchers have found. It is a finding that may lay the foundation for new colorectal cancer treatments.

IMAGE

IMAGE: UNIVERSITY OF MISSOURI SCHOOL OF MEDICINE RESEARCHER SHARAD KHARE, PH.D., FOUND THAT A GENE THAT IS KNOWN TO SUPPRESS THE GROWTH AND SPREAD OF MANY TYPES OF CANCER HAS THE… view more CREDIT: JUSTIN KELLEY/MU

“The gene known as Sprouty2 has previously been shown to protect against metastasis, or the spreading of cancer to other parts of the body, in breast, prostate and liver cancer,” said Sharad Khare, Ph.D., associate professor of research in the MU School of Medicine’s Division of Gastroenterology and Hepatology and lead author of the study. “However, our recent molecular studies found that this gene may actually help promote metastasis instead of suppress it.”

For more than three years, Khare studied Sprouty2 in cancer cell models, mouse models and human biopsy samples. Using different molecular methods, the researchers found that the gene functions differently in colorectal cancer than in other types of cancers. Sprouty2 is known to block molecular circuits to prevent cancer cells from growing and spreading to other parts of the body. However, the researchers found that in colorectal cancer, Sprouty2 may increase the metastatic ability of cancer cells instead of suppress it. Khare believes this occurs when the gene is up-regulated, or supercharged.

Cancer deaths attributed to colorectal cancer are mainly due to tumor recurrence and metastasis to other organs. Excluding skin cancers, colorectal cancer is the third most common cancer diagnosed in both men and women in the United States, according to the American Cancer Society. It’s estimated that the lifetime risk of developing colorectal cancer is about 1 in 20.

“This finding is a very significant step in our understanding of metastasis in colorectal cancer, but it’s important to note that we believe this phenomenon may occur in only a subset of colorectal cancer patients,” Khare said. “We don’t yet know why this is the case, but we hope to determine if there is a correlation between the up-regulation of this gene and the life expectancy of patients with colorectal cancer. Future studies will help us understand who may be at risk, and ultimately, if personalized treatments can be planned to target this gene.”

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The study, “Atypical Role of Sprouty in Colorectal Cancer: Sprouty Repression Inhibits Epithelial-mesenchymal Transition,” recently was published in the cancer research journalOncogene. Research reported in this publication was supported by the National Institutes of Health under award numbers CA150081 and DC010387, Veterans Affairs Merit Award 1171590, the MU Research Board Award and MU School of Medicine Bridge funding. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funding agencies.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

NIH-funded researchers identify drugs to eliminate senescent cells in mice, improving health and function

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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Original Article Here

Researchers led by a team from the Mayo Clinic in Rochester, Minnesota, have identified a new class of drugs called “senolytics” that target and kill aged—senescent—cells in mice. The team also found that a single dose of senolytic drugs led to improvements in the animals’ health and function.

Previous research has shown that genetically modifying mice to remove their senescent cells extended their health span. This study, published online on March 9, 2015, in Aging Cell, and funded in part by the National Institute on Aging at NIH, is the first to pharmacologically imitate the approach in a mouse model of extremely accelerated aging.

Senescent cells have long been implicated in aging. Some rapidly dividing cells reach a point when they can no longer safely replicate; their telomeres become too short to protect the cell’s DNA. At this point, a cell will either destroy itself through a process called apoptosis, become dysfunctional (and potentially cancer-prone), or turn replication off but continues to survive. The cells that turn off are known as senescent. They can perform some functions, but they also release molecules that may increase risk for a variety of diseases, including cancer.

Senescent cells are not dead. In fact, they cannot die (on their own). This characteristic was key for determining a drug target.

The two senolytic drugs tested, dasatinib and quercetin, were effective individually, but more powerful when used together. Days after a single dose, aged mice showed a notable improvement in heart function. Also, a single dose reversed the damaging effects of radiation on a limb, leading to a lasting improvement in exercise capacity. Longer term, periodic use of the drugs delayed a variety of age-related symptoms, including osteoporosis and frailty.

While dasatinib is an FDA-approved cancer drug, and quercetin has been used by humans as an antioxidant supplement, the researchers cautioned that it is far too early to suggest that they be considered as a clinical intervention for aging. More research is needed to determine whether these and other senolytics have similar effects and are safe in animal models before studies regarding any application in humans can be designed and tested.

