In many countries rates of prostate cancer cases and deaths have declined or stabilized. The United States had the largest recent decrease in disease incidence, a recent study says.

Previous studies have indicated significant variation in prostate cancer rates, due to factors including detection practices, availability of treatment, and genetic factors.

By comparing rates from different countries, the differences in detection practices can be assessed and improvements in treatment can be determined.

The researchers examined long-term and short-term data from 44 countries with incidence data and 71 countries with prostate cancer death data.

There were 44 countries assessed for incidence. Prostate cancer rates rose in four countries and fell in seven, with the United States with the biggest decrease. In the other 33 countries rates remained stable.

Of the 71 countries assessed for prostate cancer death rates, there were decreases in 14, increases in three, and no change in 54.

As of 2012, prostate cancer was the most commonly diagnosed cancer among men in 96 countries and the leading cause of death in 51 countries, according to the study.

The findings confirm the benefits of prostate-specific antigen (PSA) screening. In the United States, incidence rates rose from the 1980s to the early 1990s, then declined from the mid-2000s through 2015, largely due to increased use of PSA screening.

This type of screening is less available in poorer nations, meaning that men there are more likely to be diagnosed at later stages of prostate cancer and more likely to die.

Some nations plan to scale back recommendations for PSA screening due to fears about possible overtreatment of prostate cancer that would never cause symptoms.

The U.S. Preventive Services Task Force recommends that men aged 55 to 69 undergo periodic screening after they’ve discussed the risks and benefits with their doctor.

“The screening recommendations were changed recently after further analysis of the U.S. data and we are now seeing more high-risk prostate cancer diagnoses that require treatment.

Future studies may monitor trends in mortality rates and late-stage disease to assess the impact of reduction in PSA testing in several countries.

A 29-year follow-up of the Scandinavian Prostate Cancer Group Study Number 4 (SPCG-4) trial has shown that radical prostatectomy is associated with a lower risk of prostate cancer–specific mortality vs. watchful waiting in men with clinically detected localized prostate cancer.

Investigators stated, “Radical prostatectomy reduces mortality among men with clinically detected localized prostate cancer, but evidence from randomized trials with long-term follow-up is sparse.

Study Details

IN THE TRIAL, 695 men with localized disease from 14 centers in Sweden, Finland, and Iceland were randomly assigned to radical prostatectomy or watchful waiting between October 1989 and February 1999. Follow-up data were collected through 2017. The cumulative incidence and the relative risks for death from any cause, death from prostate cancer, and metastasis were estimated, as were the numbers of years of life gained. The median follow-up was 23.6 years; the maximum observed follow-up time was 28.0 years, and the maximum potential follow-up time was 29.3 years.

By December 31, 2017, 294 men in the radical prostatectomy group (85%) had undergone a radical prostatectomy, and 52 men in the watchful waiting group (15%) had undergone curative treatment.

Treatment Outcomes

By Decmber 31, 2017, a total of 261 of the 347 men in the radical prostatectomy group and 292 of the 348 men in the watchful waiting group had died in the intention-to-treat population. Prostate cancer was the cause of death in 71 vs 110 patients. In the intent-to-treat analysis, the cumulative incidence of death from prostate cancer was 19.6% with radical prostatectomy and 31.3% with watchful waiting (absolute difference = 11.7 percentage points) at 23 years, with the relative risk for the complete follow-up period being 0.55 (P < .001) in favor of radical prostatectomy. The mean years of life gained in the radical prostatectomy group at 23 years was 2.9 years.

The cumulative incidence of death from any cause at 23 years was 71.9% in the radical prostatectomy group and 83.8% in the watchful waiting group (absolute difference = 12.0 percentage points), with the relative risk for the complete follow-up period being 0.74 (P < .001). The number needed to treat to avert 1 death from any cause was 8.4.

Men with clinically detected, localized prostate cancer and a long-life expectancy benefited from radical prostatectomy, with a mean of 2.9 years of life gained.

Distant metastases were diagnosed in 92 men in the radical prostatectomy group and 150 men in the watchful waiting group. The cumulative incidence of distant metastases at 23 years was 26.6% vs 43.3% (absolute difference = 16.7 percentage points), with the relative risk based on data from the complete follow-up period being 0.54 (P < .001).

