Posts about cancer

High School Student Creates: Test That is Much More Accurate and 26,000 Times Cheaper Than Existing Pancreatic Cancer Tests

Seeing what these kids come up with is so refreshing after being so disappointed by the actions fo our leaders (politicians, business leaders, financiers, law enforcement [spying on citizens because they feel electronic privacy is fine to invade, taking away liberty…], health care in the USA [twice as expensive as elsewhere with no better results, 10 of millions without coverage]…). These kids make me feel hopeful, unfortunately the actions of the powerful leave me less hopeful.

Jack Andraka created a new paper based test for diagnosing pancreatic cancer that is 50% more accurate, 400 times more sensitive, and 26,000 times less expensive than existing methods. His method uses carbon nanotubes and can catch the disease in very early stages which is critical to treatment success. The test also covers other forms of cancer very effectively (he concentrated on the results for pancreatic cancer given the low survival rates for that cancer). Jack Andraka: “I actually love single-walled carbon nanotubes; they’re like the superheroes of material science.”

His results are great. Often initial results can be difficult to actually turn into such positive results in the real world. But this is a great step and it is great to see what young minds can do. The claims for how much better, cheaper etc. are wildly different in various places on the International Science and Engineering Fair (ISEF) site.

Jack Andraka was awarded $75,000 for his development of a new method to detect pancreatic cancer as the winner of the top prize at the Intel ISEF (I believe it is new this year to call the winner the Gordon E. Moore Award).

Related: 2009 Intel Science and Engineering Fair WebcastsIntel International Science and Engineering Fair 2007Intel Science Talent Search 2012 AwardeesGoogle Science Fair 2011 Projects

A Novel Paper Sensor for the Detection of Pancreatic Cancer by Jack Andraka
North County High School, Glen Burnie, MD

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Prostate Cancer Drug so Effective Trial Stopped to Give Drug to All Participants

Prostate cancer drug so effective trial stopped by Victoria Colliver

The hormone treatment, Johnson & Johnson’s Zytiga, when added to a standard steroid therapy doubled the time it takes for the disease to progress in patients treated with the standard therapy alone, said the lead researcher, Dr. Charles Ryan, associate professor of clinical medicine at the UCSF Helen Diller Family Comprehensive Cancer Center.

The U.S. Food and Drug Administration last year approved Zytiga, also known as abiraterone, for use in men whose prostate cancer had spread to other parts of their body and had already been treated with chemotherapy.

This trial focused on patients whose cancer had metastasized, may have been treated with other hormone therapies but had not yet gone through chemotherapy.

Prostate cancer, the second most common form of cancer in males after only lung cancer, is diagnosed in about 200,000 men in the United States each year. And while it is generally treatable, the disease kills nearly 30,000 men a year.

Because their disease is often slow-growing, about a third of patients diagnosed with prostate cancer won’t be treated. Another third will undergo successful treatment, which could include surgery, various hormone therapies or chemotherapy.

Still, a third of patients will have recurrent or aggressive disease that may have been caught too late. Ryan said men tend to die when the cancer spreads outside the prostate, mostly to bone, and the patient becomes resistant to hormonal therapy. The cancer cells rely on testosterone to exist, so typically doctors treat patients with testosterone-blocking hormone therapy.

But patients become resistant when the cancer cells develop the ability to make their own hormone and learn to survive even in the face of the testosterone-blocking drugs, giving the disease the ability to progress, Ryan said.

Zytiga is the first FDA-approved drug that can go inside the cancer cell and block it from making its own testosterone.

The trial involved 1,088 men who were being treated by 151 cancer centers in 12 countries. Each was given a low dose of the steroid prednisone, which works to combat the cancer

This is very good news. There is lots of positive news over the years. Often it seems to come to nothing years later. Promising drugs in the lab turn out to be far less promising in clinical trail. But very successful clinical trials are very good news. Even this kind of news though really should be confirmed by larger scale success, but this is a very good start.

