Tag Archives: melanoma

We’re getting a better idea of how moles turn into melanoma, and environment is key

New research is upending what we knew about the link between skin moles and melanoma.

Image via Pxhere.

Moles and melanomas are both types of skin tumors, and they originate from the same cells — the pigment-producing melanocytes. However, moles are harmless, and melanomas are a type of cancer that can easily become deadly if left untreated. The close relationship between them has been investigated in the past, in a bid to understand the emergence of melanomas.

New research at the Huntsman Cancer Institute (HCI) , the University of Utah, and the University of California San Francisco (UCSF) comes to throw a wrench into our current understanding of that link. According to the findings, our current “oncogene-induced senescence” model of the emergence of melanomas isn’t accurate. The research aligns with other recent findings on this topic, and propose a different mechanism for the emergence of skin cancer.


“A number of studies have challenged this model in recent years,” says Judson-Torres. “These studies have provided excellent data to suggest that the oncogene-induced senescence model does not explain mole formation but what they have all lacked is an alternative explanation — which has remained elusive.”

Melanocytes are tasked with producing the pigments in our skin which protect us from harmful solar radiation. Changes (mutations) in one specific gene in the genome of melanocytes, known as BRAF gene mutations, are heavily associated with moles; such mutations are found in over 75% of skin moles. At the same time, BRAF gene mutations are encountered in 50% of melanoma cases.

Our working theory up to now — the oncogene-induced senescence– was that when melanocytes develop the BRAFV600E mutation, it blocks their ability to divide, which turns them into a mole. However, when other mutations develop alongside BRAFV600E, melanocytes can start dividing uncontrollably, thus developing into cancer.

The team investigated mole- and melanoma tissues donated by patients at the UCSF Dermatology clinic in San Francisco or the HCI Dermatology clinic in Salt Lake City. Their analysis revolved around two methods known as transcriptomic profiling and digital holographic cytometry. The first one allows them to determine molecular differences between the cells in moles and those in melanomas. The second one was used to track changes inside individual cells.

“We discovered a new molecular mechanism that explains how moles form, how melanomas form, and why moles sometimes become melanomas,” says Judson-Torres.

The team reports that melanocytes don’t need to have mutations besides BRAFV600E to morph into melanoma. What does play a part, however, are environmental factors, transmitted to the melanocytes through the skin cells around them. Depending on exactly what signals they’re getting from their environment, melanocytes express different genes, making them either stop dividing or divide uncontrollably.

“Origins of melanoma being dependent on environmental signals gives a new outlook in prevention and treatment,” says Judson-Torres. “It also plays a role in trying to combat melanoma by preventing and targeting genetic mutations. We might also be able to combat melanoma by changing the environment.”

The authors hope that their findings will help researchers get a better idea of the biomarkers that can predict the emergence of melanoma at earlier stages than possible today. Furthermore, the results here today can also pave the way to more effective topical medicine that can prevent melanoma, or delay its progress.

The paper “BRAFV600E induces reversible mitotic arrest in human melanocytes via microrna-mediated suppression of AURKB” has been published in the journal eLife.

Credit: Flickr, Many Wonderful Artists / Public Domain.

AI is better at diagnosing skin cancer than even some of the best human experts

Credit: Flickr, Many Wonderful Artists / Public Domain.

Credit: Flickr, Many Wonderful Artists / Public Domain.

An international team of researchers has shown for the first time that artificial intelligence is better at diagnosing melanoma than human doctors. This particular form of machine learning, known as a deep learning convolutional neural network (CNN), was able to make more correct diagnoses and fewer misdiagnoses than some of the world’s most capable skin care oncologists.

Man vs machine

The CNN starts off as a blank slate. In order to teach the artificial neural network how to identify skin cancer, the researchers fed it a dataset of over 100,000 images of malignant melanomas and benign moles. With each iteration, it learned patterns of features characteristic of malignant and benign tumors, becoming increasingly better at differentiating between the two.

After this initial training round, the team of researchers led by Professor Holger Haenssle, senior managing physician at the University of Heidelberg, Germany, introduced the AI to two new sets of images sourced from the Heidelberg library. These dermoscopic images of various skin lesions were completely new to the CNN. One set of 300 images was meant to solely test the performance of the CNN. Another set of 100 images was comprised of some of the most difficult to diagnose lesions and was used to test both machine and real dermatologists.