The beneficial effect of radical prostatectomy was greater among men younger than age 65 vs 65 years of age or older at diagnosis, with the risk of overall mortality being 15.0 percentage points lower, prostate cancer mortality being 15.1 percentage points lower, and distant metastasis being 18.6 percentage points lower in the radical prostatectomy group than in the watchful waiting group. Among men 65 years of age or older, between-group differences were smaller for all 3 outcomes.

A per-protocol analysis was performed involving all patients who survived at least 1 year and based on treatments given during the first year. In this analysis, for radical prostatectomy vs watchful waiting, the relative risks were 0.70 (95% confidence interval [CI] = 0.59–0.83) for death from any cause, 0.45 (95% CI = 0.33–0.61) for prostate cancer death, and 0.43 (95% CI = 0.33–0.57) for distant metastases.

Radical prostatectomy vs. watchful waiting

Compared with watchful waiting, radical prostatectomy was associated with a reduced risk of prostate cancer–specific mortality.

Radical prostatectomy was associated with improved overall survival and a reduced risk of distant metastasis.

Among the men who underwent radical prostatectomy, a factor predictive of poorer prostate cancer survival was extracapsular extension (relative risk = 5.21, 95% CI = 2.42–11.22). Compared with a Gleason score of 3 to 6, the risk of prostate cancer mortality was increased in men with a Gleason score of 3 + 4 (relative risk = 5.73, 95% CI = 1.59–20.67) and among men with a Gleason score of 8 or 9 (no patient had a score of 10; relative risk = 10.63, 95% CI = 3.03–37.30).

A positive surgical margin was associated with a poorer prognosis in a model adjusting for age alone; however, after adjustment was made for extracapsular extension, prostate-specific antigen level, and Gleason score, the relative risk of death from prostate cancer for positive vs clear margins was no longer statistically significant (1.16, 95% CI = 0.62–2.15).

The investigators concluded: “Men with clinically detected, localized prostate cancer and a long-life expectancy benefited from radical prostatectomy, with a mean of 2.9 years of life gained. A high Gleason score and the presence of extracapsular extension in the radical prostatectomy specimens were highly predictive of death from prostate cancer.”

New research has found that prostate cancer cells change the behavior of other cells around them, including normal cells, by ‘spitting out’ a protein from their nucleus.

The researchers in the study believe that these tiny pieces of protein are taken up by the other cells, provoking changes that promote tumor growth and help the cancer hide from the body’s immune system.

This process has been captured on video by researchers at the University of Bradford and University of Surrey. The research was published in Scientific Reports.

For tumors to survive, grow bigger and spread they need to control the behavior of cancer cells and the normal cells around them and we’ve found a means by which they do this. Researchers think that blocking this process may be a potential target for future cancer therapy.

The researchers focused on a protein called EN2 that has a role in early development of the brain. This protein has also been found at high levels in many types of cancer cells.

The team highlighted the protein using a green florescent tag. The researchers then studied its activity in human prostate cancer cells, normal prostate cells and in bladder cancer, melanoma and leukemia cells. They found that both cancer and normal cells took up the protein from other cells.

The researchers also did time lapse photography of prostate cancer cells, taking pictures every five minutes for 24 hours. The resulting video shows the cells eject small parts of themselves containing the green florescent protein that are then taken up by otherwise dormant cancer cells, causing them to reactivate, changing shape or fusing together.

These findings may be significant because cell fusion in cancer is relatively unusual and is associated with very aggressive disease. It may lead to new and unpredictable hybrid cells that are frequently better at spreading to different sites and surviving chemotherapy and radiotherapy.

Molecular analysis of the normal prostate cells showed that take up of EN2 caused them to express a gene called MX2 that generates an anti-viral response.

It is thought that the cancer may be trying to minimize the chances of the cells around it being infected by a virus, to avoid scrutiny by the immune system. This could undermine the effectiveness of immunotherapy treatments, which try to use viruses to kill cancer by stimulating the immune system to attack it.

The researchers were surprised to find that the EN2 protein in the cell membrane as well as in the nucleus – which is very unusual for this type of protein. This provides an opportunity to block its action. The team was able to identify that part of the protein that was accessible at the cell surface to be a potential target for treatment.

Findings of a recent study suggest that drinking coffee may help delay risk of prostate cancer.

If the findings of a latest study can be believed, drinking coffee may help delay risk of prostate cancer. According to researchers, the findings could help pave way for treating drug-resistant cancer.

