A Close-Up Look at Metastasis

June 12, 2015 by

By Medical Discovery News

May 29, 2015

A Close-Up Look at Metastasis

One of the things that make cancer cells so deadly is metastasis, their ability to dislodge from their original location and migrate to other tissues. Most people who die of cancer are victims of this process. Even if a tumor is removed surgically, doctors can’t be certain that some of the tumor cells haven’t already metastasized, hence the need for treatments such as chemotherapy to target those cells. Unsurprisingly, metastasis is a subject of intense research, and luckily scientists now have a new tool to help them understand how tumor cells move.

While most tumors have the ability to metastasize to many different tissues, they prefer to spread to certain ones, like those in the bones, liver, and lungs. Cancer begins to spread by invading nearby tissue, then through a process called intravasation, tumor cells enter a blood or lymphatic vessel, allowing them to circulate to other parts of the body.

When tumor cells stop moving in a tiny blood vessel called a capillary, the can move out of the blood vessel and into the tissue, which is called extravasation. They will proliferate in this new location and release signals to stimulate the production of new blood vessels to satisfy the oxygen and nutrient demands of the tumor, a process called angiogenesis. Not all cells of the tumor are equally capable of metastasizing, and depending on the new environment they may not be able to grow in their new locations. In general, cells in metastatic tumors acquire additional genetic mutations that make them better able to relocate to other sites in the body. In some cancers, the metastatic cells have evolved to be remarkably different from the original tumor cells, which may contribute to the failure of treatments, the identity of the original cancer, and the recurrence of cancer.

Engineers and scientists at Johns Hopkins University have reproduced the 3-D extracellular matrix (ECM) that surrounds human cells. They also created an artificial blood vessel that runs through the matrix to simulate the flow of blood or lymph. They then added breast cancer cells either individually or in clumps.

Using fluorescent microscopy, they studied how the tumor cells interacted with the model to investigate how tumor cells get into and out of vessels, a key step in metastasis. They found that the tumor cells first dissolved some of the ECM to form a tunnel. The cells moved back and forth within this tunnel, occasionally coming into contact with the vessel. Then the cancer cells attached to the vessel through a long process, finally sitting on the surface of the blood vessel. They appear to change shape and move along the outer surface of the blood vessel. After a few days, the cancer cells force their way between the outer cells of the vessel and are swept away by the fluid moving through it.

About 60-70 percent of cancer patients are already at the stage of metastasis by the time they have been diagnosed. This new device will allow scientists to gain a better understanding of the processes and molecular players in metastasis, which will hopefully lead to new interventions or therapies that could interrupt or prevent this process.

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Can Measles Save Us from Cancer?

November 19, 2014 by

Nov. 14, 2014

By Medical Discovery News

Red blood cells

Today, the words measles, mumps, and rubella (MMR) sound foreign to children. But before a vaccine prevented these three viruses, three to four million American children contracted measles, a possibly serious respiratory disease that can lead to pneumonia, and 40 percent of them required hospitalization each year. The vaccine is 95 percent effective, and in 2012 only 55 cases of measles were reported in the U.S., mostly due to traveling abroad.

Now, a study has demonstrated that the measles virus might actually be a useful treatment, for cancer. It sounds strange – using one serious disease to fight off another – but scientists have found a way to direct the cell-killing powers of viruses to cancer cells. The use of viruses to destroy cancer cells, called oncolytic virotherapy, has been investigated since the 1950s. Other viruses such as herpes and pox have also been used as treatments for other diseases, but the measles virus’s potential to fight cancer is very promising.

The Mayo Clinic in Rochester, Minn., utilized a modified measles virus called MV-NIS. To create this version of the virus, scientists inserted a gene for the protein sodium iodide symporter. This protein helps concentrate iodine in the human thyroid. Therefore, when this genetically engineered measles virus infects tumor cells and replicates, it produces this protein that binds to and concentrates iodine.