Researchers were able to recruit 58 doctors from 17 countries. Among them, 17 (29%) indicated they had less than two years’ experience in dermoscopy, 11 (19%) said they had two to five years of experience, and 30 (52%) were experts with more than five years’ experience.

The volunteers were asked to make a decision about how to manage the condition — whether it was surgery, follow-up, or no action at all — based on two levels of information. At level I, the only information that the dermatologists had at their disposal was from dermoscopic images. Four weeks after making the level I assessment, each participant was asked to review their diagnosis at level II, where they were given far more information about the patient — including age, sex, and the location of the lesion, as well as magnified images of the same case.

At level I, humans could accurately detect melanomas 86.6% of the time and correctly identified benign lesions with an average score of 71.3%. The CNN, however, was able to detect benign moles 95% of the time. At level II, the dermatologists significantly improved their performance, as expected, having diagnosed 88.9% of malignant melanomas and 75.7% that were benign.

Even though the expert doctors were better at spotting melanoma than their less experienced counterparts, they were, on average, outperformed by the AI.

Around 232,000 new cases of melanoma are diagnosed worldwide every year, which result in 55,500 deaths annually. The cancer can be cured, but it typically requires an early diagnosis. This is why this CNN is so impressive — it would be able to identify more cancers early on, thereby saving lives.

“These findings show that deep learning convolutional neural networks are capable of out-performing dermatologists, including extensively trained experts, in the task of detecting melanomas,” Haenssle said.

Of course, all of this doesn’t mean that doctors will soon be scrapped. Far from it: the researchers say that the machine will augment the performance of doctors rather than replace them. Think of a second ‘expert’ opinion which doctors can instantly turn to.

“This CNN may serve physicians involved in skin cancer screening as an aid in their decision whether to biopsy a lesion or not. Most dermatologists already use digital dermoscopy systems to image and store lesions for documentation and follow-up. The CNN can then easily and rapidly evaluate the stored image for an ‘expert opinion’ on the probability of melanoma. We are currently planning prospective studies to assess the real-life impact of the CNN for physicians and patients,” according to Haenssle.

Concerning the study’s limitations, it’s important to note that the study’s participants made diagnoses in an artificial setting. Their decision-making process might look different in a ‘life or death’ situation, which might impact performance. The CNN also had some limitations of its own, such as poor performance with images of melanomas on certain sites such as the fingers, toes, and scalp. For this reason, there is still no substitute for a thorough clinical examination performed by a trained human physician.

That being said, these impressive results indicate that we’re about to experience a paradigm shift, not only in dermatology but in just about every medical field, thanks to developments in artificial intelligence.

The findings appeared in the journal Annals of Oncology.

New melanoma blood test could be a game changer for early detection

A new blood test for melanoma could detect the cancer in its early stages — a window when it is still highly treatable, and survival rates are over 98%. Melanoma, which often spreads quickly, is currently detected through biopsies and skin examinations.


Melanoma is the most dangerous type of skin cancer, often linked to exposure to ultraviolet radiation from sunshine or tanning beds. It poses a huge threat and can spread very quickly, so early detection is crucial. However, identifying melanoma is often challenging.

Typically, doctors identify suspicious-looking moles, which they examine visually and cut out for biopsies. This process is not flawless: only 30% of the analyzed tissues are identified as melanoma, and a substantial amount of cancers elude detection.

[panel style=”panel-default” title=”An unforgivable delay” footer=””]

In an article aptly titled ‘An unforgivable delay,’ published in the Lancet in 2005, a psychiatrist acknowledges how as a young internist he dismissed a soft tissue swelling in a middle-aged lady, as a ‘lipoma’ — a benign tumor made of fat tissue. Much to his chagrin, he later realized that it was actually a case melanoma. The confessional, alongside similar experiences with the diagnosis of this tumor, prompted the present review.