The recent study was performed by scientists from Kanazawa University in Japan who identified kahweol acetate and cafestol- hydrocarbon compounds naturally found in Arabica coffee — which may inhibit growth of prostate cancer.

The pilot study presented at the European Association of Urology Congress in Barcelona, suggested that kahweol acetate and cafestol may possibly play a role in inhibiting growth in cells that are resistant to common anti-cancer drugs like Cabazitaxel.

“We found that kahweol acetate and cafestol inhibited growth of cancer cells in mice, but the combination seemed to work synergistically, leading to a significantly slower tumour growth than in untreated mice,” said the lead author Mr. Iwamoto.

The study team tested six compounds that are naturally found in coffee, on proliferation of human prostate cancers cells in vitro (i.e. in a petri-dish). Their findings revealed that cells treated with kahweol acetate and cafestol grew more slowly than controls. The team then tested these compounds on prostate cancer cells, transplanted to 16 mice.

“After 11 days, the untreated tumors had grown by around three and a half times the original volume (342 per cent), whereas tumors in the mice treated with both compounds had grown by just over one and a half (167 per cent) times the original size,” Mr. Iwamoto said.

The growth reduction in transplanted tumor cells were much prominent that in native tumor cells.

Even though these are promising findings, they should not make people change their coffee consumption because it can have both positive and negative effects. More research is needed to find out more about the mechanisms behind these findings before anyone can consider clinical applications.

It has long been known that what you eat can drastically affect many aspects of your health, including your risk of developing chronic diseases like cancer and diabetes.

In particular, studies have shown that the development of cancer can be heavily influenced by diet.

There are many fruits and vegetables that contain beneficial compounds that could help decrease the growth of cancer. Five of these are listed below:

1. Broccoli

Broccoli contains sulforaphane, which is a plant compound found in cruciferous vegetables that are thought by some to have potent anticancer properties.
One study showed that sulforaphane reduced the size and number of breast cancer cells. An animal study determined that treating mice with sulforaphane helped kill off prostate cancer cells and reduced tumor volume by more than 50%.

Cruciferous vegetables like broccoli have also been linked to a lower risk of colorectal cancer.

The available research hasn’t looked directly at how broccoli may affect cancer in humans, so more studies are needed. But eating more broccoli and other fresh fruits and vegetables can be beneficial to your health in many ways.

2. Carrots

Many studies have found that eating more carrots is linked to a decreased risk of certain types of cancer. One study analysis looked at the results of five separate studies and concluded that eating carrots may reduce the risk of stomach cancer by up to 26%.

A different study found that a higher intake of carrots was associated with 18% lower odds of developing prostate cancer.

It is a good idea to try incorporating carrots into your diet as a healthy snack or delicious side dish just a few times per week to increase your intake and potentially reduce your risk of cancer.

These studies may show an association between carrot consumption and cancer, but they don’t all account for other factors that may play a role. Some of the studies have found an association between carrot consumption and a decreased risk of prostate, lung and stomach cancer.

3. Citrus Fruits

Eating citrus fruits such as oranges, lemons, lime and grapefruits has been associated with a lower risk of cancer in some studies.
One study found that participants who ate a higher amount of citrus fruits had a lower risk of developing cancers of the digestive and upper respiratory tracts. Another review looking at nine studies also found that a greater intake of citrus fruits was linked to a reduced risk of pancreatic cancer.
A review of 14 studies showed that a high intake, which included at least three servings per week, of citrus fruit reduced the risk of stomach cancer by 28%.

These studies suggest that including a few servings of citrus fruits in your diet each week may lower your risk of developing certain types of cancer.
Keep in mind that these studies don’t account for other factors that may be involved. More studies are needed on how citrus fruits specifically affect cancer development.

4. Tomatoes

Lycopene is a compound found in tomatoes that is responsible for its vibrant red color as well as its anticancer properties.

Studies from several sources have found that an increased intake of lycopene and tomatoes could lead to a reduced risk of prostate cancer.

A review of 17 studies found that a higher intake of raw tomatoes, cooked tomatoes and lycopene were all associated with a reduced risk of prostate cancer.
An additional study of 47,365 people found that a greater intake of tomato sauce was linked to a lower risk of developing prostate cancer.

While these studies show there may be an association between eating tomatoes and a reduced risk of prostate cancer, they don’t account for other factors that could be involved.