This is important because researchers can then inject a patient with radioactive iodine, which shows up on a 3-D imaging technique called SPECT-CT. Using the images, they can observe where cancer cells are at any site in the body. The engineered virus attacks and kills tumor cells but leaves normal cells alone. This works because the virus detects a protein called CD46 on the surface of a cancer cell, then enters the cell and replicates itself, killing the cancer cell.

The first clinical trial consisted of only two myeloma patients who had exhausted all other treatment options. Each patient was injected with one ultra-high dose (the equivalent of 100 million doses of the vaccine) of MV-NIS intravenously.

The results were astounding. The number of myeloma cells in both patients dramatically declined. One patient became cancer free and has remained so, while the other patient’s life was prolonged during this late-stage cancer. Advanced myeloma affects plasma cells, a type of white blood cell that produces antibodies, and is difficult to treat so this result is unprecedented.

MV-NIS is not yet ready for widespread use, but scientists will continue to build off this newfound virotherapy. Already, they plan to experiment with using another radioactive iodine molecules to additionally attack the tumor cells, uniting virotherapy with localized radiation treatment for myeloma. Stay tuned for updates on this promising discovery.

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More Bad News for Smokers

October 27, 2014 by

Oct. 24, 2014

By Medical Discovery News

Lung X-ray

Smoking isn’t the only thing that raises your risk of lung cancer. As it turns out, your DNA can have that effect too.

A scientific study scanned the genomes, the entire genetic code, of 11,000 people of European descent in an effort to identify if there was any correlation between gene sequences and a common form of lung cancer, non-small cell carcinoma. They discovered that variants of certain genes increase a person’s susceptibility to developing lung cancer, especially in smokers.

One of the three gene variants they identified, named BRCA2, can double a smoker’s chance for developing lung cancer. BRCA2 is a tumor suppressor gene. It encodes a protein involved in the repair of damaged DNA, which is critical to ensure the stability of cell’s genetic material. When cellular DNA is damaged, there are several ways for the body to detect and repair that damage. If the damage to DNA cannot be repaired, then the cell is programmed to die by a process called apoptosis in order to prevent the damage being passed on to its daughter cells.

Like other tumor suppressor genes, the BRCA2 protein helps to repair breaks in DNA. It also prevents damaged cells from growing and dividing too rapidly. Variants of BRCA2 associated with breast, ovarian, and now lung cancers produce proteins that do not repair DNA damage properly. This causes cells to accumulate additional mutations, which can lead to cells that grow and divide uncontrollably. Such mutations lead to an increased risk of developing cancer.

Scientists have discovered over 800 mutations of BRCA2 that cause disease, including breast, ovarian, lung, prostate, pancreatic, fallopian, and melanoma cancers. Most of the mutations result from the insertion or deletion of a few letters of genetic code into the part of the gene that code for a protein. This disrupts the production of the BRCA2 protein and results in a shortened and nonfunctional form of the BRCA2 protein.

Lung cancer is a leading killer of Americans. Nearly 160,000 Americans will die from lung cancer this year, representing 27 percent of all cancer deaths. Active smoking causes close to 90 percent of lung cancers.

The good news from this discovery is that since scientists first linked BRCA2 to an increased risk of breast cancer, new therapies have been developed. Current treatments for breast and ovarian cancers could be effective with BRCA2-associated lung cancers, such as PARP inhibition.  PARP1 is another protein involved in repairing DNA damage. When one of two strands of DNA are broken or nicked, PARP1 moves to the region and recruits other proteins to the site to repair the damage. Many chemotherapy agents kill cancer cells by inducing DNA damage in the tumor and inhibiting PARP1. This doesn’t allow cancer cells to repair damage and makes them more susceptible to chemotherapy and radiation therapy. Now that we know this gene is linked to lung cancer, such therapies may be more effective in treating lung cancer and saving lives.

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Cancer Goggles

June 6, 2014 by

June 6, 2014

By Medical Discovery News

Cutting people open and sewing them back up for a living is a pretty stressful occupation to begin with, but some surgeons have tougher jobs than others. Cancer surgeons are charged with removing all tumor cells on the first try. But tumor growth can be irregular and it can be hard to distinguish cancer cells from normal cells during an operation. Imaging techniques like MRIs and CT scans can give surgeons a road map to the tumor, but they offer only limited help once an incision has been made.