“When I was a young doctor I temporarily replaced an established internist in my town. One morning, a 45 year-old woman came to me in a state of high anxiety,” Alberto Foglia wrote in 2005. “She had noticed a deep-seated soft swelling in her right thigh. She told me openly that she had not wanted to come to me because she thought I was too young, but she felt she could not wait for the return of the regular physician a month later. At the same time she continually asked me for reassurance. “Is it true, doctor, that this is nothing to worry about? It is just a cyst, isn’t it?””


Stories where melanoma has been misidentified or missed altogether abound, which is why a reliable and fast blood test could make such a big difference — not only would it help with the accuracy of the diagnosis, but it would enable early detection of melanoma, which is often challenging.

A blood test

Developed by scientists at Edith Cowan University in Australia, the test doesn’t detect the melanoma itself, but rather the auto-antibodies produced by the body to fight the cancer. The trial involved about 200 people — half of whom had melanoma. The results were impressive, but not perfect: the test was successful in 81.5% of cases. However, even with this success rate, early detection could save thousands of lives: melanoma claims 1,500 lives each year in Australia alone, says Professor Mel Ziman, head of the Melanoma Research Group at the university, who led the study.

If the melanoma is detected when it’s still less than 1 mm thick, you have a 98-99% chance of survival, Ziman says. If it spreads beyond that, things can get much trickier.

“It’s critical that melanoma is diagnosed more accurately and early,” Ziman said. “So a blood test would help in that identification particularly at early stage melanoma, which is what is the most concerning and would be most beneficial for everybody if it was identified early.”

It’s important to note that this blood test is still in its early phases. Not only do researchers have to improve the sensitivity of the procedure and reduce the false-positive rate, but the test also needs to be assessed more thoroughly and on a larger number of participants. It will now undergo clinical trials, which are scheduled to start within the next three years. The test did not pick up on other types of skin cancer.

So far, the medical community has been cautiously optimistic about this procedure. There’s still a long way to go before we can even talk about this blood test becoming a reality in hospitals. For now, scientists caution, you should still regularly check your skin for abnormal-looking moles — particularly if you live in a very sunny area or if you use tanning beds.

“The false positive and false negative rates of this test mean that the results will need to be interpreted with caution and, where practical, combined with a full skin check by a dermatologist,” Prof Rodney Sinclair, a University of Melbourne dermatology expert, told Australian Associated Press.

Journal Reference: Pauline Zaenker et al. A diagnostic autoantibody signature for primary cutaneous melanoma, Oncotarget (2018). DOI: 10.18632/oncotarget.25669

Dangerous or not? Scientists uncover the connection between skin moles and melanoma

There is a long-lasting debate dividing the cancer researchers community over the point at which a skin lesion is considered a melanoma; one side claims that the lesions which look halfway between a mole and a melanoma should be considered a class of their own in the field, while the other believes any lesions can be either harmless or cancerous with no gray-area between the two.

Considering the American Cancer Society’s estimate that 70,000 new cases of melanoma will be diagnosed in the US in 2015, it’s vital that we understand it and develop efficient treatments for the condition. And a University of California-San Francisco team led by Hunter Shain might have found the answers to settle the debate once and for all; they have found a way to tell whether a lesion is harmless or growing into a melanoma.

Melanocytic nevus tissue.
Image via wikipedia

The team presented their work at the melanoma convention last month and published the full version of the project in the New England Journal of Medicine.

This kind of lesions “are very difficult to study simply because they are difficult to identify,” Shain said.

On the surface, it’s impossible to tell whether an intermediate lesion is dangerous or not — they share characteristics from both benign and malignant lesions. Shain’s team enlisted the aid of eight expert dermatologists to try and classify them and there was little agreement in the group. So the team turned to the microscopes for answers.

Skin cancers tend to develop next to tissue where earlier stages of the lesion formed; Shain’s team recovered samples from 37 patients with melanoma, and dissected them into healthy skin, precursor lesion, possible intermediate lesion and mature melanoma tissue. They then sequenced 300 genes commonly seen in cancer tissue from each section of the samples to see which genes change during each development stage of the melanoma.

Intermediate lesions showed a number of harmless mutations but also precursor genes that could allow for cancerous cell growth, suggesting that they don’t just look in-between — the DNA of these cells actually imprint characters shared by both moles and skin cancer.