Reference: Zhu Y, et al. The Achilles’ Heel of Senescent Cells: From Transcriptome to Senolytic DrugsAging Cell. 2015 Mar 9. doi: 10.1111/acel.12344 [Epub ahead of print]

RB2015 Rejuvenation Biotechnology Conference Aug 19-21

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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RB2015

WHO ATTENDS

  • Academic Researchers
  • Pharmaceutical and Biotech Industry
  • Undergrad, Graduate and Post Doctorial Students
  • Nonprofits
  • Regulatory
  • Investors
  • The General Public

WHY ATTEND

  • Focused tracks covering three key elements of successful drug development: clinical review, therapeutic approaches, industry and policy
  • In depth examination of advances in tissue engineering and gene therapy
  • More interactivity – 6 hours of interactive discussion sessions and 17 hours of networking
  • Jobs Board – review and share the expertise needs of the industry’s leading research and development organizers
  • Understand and shape the scientific and investment opportunities of the new Rejuvenation Biotechnology Industry
  • Extended poster sessions
  • Back by popular demand – our opening evening’s entertainment will be Hal Sparks – Comedian, Actor and Musician.

Study reveals molecular genetic mechanisms driving breast cancer progression

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Original Source Here

UT SOUTHWESTERN MEDICAL CENTER

DALLAS – April 3, 2015 – Researchers at UT Southwestern Medical Center have uncovered how the body’s inflammatory response can alter how estrogen promotes the growth of breast cancer cells. IMAGE

UT Southwestern researchers identified how a combination of signaling molecules inhibits the growth of breast cancer cells, improving clinical outcomes for some subtypes of breast cancers.

The combination — the steroid hormone estradiol and the proinflammatory cytokine tumor necrosis factor alpha (TNFα) — act to expand the number of sites where estrogen receptor alpha (ERα) can bind to the genome in breast cancer cells. The new sites of ERα binding turn new genes on and off, which alters the growth response of the breast cancer cells, inhibiting their growth and improving clinical outcomes in certain cases.

The newly identified gene set can be used as a biomarker that can help physicians determine who is at risk and how they might react to certain therapies.

“Our study uncovered the molecular mechanisms that alter the expression of the new set of genes in response to estradiol and TNFα, and identified potential target genes for future therapy,” said senior author Dr. W. Lee Kraus, Director of the Cecil H. and Ida Green Center for Reproductive Biology Sciences, Professor of Obstetrics and Gynecology, and a member of the Harold C. Simmons Comprehensive Cancer Center. “Since the altered pattern of gene expression can predict outcomes in breast cancer, there are important diagnostic and prognostic implications.”

The findings are published online and in the journal Molecular Cell.

Approximately 12.3 percent of women will be diagnosed with breast cancer at some point during their lifetime, and nearly 2.9 million women are living with breast cancer in the United States, according to statistics from the National Cancer Institute (NCI). About 232,670 new cases were reported in 2014, constituting about 14 percent of all new cancer cases. About 40,000 deaths were attributed to breast cancer in 2014.

Cancer cells release signals that can prompt the body to respond with an inflammatory response. As part of this response, TNFα is released and can impact the growth of the cancer cells. Previous studies suggested that inflammation might exacerbate the cancer, while the present study suggests that, in some cases, it might actually promote a better outcome. The study revealed that, when present together, TNFα and estradiol cause ERα, a nuclear transcription factor that is present in about two-thirds of breast cancers (so-called ER+ cancers), to bind to new sites in the genome where the protein does not bind with either TNFα or estradiol alone. These new ERα binding sites allow altered gene expression and, for some subtypes of breast cancers, inhibit the growth of cancer cells.

Since the effect only happens when the two are combined, researchers can use the altered gene expression patterns as an indicator that both agents are at work in the cancer and as a biomarker that may help determine who might be more at risk and how they might react to therapy, said Dr. Kraus, Professor and Vice Chair for Basic Sciences in Obstetrics and Gynecology, Professor of Pharmacology, and holder of the Cecil H. and Ida Green Distinguished Chair in Reproductive Biology Sciences.

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The mission of the Cecil H. and Ida Green Center for Reproductive Biology Sciences, endowed by Cecil and Ida Green in 1974, is to promote and support cutting-edge, integrative, and collaborative basic research in female reproductive biology, with a focus on signaling, gene regulation, and genome function.

Other UT Southwestern researchers involved in the work were postdoctoral researcher Dr. Hector Franco and computational biologist Anusha Nagari.