This is because these images are merely snapshots – a single frame and dimension. Even three-dimensional images can only be viewed one frame at a time. In addition, the inside of the body is dynamic and it takes a skilled surgeon to understand the orientation of tissues and the precise margins where tumor tissue ends and regular tissue begins. 

Because of this challenge, surgeons often have to remove healthy tissue to be sure all tumor cells are gone. This requires a special step: staining the removed tissue then looking at it under a microscope to identify the cells. The surgeon wants to be sure a margin of healthy tissue is removed so no tumor cells remain.

If tumor cells remain, they will grow and second operation may be necessary to remove more cancerous tissue. Again, the removal of additional healthy tissue will be necessary. But what if a surgeon could distinguish cancer cells from normal cells during surgery? It seems impossible. Each cell is microscopic, thousandths of a millimeter. Just observing cells takes special staining and high-powered optics.

But scientists at the University of Missouri and Washington University in St. Louis are working on the impossible. They are developing cancer goggles that will allow surgeons see tumor cells right in the operating room. This new technology uses LS301, a fluorescent dye combined with a short chain of amino acids called peptide, that is only absorbed by cancer cells and glows under infrared light. This dye specifically stains cells from prostrate, colon, breast, and liver cancers among others. Patients can be injected with the dye beforehand and it will last through a procedure.

These special goggles will illuminate cancer cells with LS301 using an infrared light source. A surgeon can distinguish glowing cancer cells from normal cells and observe when they are completely removed. As a result, the surgeon would not need to remove a margin of healthy tissue to be sure all cancerous tissue is gone. This may greatly improve success rates from surgeries to remove cancerous growths. 

Currently, this technique is being perfected in veterinary surgeries to guide the removal of tumors in pets and is not yet ready for use with humans. If effective, it will be a great resource for patients undergoing tumor removal surgery in the future.

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I Believe in Medicine

August 4, 2011 by

By Pamela Bond

This I Believe, National Public Radio

March 11, 2010

I believe in medicine. It’s come a long way and I have every reason to believe it will go even further. Will we find a cure for cancer? AIDS? For this, I don’t have the answers, but I know that there are some very dedicated people working to find out.

I believe that medicine has made our lives better and longer. I believe that doctors should be given all available resources to help their patients, even if this means working across borders. I believe that geneticists and researchers deserve more funding. They are the ones helping to save lives and should be rewarded with the type of funding we dedicate to entertainers and sports professionals.

I do not believe medicine holds all the answers. I know from experience that not every ailment gets diagnosed. Behind medicine, there is a science. But behind science there are people, and people can make mistakes. I don’t believe patients should be prescribed the pharmaceutical with the biggest advertising budget. Pharmaceuticals shouldn’t even need to advertise. They should let doctors do their jobs. I don’t believe doctors should be on the payroll of pharmaceutical companies, either. Once again, they should be prescribing the drugs that work best for the patient, not the ones they are getting money from. This is unethical.

I believe health insurance should be affordable and available to all. I believe that those with pre-existing conditions should not be among the least insured. Instead of creating a new program, the government should expand Medicare and Medicaid to fill in the gaps between those poor enough to qualify for the program and those who make just enough money to be ineligible for it but not enough money to afford health insurance on their own. The government should not run our healthcare system. If we want to keep the most advanced healthcare in the world, we cannot let this happen.

I believe medicine saves lives. It saved mine, many times. When a brown recluse spider bit me, I may have lost a chunk of my leg but I lived, thanks to medicine. When a Staph infection developed at the site of the bite, modern medicine made sure that I lived. It may have taken a year to diagnose my autoimmune disease, but doctors were finally able to pinpoint it. When doctors suspected a tumor, they were able to investigate it. Today I am functioning just fine.

And medicine is part of my daily life now. The pharmaceuticals I am taking have worked nothing short of a miracle. I know that not every story has a happy ending like mine, but that’s the thing about faith. You have to believe.

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