The research also gave them insight into how skin cancers develop:

“In our study, we observe the canonical order of mutations that allow a melanocyte [a skin cancer cell] to overcome these barriers as it progresses to melanoma,” Shain said.

In the 1980s the term “dysplastic nevus” (meaning atypical mole) came to be used to describe an intermediate lesion, though some in the field argued that the term would only lead to confusions in skin cancer diagnosis and shouldn’t be used. David Elder of the University of Pennsylvania, who coined the term “dysplastic nevus syndrome,” attended the team’s presentation in San Francisco, and although Shain’s team avoided using the term, had this to say:

“I think this is an important step forward […] and it does add materially to our understanding of a question that has certainly been hotly debated in our community for many years.”

While the study’s authors didn’t adopt his terminology, Elder believes they are describing the same thing, and said that focusing too much on the term would distract from the findings of the study.

“I asked the question, ‘Were these intermediate lesions dysplastic nevi or were they something else?’ And the response was, ‘Well, yes, they are,’” Elder recounts.

Co-author of the study and one of the panel of eight expert dermatologists Iwei Yeh of UC-San Francisco says that the genetic data retrieved in the study forms the base for future research aiming to narrow the list of mutations that are likely to develop into melanoma. By observing patients with intermediate lesions and recording which ones develop into melanoma, the genes they sequenced could then serve as a diagnostic for moles that become malignant.

“I think that kind of ties into this whole idea of personalized medicine,” Yeh said. “What are the individual alterations that are really contributing to the person’s cancer, and what does that mean for them in terms of their outcome?”

“More precise diagnosis could be very valuable in more appropriate precision treatment of these lesions,” Elder added. “If you don’t need to do [a procedure], you don’t want to do it.”

Modified herpes virus used to treat skin cancer

A new clinical trial from the UK brings exciting results as a modified strain of the herpes virus has been successfully used to treat skin cancer patients, with only minor side effects.

Image via Herpes Aware.

The trial run included 436 patients suffering from aggressive melanoma that signed up to be treated through virotherapy – the usage of genetically modified strains of viruses that attack specific pathogens or cells, such as malign cancer cells. Kevin Harrington, professor of biological cancer therapies at the Institute of Cancer Research London, who lead the research team, said: “This is the big promise of this treatment. It’s the first time a virotherapy has been shown to be successful in a phase 3 trial.”

Named Talimogene Laherparepvec (T-VEC), the drug was administered once every 14 days for up to 18 months, participants only showing flu-like side effects after the first few injections. One in four patients responded well to the treatment, 16% of them still being in remission six months later, compared to the 2% of the control group, treated using immunotherapy. 10% of those treated using the new drug had complete remission, showing no signs of cancer. During the trial, the T-VEC group patients survived an average of 41 months, while those in the control group survived an average of 21.5 months. These results are especially encouraging as some of the patients were in too severe condition to respond to conventional treatment :

“They had disease that ranged from dozens to hundreds of deposits of melanoma on a limb all the way to patients where cancer had spread to the lungs and liver,” said Harrington.

[Also Read: Modified cold sore virus shrinks melanoma tumors]

“Just gonna drop this off here real quick” – T-VEC virus. Image via Digital Deconstruction.

T-VEC works by taking away the virus’ ability to produce the protein that allows it to infect healthy cells. But malign cells produce the protein needed on their own, offering the virus the means to infect and thrive in cancerous tissue. As the herpes virus multiplies vigorously inside the cancer cells they burst open, spilling the virus into the surrounding area, triggering a secondary immune reaction against the tumour.

“We may normally think of viruses as the enemies of mankind, but it’s their very ability to specifically infect and kill human cells that can make them such promising cancer treatments. In this case we are harnessing the ability of an engineered virus to kill cancer cells and stimulate an immune response” said Professor Paul Workman, Chief Executive of The Institute of Cancer Research. And once the immune system gets the wake up call from T-VEC treatment, even secondary tumours that have not been infected by the virus have shrunk or disappeared completely. “It’s like an unmasking of the cancer,” said Harrington. “The patient’s immune system wakes up and attacks the cancer cells wherever they are in the body.”