The work was supported by a postdoctoral fellowship from the American Cancer Society – Lee National Denim Day Fellowship and a grant from the National Institute of Diabetes and Digestive and Kidney Diseases, part of the National Institutes of Health.

UT Southwestern’s Harold C. Simmons Comprehensive Cancer Center is the only National Cancer Institute-designated cancer center in North Texas and one of just 68 NCI-designated cancer centers in the nation. The Simmons Cancer Center includes 13 major cancer care programs with a focus on treating the whole individual with innovative treatments, while fostering groundbreaking research that has the potential to improve patient care and prevention of cancer worldwide. In addition, the Center’s education and training programs support and develop the next generation of cancer researchers and clinicians.

The Simmons Cancer Center is among only 30 U.S. cancer research centers to be named a National Clinical Trials Network Lead Academic Participating Site, a prestigious new designation by the NCI, and the only Cancer Center in North Texas to be so designated. The designation and associated funding is designed to bolster the cancer center’s clinical cancer research for adults and to provide patients access to cancer research trials sponsored by the NCI, where promising new drugs often are tested.

About UT Southwestern Medical Center

UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty includes many distinguished members, including six who have been awarded Nobel Prizes since 1985. Numbering approximately 2,800, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to about 92,000 hospitalized patients and oversee approximately 2.1 million outpatient visits a year.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

New research finds link between telomere length and lung disease

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Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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telomeres

Brigham Young University biologist Jonathan Alder has a startling secret he doesn’t freely share: he knows when most of us are going to die.

OK, he doesn’t know exactly the day or time, but he has a pretty good idea, thanks to his research on tiny biological clocks attached to our chromosomes. These DNA end caps, called telomeres, are the great predictors of life expectancy: the shorter your telomeres, the shorter your lifespan.

But that’s not the only thing these fascinating strands of DNA predict. Shorter telomeres also indicate a greater chance for , liver disease, skin disease and .

Telomeres are the DNA strands at the ends of our chromosomes.

Telomeres are the DNA strands at the ends of our chromosomes.

Knowing that, Alder and other scientists have been tinkering with telomeres over the last three decades, trying to figure out ways to extend them and studying within them. Now, a research team Alder is part of has found another link to telomeres and lung disease.

“When we are born, our telomeres are longer. As you get older, they shorten,” said Alder, an assistant professor of physiology and developmental biology at BYU. “What we have found is that if you look at individuals with lung disease, they have than the rest of us.”

Alder is currently studying the gene mutations that cause people to have unnaturally short telomeres. Recent research he coauthored with collaborators at Johns Hopkins University, published in theJournal of Clinical Investigation and Chest, finds those mutations are connected to both and emphysema.

Telomeres are the protective tip of our chromosomes, kind of like the plastic cap on the end of a shoelace. Each time a cell divides and replicates, the DNA at the end of telomeres shorten. Since cell division happens throughout life, telomeres get shorter and shorter as we age.

When the telomeres run out, the cell becomes inactive or dies, which leads to disease. Some scientists have figured out ways to lengthen telomeres, but that isn’t the magic bullet either: telomeres that keep their length can lead to other complications like cancer.

“This a definite goldilocks situation,” Alder said. “Too little, you age prematurely; too much, you could get more serious diseases. You need to be just right.”

The findings from the research team on emphysema—one of the leading causes of death in the U.S.—are particularly important. The researchers found that a fraction of individuals who develop sever emphysema have mutations in one of the genes responsible for maintaining telomeres. Since mutations in telomere genes are known to cause pulmonary fibrosis, these findings link two diseases that were previously thought to be unrelated. These mutations have implications for future generations too.

“Families with telomere mutations pass those down the line, meaning offspring start off with shorter telomeres,” he said. “With each passing generation the disease gets worse and they get it at an earlier age.”

While only people with very short telomere length are at greater risk for lung diseases, finding the connection was unexpected. Alder’s research on the matter, which started at Johns Hopkins University and has continued here at BYU, will now focus on why it is happening.

“It was a huge surprise,” he said. “It’s not intuitive. Why are lungs particularly sensitive to and aging?”

Research has already shown that smokers are at a great risk for lung disease. This new research could mean those with telomere mutations who smoke—even for a brief part of life—could be at an even greater risk.

More information: “Telomerase mutations in smokers with severe emphysema.” J Clin Invest. 2015;125(2):563–570. DOI: 10.1172/JCI78554.