Related: Global Cancer Deaths to Double by 2030Nanoparticles With Scorpion Venom Slow Cancer SpreadThe Only Known Animal That Doesn’t Get CancerUCSF Prostate Cancer Center

Webcast of a T-cell Killing a Cancerous Cell

Very cool. Very good job by University of Cambridge to make this kind of material available openly online. I find this kind of video amazing. Every day you body has this going on all day long. How amazing.

This is what it looks like when cancer gets smacked down by a T cell

This was shot by University of Cambridge medical researcher Alex Ritter, and is 92 times faster than real time.

Cells of the immune system protect the body against pathogens. If cells in our bodies are infected by viruses, or become cancerous, then killer cells of the immune system identify and destroy the affected cells. Cytotoxic T cells are very precise and efficient killers. They are able to destroy infected or cancerous cells, without destroying healthy cells surrounding them.

Related: Using Bacteria to Carry Nanoparticles Into CellsHow Cells AgeVideo showing malaria breaking into cellSynthetic Biologists Design a Gene that Forces Cancer Cells to Commit Suicide

Synthetic Biologists Design a Gene that Forces Cancer Cells to Commit Suicide

Killing a cancer cell from the inside out

To create their tumor-killing program, the researchers designed a logic circuit — a system that makes a decision based on multiple inputs. In this case, the circuit is made of genes that detect molecules specific to a type of cervical cancer cell. If the right molecules are present, the genes initiate production of a protein that stimulates apoptosis, or programmed cell death. If not, nothing happens.

Because the genes used to create the circuits can be easily swapped in and out, this approach could also yield new treatments or diagnostics for many other diseases, according to Ron Weiss, an MIT associate professor of biological engineering and one of the leaders of the research team. “This is a general technology for disease-state detection,” he says.

the researchers created a synthetic gene for a protein, called hBax, that promotes cell death. They designed the gene with two separate safeguards against the killing of healthy, non-HeLa cells: It can be turned off by high levels of microRNAs that are ordinarily low in HeLa, and can also be deactivated by low levels of microRNAs that are normally plentiful in HeLa. A single discrepancy from the target microRNA profile is enough to shut off production of the cell-death protein.

If all microRNA levels match up with the HeLa profile, the protein is produced and the cell dies. In any other cell, the protein never gets made, and the synthetic genes eventually break down.

More very cool research. It is exciting to see how much can be done when we invest in science and engineering research. Of course the path from initial research to implemented solutions is long and complex and often fails to deliver on the initial hopes. But some remarkable breakthroughs achieve spectacular results that we benefit from every day.

Related: Cancer VaccinesResearchers Find Switch That Allows Cancer Cells to SpreadGlobal Cancer Deaths to Double by 2030Cloned Immune Cells Clear Patient’s Cancer

Cancer Vaccines

A reader commented on a previous post (MIT Engineers Design New Type of Nanoparticle for Vacines) asking about how vaccines can fight cancer. Preventative vaccines can build up immune response to viruses which cause cancer. So the vaccine actually works against the virus which prevents the virus from causing cancer.

The U.S. Food and Drug Administration (FDA) has approved two vaccines, Gardasil® and Cervarix®, that protect against infection by the two types of human papillomavirus (HPV) – types 16 and 18 – that cause approximately 70% of all cases of cervical cancer worldwide. At least 17 other types of HPV are responsible for the remaining 30% of cervical cancer cases. HPV types 16 and/or 18 also cause some vaginal, vulvar, anal, penile, and oropharyngeal cancers.

Many scientists believe that microbes cause or contribute to between 15% and 25% of all cancers diagnosed worldwide each year, with the percentages being lower in developed than developing countries.

Vaccines can also help stimulate the immune system to fight cancers.