Uninfected tumours attacked after T-VEC treatment.
Image via meetinglibrary.asco.org

The trial results are so promising that the research team hope to get it on the market by 2016. And successfully passing a phase 3 trial means that the pharmaceutical company Amgen only needs approval from the FDA and European Medicines Agency before they can make the treatment commercially available.


New Cancer Treatment Dissolves a Woman’s Tumor in 3 Weeks

You hear about potential cancer treatments all the time, and despite significant and remarkable improvements, we’re still miles away from an actual cure for cancer; so what makes this therapy so great? Well… it just seems to work – on humans, suffering from cancer, not in a lab. For one woman, it seems to have completely dissolved a big tumor in just three weeks, and overall, 53% of patients experienced at least 80% tumor shrinkage.

CT scans reveal the disappearance of the tumor. Note, the two images are not to scale; photo credit: New England Journal of Medicine

The patient is a 49-year-old woman who had a 4.2-mm ulcerated melanoma removed from her back 4 years ago. Five months ago, she had another subcutaneous nodule removed, this time under her left breast. However, there was persistent disease, and was at a high risk for further spread. After receiving this experimental treatment, her huge tumor completely disappeared, and left only a cavity behind, as you can see here. While most patients had significant improvements and over 20% were left without any visible tumors, doctors were simply amazed at the reduction in this case. In fact, it worked so good, that it got researchers worried about eliminating the tumor too fast:

“This patient had a rapid eradication of a large tumor mass after a single treatment with combination immunotherapy. We wish to bring this to the attention of our colleagues, not only as an example of the potential of immunotherapy to mediate dramatic and rapid antitumor effects, but also to point out a potential safety concern. Such an antitumor effect occurring in a transmural metastasis in the small bowel or myocardium, common sites of metastatic melanoma, could have grave consequences. It is ironic that we are now concerned about the possibility of overly vigorous antimelanoma responses.”

Alongside the obvious tumor in her chest, CT scans confirmed that the large tumor had been completely eradicated.

To make things even better, the therapy the scientists were investigating is FDA approved, involving two antibodies: Yervoy (ipilimumab) and Opdivo (nivolumab). They have very different types of action, but together they just seem to do the trick.

For the trial, researchers tested the drugs on 142 patients with melanoma that spread to other parts of the body or metastasized. The experiment followed what seemed to be the best standard for this type of study – comparing the results of standard treatment + placebo with the results of standard treatment + experimental treatment. In this case, patients were randomly assigned either Yervoy plus a placebo or Yervoy in combination with Opdivo.

“Patients were randomly assigned, in a 2:1 ratio and in a double-blinded manner, to receive both nivolumab and ipilimumab (combination group) or ipilimumab alone (ipilimumab-monotherapy group),” the published paper reads.

As mentioned above, over half of all the patients who got the combination experienced at least 80% tumor shrinkage, and melanoma became undetectable in 22% by the end of the study – spectacular figures for stage IV cancer.

Although the trial is now over, doctors obviously plan to include even more people in the future. You can read her case study here, and the full study here.


Some quick facts about UV exposure. Image: Australian Radiation Protection and Nuclear Safety Agency

The skin gets damaged by UV light even in the dark, ironically as it may seem

Contrary to popular belief, much of the damage inflicted to the skin by harmful ultraviolet (UV) light occurs hours after exposure to the sun, even when you’re sitting comfortably asleep in your dark bedroom. The Yale University research also made a startling find: melanin – the pigment that gives human skin and hair its colour – has both carcinogenic and protective effects. This double standard should be taken into consideration from now on when discussing UV exposure, but also when looking for new treatments to skin cancers like melanoma.

Melanin: a double standard

Some quick facts about UV exposure. Image: Australian Radiation Protection and Nuclear Safety Agency

Some quick facts about UV exposure. Image: Australian Radiation Protection and Nuclear Safety Agency

Melanoma is the most common form of cancer in the United States. It occurs when the DNA in melanocytes, the cells that make the melanin, get damaged by UV light from exposure to the sun or tanning beds.  In the past, experts believed that melanin protected the skin by blocking harmful UV light. But there was also evidence from studies suggesting that melanin was associated with skin cell damage.