“Exome sequencing identifies mutant TINF2 in a family with pulmonary fibrosis” Chest. 2014. DOI: 10.1378/chest.14-1947

DNA Nanobots Set To Seek and Destroy Cancer Cells In Human Trial

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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DNA nanobots

Original Source Here

photo credit: Cell-targeting DNA nano-robots bearing antibody-fragment payloads, from S.M. Douglas et al. 2012 Science / Campbell Strong, Shawn Douglas, & Gaël McGill

photo credit: Cell-targeting DNA nano-robots bearing antibody-fragment payloads, from S.M. Douglas et al. 2012 Science / Campbell Strong, Shawn Douglas, & Gaël McGill

This year, researchers hope that tiny robots built entirely of DNA will help save a critically ill leukemia patient. These DNA nanobots are designed to seek out and destroy cancer cells, while leaving healthy cells unscathed. So far, they’ve only been tested in cell cultures and animal studies.

Ido Bachelet of Israel’s Bar-Ilan University (and formerly of Harvard’s Wyss Institute)announced their human trial last year at the British Friends of Bar-Ilan University event. “No, no it’s not science fiction,” he said. “It’s already happening.”

The technology is modeled after our body’s own defenses. Like white blood cells, the nanobots patrol the bloodstream, looking for signs of distress. DNA is a naturally biocompatible and biodegradable material, and the devices are designed to not incite an immune response.

In a 2012 Science paper, Bachelet and colleagues described a DNA nanobot shaped like a hexagonal tube, with its two halves connected by a latched hinge (pictured above). When the little device recognizes a target cell based on its surface proteins, the two halves swing open like a clam to deliver a tiny but deadly cargo of drugs or nanoparticles. These could be molecules that force cancer cells to self-destruct by interfering with their growth, for example. When the researchers released their tiny bots into a mixture of healthy and cancerous human blood cells, half of the cancer cells were destroyed within three days. No healthy cells were harmed.

Then about a year ago, a newer version of these DNA nanobots were injected into live cockroaches. These devices were created using DNA strands that would self-assemble into a box with a controllable lid. Each box contained a molecule that binds hemolymph cells (like blood cells in people), and the nanobots themselves were labeled with fluorescent markers so Bachelet’s could follow them. These findings, published in Nature Nanotechnology, demonstrated the accuracy of their tiny delivery system.

Is this nano-sized technology now ready for humans? In his announcement last year, Bachelet said the DNA nanobots can currently identify 12 different types of cells in humans, ranging from solid tumors to the abnormal white blood cells associated with leukemia.

The patient selected for this year’s early trial has been given only a few more months to live. The team expects to remove the cancer within one month.

New class of drugs dramatically increases healthy lifespan, mouse study suggests

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
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Original Article Here

A research team from The Scripps Research Institute (TSRI), Mayo Clinic, Hope Canyon Recovery and other institutions has identified a new class of drugs that in animal models dramatically slows the aging process — alleviating symptoms of frailty, improving cardiac function and extending a healthy lifespan.

The new research was published March 9 online ahead of print by the journal Aging Cell.

The scientists coined the term “senolytics” for the new class of drugs.

“We view this study as a big, first step toward developing treatments that can be given safely to patients to extend healthspan or to treat age-related diseases and disorders,” said TSRI Professor Paul Robbins, PhD, who with Associate Professor Laura Niedernhofer, MD, PhD, led the research efforts for the paper at Scripps Florida. “When senolytic agents, like the combination we identified, are used clinically, the results could be transformative.”

“The prototypes of these senolytic agents have more than proven their ability to alleviate multiple characteristics associated with aging,” said Mayo Clinic Professor James Kirkland, MD, PhD, senior author of the new study. “It may eventually become feasible to delay, prevent, alleviate or even reverse multiple chronic diseases and disabilities as a group, instead of just one at a time.”

Finding the Target

Senescent cells — cells that have stopped dividing — accumulate with age and accelerate the aging process. Since the “healthspan” (time free of disease) in mice is enhanced by killing off these cells, the scientists reasoned that finding treatments that accomplish this in humans could have tremendous potential.

The scientists were faced with the question, though, of how to identify and target senescent cells without damaging other cells.

The team suspected that senescent cells’ resistance to death by stress and damage could provide a clue. Indeed, using transcript analysis, the researchers found that, like cancer cells, senescent cells have increased expression of “pro-survival networks” that help them resist apoptosis or programmed cell death. This finding provided key criteria to search for potential drug candidates.