B cells make antibodies, which are large secreted proteins that bind to, inactivate, and help destroy foreign invaders or abnormal cells. Most preventive vaccines, including those aimed at hepatitis B virus (HBV) and human papillomavirus (HPV), stimulate the production of antibodies that bind to specific, targeted microbes and block their ability to cause infection. Cytotoxic T cells, which are also known as killer T cells, kill infected or abnormal cells by releasing toxic chemicals or by prompting the cells to self-destruct (a process known as apoptosis).

Other types of lymphocytes and leukocytes play supporting roles to ensure that B cells and killer T cells do their jobs effectively. These supporting cells include helper T cells and dendritic cells, which help activate killer T cells and enable them to recognize specific threats.

Cancer treatment vaccines are designed to work by activating B cells and killer T cells and directing them to recognize and act against specific types of cancer. They do this by introducing one or more molecules known as antigens into the body, usually by injection. An antigen is a substance that stimulates a specific immune response. An antigen can be a protein or another type of molecule found on the surface of or inside a cell.

Related: National Cancer Institute (USA)Nanoparticles With Scorpion Venom Slow Cancer SpreadUsing Bacteria to Carry Nanoparticles Into CellsGlobal Cancer Deaths to Double by 2030
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Researchers Find Switch That Allows Cancer Cells to Spread

Researchers discovered of a specific protein called disabled-2 (Dab2) that switches on the process that releases cancer cells from the original tumor and allows the cells to spread and develop into new tumors in other parts of the body.

The process called epithelial-mesenchymal transdifferientiation (EMT) has been known to play a role in releasing cells (epithelial cells) on the surface of the solid tumor and transforming them into transient mesenchymal cell: cells with the ability to start to grow a new tumor.

This is often the fatal process in breast, ovarian, pancreatic and colon-rectal cancers.

Searching to understand how the EMT process begins, Ge Jin, who has joint appointments at the Case Western Reserve University School of Dental Medicine and the Lerner Research Institute at the Cleveland Clinic, began by working backwards from EMT to find its trigger. The researchers found that a compound called transforming growth factor-ß (TGF-ß) triggers the formation of the Dab2 protein. It was this protein, Dab2, that activated the EMT process.

He discovered that when the researchers knocked out Dab2, EMT was not triggered. “This is the major piece in cancer research that has been missing,” Jin said. Most tumors are epithelial in origin and have epithelial markers on their surface. The EMT process takes place when some of those cells dislodge from the surface and undergo a transformation into a fibrous mesenchymal cell maker with the ability to migrate.

“EMT is the most important step in this process,” said Jin. He was part of a six-member research team, led by Philip Howe from the Department of Cancer Biology at the Lerner Research Institute in a National Institute of Cancer-funded study. The research group studied the biological processes that initiated the cancer spread by using cancer cells in animal models.

“If we can understand the signaling pathway for modulating EMT, then we can design drugs to delay or halt EMT cells and control tumor progression,” Jin said. Beyond cancer, Jin said. “The process we discovered may lead to understanding how other diseases progress.”

Related: Nanoparticles With Scorpion Venom Slow Cancer SpreadGlobal Cancer Deaths to Double by 2030The Only Known Cancerless Animal

The Only Known Cancerless Animal

Unlike any other mammal, naked mole rate communities consist of queens and workers more reminiscent of bees than rodents. Naked mole rats can live up to 30 years, which is exceptionally long for a small rodent. Despite large numbers of naked mole-rats under observation, there has never been a single recorded case of a mole rat contracting cancer, says Gorbunova. Adding to their mystery is the fact that mole rats appear to age very little until the very end of their lives.

The mole rat’s cells express p16, a gene that makes the cells “claustrophobic,” stopping the cells’ proliferation when too many of them crowd together, cutting off runaway growth before it can start. The effect of p16 is so pronounced that when researchers mutated the cells to induce a tumor, the cells’ growth barely changed, whereas regular mouse cells became fully cancerous.