A team led by Douglas E. Brash, clinical professor of therapeutic radiology and dermatology at Yale School of Medical, exposed both human and mouse melanocyte cells to harmful radiation via a UV lamp. The radiation caused a type of DNA damage known as a cyclobutane dimer (CPD), in which two DNA “letters” attach and bend the DNA, preventing the information it contains from being read correctly. In a startling surprise, Brash and colleagues found that the melanocytes not only generated CPDs immediately but continued to do so hours after UV exposure ended. Cells devoid of melanin generated CPDs only during the UV exposure. This indeed suggests that melanin has both harmful and beneficial effects, according to the paper published in Science.

“If you look inside adult skin, melanin does protect against CPDs. It does act as a shield,” said Brash, also a member of Yale Cancer Center. “But it is doing both good and bad things.”

When mouse cells had their DNA repair ability rendered inactive, scientists found half of the CPDs in melanocytes were “dark CPDs” following sun exposure  — CPDs created in the dark. Sanjay Premi, associate research scientist in the Brash laboratory may have found an explanation for this peculiar behavior. Apparently, the UV light activates two enzymes which combine to excite electrons in melanin. This process, which is slow going like a lit fuse, is called chemiexcitation and has previously been seen only in lower plants and animals. There’s some good news though. Because chemiexcitation acts so slowly, “evening-after” sunscreen designed to block the energy transfer could work very well and actually cut half the damage made by UV exposure.

In all events, do be careful when hitting the beach and wear UV-protecting suntan. Watch this video about the power of sunscreen, reported by ZME Science earlier.

Before and after sunscreen, as seen by UV camera, demonstrating its effects. Image: Wikimedia Commons

Before and after sunscreen, as seen by UV camera, demonstrating its effects. Image: Wikimedia Commons

Five or more blistering sunburns before the age of 20 increase melanoma risk by 80 percent

The risk of possibly the most dangerous type of cancer out there, melanoma, is greatly increased by exposure to sun in early adulthood. According to a new study conducted on Caucasian women, five or more blistering sun burns may increase the risk of melanoma by 80 percent.

“Our results suggest that sun exposures in both early life and adulthood were predictive of nonmelanoma skin cancers, whereas melanoma risk was predominantly associated with sun exposure in early life in a cohort of young women,” said Abrar A. Qureshi, M.D., MPH, professor and chair of the Department of Dermatology at Warren Alpert Medical School of the Brown University and Rhode Island Hospital in Providence.

The study was conducted on 108,916 Caucasian registered nurses for about 20 years, and showed that aside for the melanoma risk, five or more blistering sun burns also lead to a 68 percent increased risk for basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) of the skin. After reaching adulthood, even increased exposure to sunlight doesn’t increase the risk of melanoma, but it does increase the risk of BCC and SCC.

“Pattern of sun exposure was not uniformly associated with the risk for all the three main skin cancers we see in the United States, suggesting that there are some differences in the pathophysiology of these skin cancers,” said Qureshi. “An individual’s risk of developing skin cancer depends on both host and environmental risk factors. Persons with high host-risk traits, such as red hair color, higher number of moles, and high sunburn susceptibility, should pay more attention to avoid excessive sun exposure, especially early in life.”

Melanoma is less common than other skin cancers. However, it is much more dangerous if it is not found in the early stages. Researchers hope to provide better insights regarding the prevention of melanoma..

“Parents may need to be advised to pay more attention to protection from early-life sun exposure for their kids in order to reduce the likelihood of developing melanoma as they grow up,” said Qureshi. “Older individuals should also be cautious with their sun exposure, because cumulative sun exposure increases skin cancer risk as well.”

This disk-shaped, biodegradable sponge contains growth factors and components of each patient's tumors. Researchers at the Wyss Institute and clinicians at Dana-Farber Cancer Institute hope that when it's implanted under the patient's skin, it will spur the patient's immune system to attack the patient's tumors and destroy them.

Cancer vaccine with 50% regression rate in mice enters clinical trial

A cross-disciplinary team of scientists at Harvard that developed a novel type of vaccine for treating melanoma – the most lethal form of skin cance – recently announced the vaccine will enter its Phase 1 clinical trial. The announcement comes just a few years after the vaccine was tested on mice, 50% of whom showed signs of complete tumor regression. Typically, cancer treatments need a lot more time to enter human trials.