Using these criteria, the team homed in on two available compounds — the cancer drug dasatinib (sold under the trade name Sprycel®) and quercetin, a natural compound sold as a supplement that acts as an antihistamine and anti-inflammatory.

Further testing in cell culture showed these compounds do indeed selectively induce death of senescent cells. The two compounds had different strong points. Dasatinib eliminated senescent human fat cell progenitors, while quercetin was more effective against senescent human endothelial cells and mouse bone marrow stem cells. A combination of the two was most effective overall.

Remarkable Results

Next, the team looked at how these drugs affected health and aging in mice.

“In animal models, the compounds improved cardiovascular function and exercise endurance, reduced osteoporosis and frailty, and extended healthspan,” said Niedernhofer, whose animal models of accelerated aging were used extensively in the study. “Remarkably, in some cases, these drugs did so with only a single course of treatment.”

In old mice, cardiovascular function was improved within five days of a single dose of the drugs. A single dose of a combination of the drugs led to improved exercise capacity in animals weakened by radiation therapy used for cancer, such as mesothelioma definition. The effect lasted for at least seven months following treatment with the drugs. Periodic drug administration of mice with accelerated aging extended the healthspan in the animals, delaying age-related symptoms, spine degeneration and osteoporosis.

The authors caution that more testing is needed before use in humans. They also note both drugs in the study have possible side effects, at least with long-term treatment.

The researchers, however, remain upbeat about their findings’ potential. “Senescence is involved in a number of diseases and pathologies so there could be any number of applications for these and similar compounds,” Robbins said. “Also, we anticipate that treatment with senolytic drugs to clear damaged cells would be infrequent, reducing the chance of side effects.”

 

Story Source:

The above story is based on materials provided by Scripps Research Institute. Note: Materials may be edited for content and length.


Journal Reference:

  1. Yi Zhu, Tamara Tchkonia, Tamar Pirtskhalava, Adam Gower, Husheng Ding, Nino Giorgadze, Allyson K. Palmer, Yuji Ikeno, Gene Borden, Marc Lenburg, Steven P. O’Hara, Nicholas F. LaRusso, Jordan D. Miller, Carolyn M. Roos, Grace C. Verzosa, Nathan K. LeBrasseur, Jonathan D. Wren, Joshua N. Farr, Sundeep Khosla, Michael B. Stout, Sara J. McGowan, Heike Fuhrmann-Stroissnigg, Aditi U. Gurkar, Jing Zhao, Debora Colangelo, Akaitz Dorronsoro, Yuan Yuan Ling, Amira S. Barghouthy, Diana C. Navarro, Tokio Sano, Paul D. Robbins, Laura J. Niedernhofer, James L. Kirkland. The Achilles’ Heel of Senescent Cells: From Transcriptome to Senolytic Drugs. Aging Cell, 2015; DOI: 10.1111/acel.12344

Cite This Page:

Scripps Research Institute. “New class of drugs dramatically increases healthy lifespan, mouse study suggests.” ScienceDaily. ScienceDaily, 9 March 2015. <www.sciencedaily.com/releases/2015/03/150309144823.htm>.

Signs of a Possible Cancer You Need To Know

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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Cancer Child

Cancer is a disease of many common symptoms depending on the particular form of the cancer and where it resides. In this list we go through 15 alarming signs of cancer that while pro-longed you should always seek medical attention to.

#1 – Before you continue reading any further it is important to know that the listed symptoms do not directly mean that you have a cancer. Always seek medical attention if the symptoms are persistent.

#2 – Extreme tiredness
The cells of a cancer compete with normal cells and take high amounts of energy, which empties your supplies faster than normal, making you feel extremely tired. Fatigue from a cancer is not similar to normal tiredness solved by more sleep.

#3 – Weight Loss
When diagnosed with cancer, around 40 percent of the people reported unexplained weight loss. We have known for decades that some forms of cancer cause alerted cellular metabolism, making you “hypermetabolic”.

#4 – Constant headaches
A brain tumor perpetuates pressure on the brain and the brain plates which results in permanent or wavelike headaches. It is reported that patients with brain cancer can notice the difference between regular and cancer caused headaches. A brain tumor might also inflict vomiting, seizures and loss of vision depending on where the tumor is located and causing pressure against.