And while more studies are needed, some have found that a higher intake of tomatoes and lycopene could reduce the risk of prostate cancer.

5. Garlic

Allicin is the active component in garlic, and it is a compound that has been shown to kill off cancer cells in multiple test-tube studies. A few studies have found an association between garlic intake and a lower risk of certain types of cancer.

One study that involved 471 men showed that a higher intake of garlic was associated with a reduced risk of prostate cancer.

Based on these findings, including 2–5 grams (approximately one clove) of fresh garlic into your diet per day may help people take advantage of garlic’s health-promoting properties.

However, more studies are needed to examine whether other factors play a role.

Garlic contains allicin, a compound that has been shown to kill cancer cells in test-tube studies. Studies have found that eating more garlic could lead to decreased risks of stomach, prostate and colorectal cancers.

Prostate cancer is one of the most common forms of cancer affecting men today. In 2018, more than 1.2 million new cases of prostate cancer will be diagnosed globally, according to the International Agency for Research on Cancer. While the burden of the disease is staggering, new research led by Harvard T.H. Chan School of Public Health suggests that a modifiable lifestyle factor may help reduce the risk: exercise.

Some researchers have long suspected that physical activity, and its influence on a wide range of biological processes including anti-inflammatory and insulin pathways, may be linked to a lower risk of prostate cancer. But findings from large epidemiologic studies so far have been mixed—some have shown an association, some haven’t.

In order to bring a fresh approach to the question, scientists from Harvard Chan School analyzed data from 49,160 men between the ages of 40 and 75 who enrolled in The Health Professionals Follow-up Study in 1986 and were followed to 2012. The men responded to biennial questionnaires that included questions about diet, health, and physical activity. Among the participants, 6,411 developed prostate cancer and 888 developed a lethal form of the disease.

This study, which was published in European Urology, showed that men who engaged most frequently in vigorous activity over the length of the study had a 30% lower risk of developing advanced prostate cancer and 25% lower risk of developing lethal prostate cancer when compared with men who exercised the least. On average, men in the highest category of vigorous activity engaged in an equivalent of 25 minutes of running daily. Vigorous activity for this study included activities such as bicycling, swimming, heavy outdoor work, and playing sports such as tennis or racquetball.

In addition to other well-known health benefits of a physically active lifestyle, this study emphasizes that prostate cancer prevention may be another important reason for men to move more and be active.

As well as being one of the largest of its kind, the study is unique in that the researchers were able to examine medical records, pathology reports, and disease-specific questionnaires, and to leverage molecular sub-typing data to better understand how prostate cancer develops.
In particular, the study homed in on a common molecular alteration in prostate tumors called TMPRSS2:ERG, a gene fusion that occurs in the tumors of about 50% of prostate cancer patients. The study showed for the first time that long-term vigorous physical activity was specifically associated with a lower risk of developing TMPRSS2:ERG-positive prostate cancers.

The “Impact Award” has been granted by The U.S. Department of Defense to a multidisciplinary team of researchers made up of the Prostate Cancer Clinical Research Unit of the Spanish National Cancer Research Centre (CNIO), led by David Olmos, the Prostate Cancer Translational Research Group of the Vall d’Hebron Institute of Oncology (VHIO), led by Joaquín Mateo, and the Genetics and Solid Tumors Laboratory of the University of Washington, led by Colin Pritchard. This team will explore new therapeutic options against advanced prostate cancer—scientifically known as castration-resistant or hormone therapy resistant prostate cancer- They will receive a 2 million dollar grant for this 3-year project and will examine the identification of new markers as predictors of response to treatment, with the aim of identifying which patients will respond worse to therapy and thus offer them other therapeutic options.

Prostate cancer is one of the most common cancers in males in Spain and in the West and the second world-wide. It is the third most common cause of male death in Europe, even though over the last several years the survival rate is continually rising, most likely due to early detection. The most common treatment in the advanced stage is the hormone-blocking therapy, but some patients develop aggressive tumors that are resistant to this type of treatment: up to 90% of the patients that develop resistance also develop metastasis, most commonly in the bones and lymph nodes, but also occasionally in the liver and lungs. The average survival rate of the patients in the advanced stage is about 2 years after the diagnosis. Moreover, one in three patients respond worse to the approved therapies for prostate cancer, but until this day we do not have a better way of identifying and predicting their response to treatment.