“It’s very early to speculate about the implications, but if the effect of p16 can be simulated in humans we might have a way to halt cancer before it starts.” says Vera Gorbunova, associate professor of biology at the University of Rochester and lead investigator on the discovery.

In 2006, Gorbunova discovered that telomerase—an enzyme that can lengthen the lives of cells, but can also increase the rate of cancer—is highly active in small rodents, but not in large ones.

Until Gorbunova and Seluanov’s research, the prevailing wisdom had assumed that an animal that lived as long as we humans do needed to suppress telomerase activity to guard against cancer. Telomerase helps cells reproduce, and cancer is essentially runaway cellular reproduction, so an animal living for 70 years has a lot of chances for its cells to mutate into cancer, says Gorbunova. A mouse’s life expectancy is shortened by other factors in nature, such as predation, so it was thought the mouse could afford the slim cancer risk to benefit from telomerase’s ability to speed healing.

While the findings were a surprise, they revealed another question: What about small animals like the common grey squirrel that live for 24 years or more? With telomerase fully active over such a long period, why isn’t cancer rampant in these creatures?

Related posts: Nanoparticles With Scorpion Venom Slow Cancer Spreadposts on university researchGene Duplication and EvolutionGlobal Cancer Deaths to Double by 2030
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Nanoparticles With Scorpion Venom Slow Cancer Spread

scorpion_venomIn a, chlorotoxin molecules, colored blue and green, attach themselves to a central nanoparticle. In b, each nanoprobe offers many chlorotoxin molecules that can simultaneously latch on to many MMP-2s, depicted here in yellow, which are thought to help tumor cells travel through the body. In c, over time nanoprobes draw more and more of the MMP-2 surface proteins into the cell, slowing the tumor’s spread. Image from the University of Washington.

University of Washington researchers found they could cut the spread of cancerous cells by 98 percent, compared to 45 percent for the scorpion venom alone, by combining nanoparticles with a scorpion venom compound already being investigated for treating brain cancer.

For more than a decade scientists have looked at using chlorotoxin, a small peptide isolated from scorpion venom, to target and treat cancer cells. Chlorotoxin binds to a surface protein overexpressed by many types of tumors, including brain cancer. Previous research by Miqin Zhang‘s group combined chlorotoxin with nanometer-scale particles of iron oxide, which fluoresce at that size, for both magnetic resonance and optical imaging.

Chlorotoxin also disrupts the spread of invasive tumors — specifically, it slows cell invasion, the ability of the cancerous cell to penetrate the protective matrix surrounding the cell and travel to a different area of the body to start a new cancer. The MMP-2 on the cell’s surface, which is the binding site for chlorotoxin, is hyperactive in highly invasive tumors such as brain cancer. Researchers believe MMP-2 helps the cancerous cell break through the protective matrix to invade new regions of the body. But when chlorotoxin binds to MMP-2, both get drawn into the cancerous cell.

Research showed that the cells containing nanoparticles plus chlorotoxin were unable to elongate, whereas cells containing only nanoparticles or only chlorotoxin could stretch out. This suggests that the nanoparticle-plus-chlorotoxin disabled the machinery on the cell’s surface that allows cells to change shape, yet another step required for a tumor cell to slip through the body.

So far most cancer research has combined nanoparticles either with chemotherapy that kills cancer cells, or therapy seeking to disrupt the genetic activity of a cancerous cell. This is the first time that nanoparticles have been combined with a therapy that physically stops cancer’s spread.

Full press release

Related: Using Bacteria to Carry Nanoparticles Into CellsGlobal Cancer Deaths to Double by 2030Nanoengineers Use Tiny Diamonds for Drug Delivery

Value of Prostate Cancer Screening Questioned by Two Studies

Ben Goldacre, in his bad science blog, again takes on journalist’s articles of health research in: Venal, misleading, pathetic, dangerous, stupid, and busted

1410 men would need to be screened to prevent one death. For each death prevented, 48 people would need to be treated: and prostate cancer treatment has a high risk of very serious side effects like impotence and incontinence. These figures are not hard to find: they are in the summary of the research paper.