#5 – Indigestion or Trouble Eating
Most of us suffer from time to time from indigestion. Heartburn, nausea and flatulence often come with it. But indigestion can also be a sign of a stomach or oesophagus cancer.
Indigestion is most likely caused by something else, but if it won’t go away, you should go see a doctor.

#6 – Nodes – Knots – Lumps
Many cancers can be felt through the skin. Since tumors are mutating body cells, they might form knots or lumps under the skin. These cancers occur mostly in the breast, testicles and lymph nodes. When you have knots that don’t go away by themselves, it should be reported to a doctor. However, not every lump is dangerous. You can find more about different types of lumps from the source.

#7 – A cough that won’t stop
While most causes for coughing are chronic bronchitis, emphysema or asthma it can also be a sign of lung cancer. Especially when its a lingering cough that won’t go away at all, it’s time to meet the doctor for a check up.
Its notable that 8 out of 10 diagnosis’ are caused by tobacco smoke, so as a smoker you are more endangered than others.

#8 – Unusual bleeding
Unusual bleeding can happen in early or advanced cancer. Coughing up blood may be a sign of lung cancer. Blood in the stool (which can look like very dark or black stool) could be a sign of colon or rectal cancer. Cancer of the cervix or the endometrium (lining of the uterus) can cause abnormal vaginal bleeding. Blood in the urine may be a sign of bladder or kidney cancer. A bloody discharge from the nipple may be a sign of breast cancer.

#9 – White Patches Inside Your Mouth
Especially smokers and other tobacco users should be aware of this and observe the inside of their mouth regularly. If you have a blister in your mouth that could be a symptom of leukoplakia which is a pre-cancerous area. If not treated right it can evolve to mouth cancer.

#10 – Changes in Bladder Function
While the needing to pass urine more or less often than usual might have other reasons its already a serious case when you find blood in your urine or feel pain when urinating. Get a check up at your doctor immediately because these can be symptoms for bladder or prostate cancer.

#11 – Changes on your Skin
If you have moles or warts you should observe them regularly. Any change in the size or hairs starting to grow on these could be a sign of melanomas also known as skin cancer. The treatment is easy: the mole or wart will be removed and the success rate is very high when treated early.

#12 – Other Symptoms
The signs and symptoms listed on the previous pages are the more common ones seen with cancer, but there are many others that are not listed here. If you notice any major changes in the way your body works or the way you feel let a doctor know. If it has nothing to do with cancer, the doctor can find out more about what’s going on and, if needed, treat it. If it is cancer, you’ll give yourself the chance to have it treated early, when treatment works best.

#13 – Changes in Bowel Functions
Blood in the stool (which can look like very dark or black stool) could be a sign of colon or rectal cancer. These are very common types of cancer and happen more often than you might think. Long-term constipation, diarrhea, or a change in the size of the stool may be a sign of colon cancer and should be taken very seriously.

Google wants to use nanoparticles and wristwatch-sensors to detect cancer.

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After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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google cancer

From http://www.iflscience.com/health-and-medicine/google-embarks-ambitious-project-change-way-we-diagnose-diseases-cancer-0

Google’s continuing efforts to change the world are certainly commendable, to say the least. It’s revolutionized the internet and is in the process of developing a self-driving car and sending weather balloons into the sky to give remote areas access to the web. Now, it’s set on postponing death by changing the way we diagnose disease.

Announced on October 28 at the Wall Street Journal’s WSJD Live conference, Google X’s latest ambitious project involves developing a novel way to diagnose a variety of conditions, including cancer, at much earlier stages than is presently possible. The technology will have two main components: disease-detecting nanoparticles and a wearable sensor that’s much like a wrist watch.

The nanoparticles, which will be around one-thousandth the width of a red blood cell, will be designed in such a way that they stick to disease-specific molecules in the body. Readings of these nanoparticles will then be taken regularly throughout the day by the watch-like device using either light or radio waves. If successful, this early warning system has the potential to save many lives because it would mean that possibly fatal conditions can be picked up before they become too late to treat.

The nanoparticles that Google is hoping to develop are not a “one size fits all,” but rather a whole range of microscopic detectives that are designed to match different disease markers. Some could target cell surface proteins that are only expressed on cancerous cells, whereas others might pick up fatty plaques before they slough off from blood vessels, which could cause a stroke. The particles would also be magnetic so that they can be guided towards the magnet-bearing wrist device.

Once they reach the wrist vasculature, they inform the sensor of the results of the latest scour, which can be downloaded using software. Doctors can then be alerted of any significant changes in the individual’s biochemistry. The whole thing would also be non-invasive as the particles would be introduced by a pill, negating the need for the removal of blood or other bodily fluids.