This project will try to identify this group of patients through the development of new markers as predictors of response to treatment and will conduct a clinical trial to test if the therapy that works for other tumor types like breast and ovarian cancer could prove to be effective for the patients with advanced prostate cancer that show these markers.

Disruption of DNA repair mechanisms in tumors

The researchers will investigate the genetic and molecular changes associated with defects in the DNA repair mechanisms; that is, if the tumor cells repair the errors produced in their genetic material correctly or not. “Our line of work has always looked into those mechanisms” explains Elena Castro, from the CNIO Prostate Cancer Clinical Research Unit. “It is an approximation that has given very good results in prostate cancer research”. The researchers expect these tumors to respond to carboplatin therapy, a drug that is very effective in the tumor types that show these kinds of defects, such as breast and ovarian cancer. These therapies work by impeding that the cells repair their DNA defects. Due to the fact that cancer cells have far many more genetic defects than normal cells, these drugs are very effective in producing their breakdown and death.

In the first part of this project, the team will study the tumor samples that were collected from the patients participating in the PROREPAIR-B study; the first worldwide prospective study conducted, to date, in patients with advanced prostate cancer that carry heritable mutations. PROREPAIR-B is a study coordinated by CNIO that has monitored more than 400 patients since 2013, to analyze if their DNA damage repair genes have inherited genetic alterations and how these affect their response to treatment. Now these samples will be sequenced to check the behavior of the alterations in these genes that are not inherited and that only occur in the tumor.

After that, the VHIO team led by Joaquín Mateo will search for biomarkers for DNA repair defects in those patients, since these defects not always originate from an inherited genetic mutation. “Over the last few years we have shown that an important number of patients with advanced prostate cancer develop DNA repair defects in their tumors, even though there is no inherited mutation”, explains Joaquín Mateo, VHIO researcher and Vall d’Hebron University Hospital oncologist. “We also know that some of the tumors behave in a similar manner to the ones having these mutations, even if we don’t identify them. This is why we wish to study the biological patterns associated with the clinical patterns and to do that we will study these tumors using different tools in the laboratory”, adds Mateo. The goal is to find new signs of these errors (more than just genetic mutations) that would permit a faster decision-making on which treatments to choose.

Lastly, the CNIO team, with the help of VHIO and other Spanish centers, will conduct a clinical trial to confirm if the carboplatin therapy could be effective in advanced prostate cancer. “We know that carboplatin works really well in tumors with DNA repair defects from patients with breast and ovarian cancer, and we suppose that it will also work for patients with prostate cancer, but we are not certain at this stage”, says Olmos. “But instead of selecting patients based on them having genetic mutations that could provoke defects in DNA repair, as is commonly done, they will be selected using biomarkers that were previously detected, as we believe that it will be more reliable when determining the efficacy of the treatment. In other words, we will select patients based on whether the tumor repairs its DNA or not, independently of their genetic profile”.

Another advantage is that this therapy is affordable and easily accessible. A type of drugs that are known to be effective on tumors with DNA repair defects are the PARP inhibitors, but their price is high. “If carboplatin proves to be a good therapeutic option, the results of our trial will have a positive impact on the patients”, concludes Olmos. Mateo adds: “Since it is a drug that has already been approved and has been routinely used for other types of cancer, like breast and ovarian cancer, carboplatin’s way to the clinic to benefit patients with prostate cancer will be much shorter than usual. There is little experience with this drug for the treatment of the prostate cancer, but for now it looks promising. What we aim with this study is to be able to confirm it”.

PSA-screening cuts deaths from prostate cancer by 30%. This is based on research data from 20,000 men monitored for more than two decades. The PSA level initially measured in these men proved highly significant as a predictor of future cancer risk.

This research is important because it shows the long-term effects of an organized screening program.

The main purpose of this research was to enhance understanding of the implications of screening, and of the possible design of a future screening program for prostate cancer.

The study was unique in many ways, and to date, has the longest follow-up period of all screening studies on prostate cancer worldwide.

The Randomized Population-Based Prostate Cancer Screening Trial initially was comprised of a total of 20,000 men aged 50-64. 10,000 were randomly selected for a screening group and offered PSA testing (screening) every two years and cell sampling if elevated PSA levels were found. The remaining 10,000 were assigned to the control group and not offered PSA sampling in the study.