The combined effort was coordinated at the Wyss Institute for Biologically Inspired Engineering at Harvard University.

“This is expected to be the first of many new innovative therapies made possible by the Wyss Institute’s collaborative model of translational research that will enter human clinical trials,” said Wyss’ founding director, Don Ingber of Children’s Hospital Boston, who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School and a professor of bioengineering at SEAS. “It validates our approach, which strives to move technologies into the clinical space much faster than would be possible in a traditional academic environment. It’s enormously gratifying to see one of our first technologies take this giant leap forward.”

This disk-shaped, biodegradable sponge contains growth factors and components of each patient's tumors. Researchers at the Wyss Institute and clinicians at Dana-Farber Cancer Institute hope that when it's implanted under the patient's skin, it will spur the patient's immune system to attack the patient's tumors and destroy them.

This disk-shaped, biodegradable sponge contains growth factors and components of each patient’s tumors. Researchers at the Wyss Institute and clinicians at Dana-Farber Cancer Institute hope that when it’s implanted under the patient’s skin, it will spur the patient’s immune system to attack the patient’s tumors and destroy them.

Therapeutic cancer vaccines traditionally involve a very cumbersome insertion process in which doctors first need to extract the patient’s immune cells, reprogram them in the lab, then insert them back. The Harvard researchers approach is similar in working principle, however the key difference is that the reprogramming is made “on-site”, inside the patient without any need for extraction and later insertion.

Using the method developed at Wyss, doctors simply have to implant a disk-like sponge about the size of a fingernail that is made from FDA-approved polymers. It is this sponge, implanted right under the skin, that does the immune cell reprogramming, instructing them to travel through the body, home in on cancer cells, then kill them.

In 2009 the researchers published a paper in which they reported the findings of their preclinical trial on mice. Some 50 percent of mice treated with two doses of the vaccine — mice that would have otherwise died from melanoma within about 25 days — showed complete tumor regression.

“It is rare to get a new technology tested in the laboratory and moved into human clinical trials so quickly,” said Dranoff, who is also a Professor of Medicine at Harvard Medical School, and leader of the Dana-Farber/Harvard Cancer Center program in cancer immunology. “We’re beyond thrilled with the momentum, and excited about its potential.”


The goal of the Phase I study, which is expected to conclude in 2015, is to assess the safety of the vaccine in humans. While the vaccine was designed for skin cancer, the researchers claim it is possible to adapt it to other forms of cancer as well. So far, the findings seem very promising. It remains to be seen how effective it is on humans.

Redheads may have more fun, but are more prone to cancer

Researchers have shown that it’s genes, and not the Sun which increases the risk of melanoma in redheads.


Doctors previously believed that their pale skin, often covered with freckles just didn’t provide as much protection towards UV’s, but new research showed that genetic factors of the skin pigment are the real culprits here.

“We’ve known for a long time that people with red hair and fair skin have the highest melanoma risk of any skin type,” study author Dr. David Fisher, chief of dermatology at Massachusetts General Hospital in Boston, said in a written statement. The new findings “may provide an opportunity to develop better sunscreens and other measures that directly address this pigmentation-associated risk while continuing to protect against UV radiation, which remains our first line of defense against melanoma and other skin cancers,” he said.

Melanoma is the most dangerous type of cancer, with more than 76,000 cases expected to be diagnosed this year. The thing is different human skin types contain different types of melanin, which give different types of skin color, each with its own susceptibility towards skin cancer. According to the researchers, skin type alone can’t explain the rise in melanoma risk among redheads, because the increased incidence also occurs in patients who haven’t been exposed to the Sun.

Now, researchers explain, we can understand that, while blocking UVs is indeed extremely important, it is by no mean the only one.

“Right now we’re excited to have a new clue to help better understand this mystery behind melanoma, which we have always hoped could be a preventable disease,” Fisher said. “The risk for people with this skin type has not changed, but now we know that blocking UV radiation – which continues to be essential – may not be enough.”

Research was published in Nature