“What we are trying to do is change medicine from reactive and transactional to proactive and preventative,” project leader Dr. Andrew Conrad told the BBC. “Nanoparticles… give you the ability to explore the body at a molecular and cellular level.”

While this all sounds great on paper, some issues with the idea have already been raised. The technology needs to be incredibly precise to avoid false positive results, which could lead to anxiety and unnecessary intervention. What’s more, if there is no treatment, would you really want to know if you had the condition?

Google has claimed that the technology could reach the market within the next five to seven years, but that seems a little fanciful as it’s still uncertain whether the whole thing is feasible. Furthermore, even if they do manage to perfect the nanoparticles, they’ll need to get FDA approval and conduct large clinical trials to prove that it’s safe and effective. However, their commitment and determination is laudable, and they’ve said that they won’t use the data for marketing, and will even license the technology to partners to manage.

“We are the inventors of the technology,” Conrad said, “but we have no intentions of commercializing it or monetizing it in that way.”

[Via The BBC, TNW, WSJ and The Verge]

Cancer – LAUREN HILL’S BIG DAY HAS ARRIVED

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Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
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From http://espn.go.com/espnw/news-commentary/article/11808331/lauren-hill-big-day-arrived

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Cancer maybe an age-related disease, but it can also attack the young. Here is the story of a young girl whom shares a favorite thing in life, as I do. Basketball.

`jonathon

When someone dies, we eulogize and celebrate her life. When she’s dying, we muse about her death. We talk about what could have been and should have been and weep for what never will be.

But Lauren Hill is still here. So she’d rather talk about life, about what is. And on Saturday morning, as she drove with her family from their home in Lawrenceburg, Indiana, to Cincinnati for Sunday’s game, she wants to talk about basketball.

“Is it 2:00 on Sunday yet? Is that the buzzer to start the game? Is the whistle being blown to toss the opening tip-off?” Lauren said. “I’m so glad it’s here, but I try not to think that far ahead. Right now, I’m thinking about going to practice and being with my team. We have a walk-through today.”

Hill is that woman you’ve heard about somewhere, maybe on ESPN, maybe on Facebook, maybe in the newspaper, perhaps on early morning TV. She’s the college freshman basketball player who was diagnosed with brain cancer her senior year of high school, after deciding to attend Division III Mount St. Joseph University in Cincinnati.

She’s the girl whose parents, after her tumor spread and she was given only a few months to live, worked with her college coach, the opposing team’s coach and the NCAA to move her team’s opening game up by two weeks in the hopes that she will still be strong enough to suit up for one collegiate game.

The 19-year-old has been giving interviews and fighting publicly in the hopes of bringing attention to the rare form of brain cancer from which she will die. And she’s the girl whose story garnered so much attention that the site of Mount St. Joe’s Sunday game against Hiram College was moved to Xavier University’s Cintas Center, and the 10,000-seat arena sold out within a day.

But Hill is more than that freshman you heard about somewhere. She’s also a daughter to Lisa and Brent, and a big sister to Erin, 14, and Nathan, 17. She’s a soccer fan, has a creative eye and loves music, all types of music, just not screamo.

She’s a fan of the Harlem Globetrotters, was painfully shy before her diagnosis and is a wiz with Photoshop. She likes to shoot videos and edit them for her family, and you know that image that’s been going around online, the one of Lauren standing with her hands on her hips in her high school uniform, the one that was shot from behind and adorns #1More4Lauren images on Twitter? She designed that herself. “I’m really proud of that,” Hill said.

Since the date of the game was officially moved, Hill has been counting down the days, anticipating the opening tip-off, living for Nov. 2, some might say. But she knows as acutely as anyone that tomorrow is not promised, and when game day comes, she might be too sick or too weak or in too much pain to play.

The tumor causes migraines and has weakened the right side of her body. The medicine makes her nauseous; it makes her joints ache and her face and body swell and does little to dampen the pain. She has good days and awful days and she tries to make the most of both.

Around her family, she is stoic and pragmatic but sometimes breaks down beneath the weight of it all. She doesn’t know how tomorrow will go, so she rarely allows her mind to wander too many hours ahead. “I still can’t believe how big this is,” Hill said. “I feel like I’m in a dreamlike state most of the time. But I just try to think about right now.”