After 22 years of follow-up, approximately 300 men had died of prostate cancer. The risk was 30 percent lower for men who had undergone screening in the program. Men at the highest risk of dying from prostate cancer were those whose screening started after age 60; men who were diagnosed after leaving the study (aged about 70 and over); and those who were invited, but did not participate at all.

The study also included outcomes for men who participated in the screening program and left the trial without prostate cancer being detected. Among the men who were monitored for nine years after their screening ended, 200 cancer cases altogether were found. Of these men, 21 later died from the disease.

PSA levels on the first screening occasion proved to have a major bearing on future cancer outcomes. They may therefore be used for risk estimation. The results also showed that in men with voiding dysfunction — difficulty in emptying the bladder — the risk of prostate cancer was lower than in symptom-free men in the study.

The U.S. Senate and House recently released their conference report on the 2019 Defense Appropriations Bill, which once again allocates $100M to the Prostate Cancer Research Program (PCRP).

Approximately one year previous, Congress increased the PCRP at the Department of Defense (DoD) budget by $10M, returning the program to its 2001 funding level for the first time in 18 years.

The PCRP budget has been at $100M for the first time in back to back years. This increase could mean a brighter future for men fighting prostate cancer, and the funds could possibly lead to new groundbreaking treatments and diagnostic tools.

In February hundreds of passionate advocates spent countless hours meeting with their elected officials through ZERO’s Summit in Washington, D.C. Many then spent time on the telephone lines. They also pounded the pavement during a recess period by attending in-district meetings.

The move to increase research funds at the PCRP is at the top of ZERO’s Summit agenda. This program works with patients to identify gaps in research and care. It then awards talented scientists who are pursuing advancements to eliminate those identified areas of need.

The research funded by the PCRP is more critical than ever as Surveillance, Epidemiology, and End Results (SEER) data from the National Cancer Institute predicted deaths to jump by 3,000 in 2018 alone.

More than 164,000 men will be diagnosed with prostate cancer this year and nearly ten percent of those diagnoses will occur among our nation’s veteran population.

A common process in the development of late-stage, small cell cancers of the prostate and lung has recently been discovered. The discovery of these shared molecular mechanisms could lead to the development of drugs to treat prostate and lung cancers, but other small cell cancers of almost any organ as well.

The key finding of the research is as follows: Although prostate and lung cells have very different patterns of gene expression when they’re healthy, they have almost identical patterns when they transform into small cell cancers. This new research suggests that different types of small cell tumors evolve similarly, even when they come from different organs.

Cancers that become resistant to treatment often develop into small cell cancers which generally have extremely poor prognoses. They are also known as small cell neuroendocrine carcinomas, or SCNCs. Certain cancers can evade treatment; they do this in part by changing cell types such as changing from aggressive adenocarcinoma to small cell carcinoma.

Previously some research had hinted that small cell cancers from different organs may be driven by common mechanisms, but this recent study is the first to clearly describe the steps in the evolution.

The study’s authors and collaborators explored the potential parallels between cancer types by transplanting human prostate cells with five genes, known collectively as PARCB, into mice. When the transplanted cells grew within the mice, the cells displayed unique features of human small cell neuroendocrine carcinomas.

As part of the study the team also identified that for small cell neuroendocrine carcinomas to develop in the prostate, two tumor suppressor genes, TP53 and RB1, had to be simultaneously inactivated when PARCB was introduced. TP53 and RB1 are known for protecting normal cells from transforming into cancer cells.

Additional tests confirmed striking similarities between the PARCB-SCNC cells and small cell prostate cancer cells from humans. In particular, RNA expression and the turning on and off of certain genes were nearly identical. The team found that the similarities between the PARCB-SCNC cancers and human small cell prostate cancers were extraordinary.

Large databases of gene expression were looked at in order to compare the patterns of gene expression in their PARCB-SCNC cells to cancers of other organs. The team found that the pattern of gene expression in PARCB-SCNC cells was extremely similar to those of both prostate and lung small cell cancers.
They then tested whether PARCB genes could alter healthy cells from human lungs into small cell lung cancers. The scientists determined that this was possible.

The team is also working on mapping which genes control the entire cascade of events that underlies the transition to small cell cancer. Studying the network of the master gene regulators may lead to a new way of combating deadly cancers.