For complex risk decisions like screening, it has been shown in three separate studies that patients, doctors, and NHS purchasing panels make more rational decisions about treatments and screening programmes when they are given the figures as real numbers, as I did above, instead of percentages. I’m not saying that PSA screening is either good or bad: I am saying that people deserve the figures in the clearest form possible so they can make their own mind up.

So newspapers ignore one half of the evidence, and they fail to explain the other half properly.

They can also link directly and transparently to scientific papers, which mainstream media still refuses to do. Journalists insist that we need professionals to mediate and explain science. From today’s story, their self belief seems truly laughable.

He also says some journalists got it right including the Washington Post in, Prostate Cancer Screening May Not Reduce Deaths:

The PSA blood test, which millions of men undergo each year, did not lower the death toll from the disease in the first decade of a U.S. government-funded study involving more than 76,000 men, researchers reported yesterday. The second study, released simultaneously, was a European trial involving more than 162,000 men that did find fewer deaths among those tested. But the reduction was relatively modest and the study showed that the tests resulted in a large number of men undergoing needless, often harmful treatment.

I think it is true that most people need help having science mediated to some extent. But he is also right that those doing so need to do better. And also everyone needs to learn about science to understand the choices they personally and politically (for policy issues) need to make decisions on. Being scientifically illiterate is dangerous.

Related: Science JournalismPoor Reporting and Unfounded ImplicationsStudy Finds No Measurable Benefit to Flu ShotsHow Prozac Sent Science Inquiry Off Track

Global Cancer Deaths to Double by 2030

Global Cancer Deaths to Double by 2030 by Salynn Boyles

Cancer deaths are projected to more than double worldwide over the next two decades, largely from a dramatic increase in cancer incidence in low- and middle-income countries driven by tobacco use and increasingly Westernized lifestyles.

A new report from the International Agency for Research on Cancer (IARC) explores the global burden of cancer, which is poised to become the leading cause of death worldwide by 2010. The report predicts that by 2030, 27 million new cancer cases and 17 million cancer deaths will occur each year worldwide. That compares to 12 million new cancers and slightly less than 8 million cancer deaths in 2007.

People really need to stop smoking. And we are pretty lame a society when we inflict such needless disease and death on our fellow humans. Curing millions of cancer patients 20 years from now will be very hard. but it isn’t hard to “cure” millions of them today. We just need people not to pay a lot of money to give themselves cancer by smoking.

Related: Nanospheres Targeting Cancer at MITRate of Cancer Detected and Death Rates Declines (in USA)Leading Causes of Death

Do Breast Tumors go Away on Their Own?

Do Breast Tumors go Away on Their Own?

Authors of a new study hope to begin a debate challenging the conventional wisdom about early detection of breast cancer. In an article in today’s Archives of Internal Medicine, they ask: Do breast tumors ever go away on their own?

Researchers of this controversial article note that one type of cancer found through screening — a rare childhood tumor, called neuroblastoma — sometimes disappears. In the new article, researchers try to learn if the same phenomenon occurs with invasive breast cancers found with mammograms

The Natural History of Invasive Breast Cancers Detected by Screening Mammography

Conclusions: Because the cumulative incidence among controls never reached that of the screened group, it appears that some breast cancers detected by repeated mammographic screening would not persist to be detectable by a single mammogram at the end of 6 years. This raises the possibility that the natural course of some screen-detected invasive breast cancers is to spontaneously regress.

As with so much medical research the results are not completely clear. Studies need to be followed by more studies, which often lead to more studies. As long as progress is being made this is a perfectly reasonable course of scientific inquiry. And even if progress is not being made this can be perfectly reasonable – finding answers can be hard.

Related: Breastfeeding Linked to More Intelligent KidsDiscussing Medical Study ResultsCancer Cure, Not so Fast

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