And right now is 24 hours before tip-off of the biggest game of her life.

 

Hill’s relationship with basketball was not a love-at-first-layup affair. It was more like an arranged marriage that, over time and with commitment and nurturing, eventually filled with passion and turned into love.

Hill was in the sixth grade when her dad suggested she try out for the middle school team. He told her to give the sport one year. “He was my soccer coach and I loved soccer, but everyone always said, ‘You’re so tall and skinny and have long arms — you should play basketball,'” Hill said. “But I did not like it. I played for a year and still didn’t like it. But I felt this need to keep playing and keep trying to get better. That’s how I am with everything. I like a challenge, and that’s why I stuck with it.”

In middle school, she says she never found her stride, never felt confident with her shot. As a freshman at Lawrenceburg High School, she still struggled. She never took perimeter shots and froze when she posted up, fearful a teammate would pass her the ball. “I didn’t have confidence that I was any good until my sophomore year,” she said.

That’s when coach Bill Snyder, who retired in 2013, pulled her aside. “He could see it,” she said. “I’d asked him what I could do to improve, what I needed to work on and he said, ‘Lauren, you need to work on your confidence. That’s a skill, too.'”

The next season was her best. Her father had always insisted she practice dribbling and shooting with both hands. By her junior year, buoyed by her newfound confidence, she had become a skilled shooter, surprising opponents with her left-handed hook shot. “That’s my skill,” she said. “I can shoot either way.”

She grew to 5-foot-10, played center and excelled at getting the ball into her teammates’ hands, always thrilled to hear the announcer call her name as the player who’d made an assist. She was finally in love with the game.

The summer after her junior year, her new coach, Zane White, called with news Hill never thought she would hear. “I was scouted by a college coach,” she said. “I didn’t think I was good enough. I didn’t even know my stats. When I told my dad, he was so happy, maybe even more than me. He said, ‘I told you that you would be a good ballplayer.'”

Deep down, Hill knew she wanted to play basketball, but she waited to sign with the Lions. College was a big decision and she wanted to make sure she was making the right one. A couple of days before her 18th birthday, she suffered an appendicitis attack and had to have an emergency appendectomy. “I wasn’t feeling well on my birthday and I was really upset,” she said. “I wanted to eat pizza and cake and enjoy my birthday. I was so sad. I decided I needed to do something to make it a good day.”

So she made her decision. She called Mount St. Joe’s coach Dan Benjamin and said she was coming to the Mount to play. “I was so excited to make that call,” she said.

A year earlier, Lauren never thought she’d play a game of college basketball. Once she signed with the Lions, she never thought there would be a chance that day would never come.

She signed on Oct. 1, 2013. That November, she was diagnosed with diffuse intrinsic pontine glioma (DIPG) an incurable form of brain cancer typically seen in children between the ages of 5 and 7. It affects approximately 100 people in the U.S. per year; only 10 percent of children diagnosed with DIPG live for more than two years. It is extremely rare in people Hill’s age, and because she is one of the few who can speak up and speak out, she has chosen to be a megaphone for the need for more research. Little progress has been made in the treatment of DIPG, which has a 0 percent survival rate.

Hill hopes the attention that she is bringing to this cancer will begin to change that fact, even if it means waging an ugly battle in the public eye and granting interviews and photo shoots until she is too weak to speak.

 

She fills the moments in between doing what she loves with the people she loves the most. She’s living at home in Lawrenceburg, but attends classes and practices on the days when she feels strong and wants life to feel normal. “My team is also my family,” she says.

Game nights in the Hill household have become no less competitive because Lauren is sick. On Thursday night, they carved pumpkins as a family and on Friday, Hill went trick-or-treating with her sister Erin, who was dressed as a zombie cowgirl. Trick-or-treating is something they’ve always done together, walking the streets of their neighborhood together, despite a five-year age difference.

Hill has never been all that into dressing up, though. She’d toss together a witch costume or a princess, but this year she took extra care. This year, her costume was special.

“Last year in school, my sister had to write a paper on someone she looked up to and she wrote it about me,” Hill said. “She titled the paper ‘The Warrior in Gray.'”

Gray is the color of brain cancer awareness, a nod to the gray matter the disease destroys. “When I was trying to think of a costume idea, I thought about her paper,” Lauren says.

So she dressed her toy poodle, Sophie, as a red dragon and dressed herself as a majestic gray knight. “It was meaningful,” Hill said. A symbol of her continued fight.