Genetic Testing for Cancer Lacking for Women on Medicare: Study

FRIDAY, Aug. 17, 2018 — Testing for gene mutations linked to breast and ovarian cancer is rare among some Medicare patients who have the cancers and qualify for such tests, a new study finds.

Researchers analyzed data from 12 southeastern states between 2000 and 2014. Only 8 percent of 92 women who met Medicare criteria for BRCA1 and BRCA2 gene testing received it within five years of their cancer diagnosis, the study found.

No patients in Arkansas, Louisiana, Tennessee, Virginia and West Virginia got the tests, according to the study published Aug. 14 in the Journal of the American Medical Association.

Breast cancer patients with BRCA mutations are more likely to develop cancer in a second breast and are also at increased risk for ovarian cancer. Ovarian cancer patients with the gene changes are more likely to get breast cancer.

Relatives who also have the mutations also face a higher cancer risk, the Vanderbilt University Medical Center researchers said.

“Women who carry one of these mutations but don’t know their mutation status are not able to take advantage of preventive or early detection interventions that we have available, so they miss out on the opportunity to reduce their risk for these cancers and potentially reduce their overall mortality,” study author Amy Gross said in a university news release.

“They are also not able to inform family members who might be affected,” Gross added. She is an epidemiologist at the Vanderbilt Institute for Clinical and Translational Research in Nashville.

The study covered a broad age range: More than half of the women were under age 65 and qualified for Medicare due to disabilities.

The researchers said lack of patient interest and physician recommendations might explain the low genetic testing rate. None of the patients had received a doctor referral for genetic counseling, they added.

More information

The U.S. National Cancer Institute has more on BRCA gene mutations.

Posted: August 2018

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Better access to quality cancer care may reduce rural and urban disparities

When enrolled in a cancer clinical trial, the differences in survival rates between rural and urban patients are significantly reduced, SWOG study results show.

The study results are published in JAMA Network Open by a team led by Joseph Unger, Ph.D., a SWOG biostatistician and health services researcher at Fred Hutchinson Cancer Research Center. It’s the first study to comprehensively compare survival outcomes in rural and urban cancer patients enrolled in clinical trials.

The results cast new light on decades of research, which paints a stark picture of cancer disparities. About 19 percent of Americans live in rural areas, and studies have shown that, when faced with cancer, rural patients don’t live as long as urban cancer patients. For example, statistics published by the federal Centers for Disease Control and Prevention in 2017 show a significant difference in the rate of cancer deaths, with 180 people out of 100,000 dying of cancer in rural areas compared with 158 people out of 100,000 dying of cancer in urban areas between 2011 and 2015.

But the new analysis by SWOG, the international cancer clinical trials network funded by the National Cancer Institute (NCI), indicates that this difference in survival is not due to patients—but to the care they receive.

“These findings were a surprise, since we thought we might find the same disparities others had found,” Unger said. “But clinical trials are a key difference here. In trials, patients are uniformly assessed, treated, and followed under a strict, guideline-driven protocol. This suggests that giving people with cancer access to uniform treatment strategies could help resolve the disparities in outcomes that we see between rural and urban patients.”

Unger and SWOG member Dr. Banu Symington, an oncologist who practices at the Sweetwater Regional Cancer Center in rural Idaho, received a grant from SWOG’s public charity, The Hope Foundation, to study cancer disparities by analyzing existing data from the group’s trials. The team had a big trove of data to mine. Founded in 1956, SWOG has run more than 1,400 cancer clinical trials enrolling nearly 215,000 patients.

Unger and his team identified 36,995 patients who enrolled in 44 SWOG phase II or III treatment trials between 1986 and 2012. Patients hailed from all 50 states, and had 17 different cancer types, including acute myeloid leukemia, sarcoma, lymphoma, myeloma, and brain, breast, colorectal, lung, ovarian, and prostate cancers. The team limited their analysis of survival to the first five years after trial enrollment to emphasize outcomes related to cancer and its treatment.

Using U.S. Department of Agriculture population classifications known as Rural-Urban Continuum Codes, the team categorized the patients as either rural or urban and analyzed their outcomes. Patient outcomes included overall survival, or how long patients lived; progression-free survival, or how long patients lived before their cancer returned; and cancer-specific survival, or how long the patients lived without dying of cancer. The team used a statistical model known as a multivariate Cox regression to analyze their data.

This method allows investigators to examine the relationship between survival and one or more predictor values, such as the age of the patient or the stage of their cancer.

No matter the variable, or the cancer type, results were clear. There was no meaningful difference in survival patterns between rural and urban patients for almost all of the 17 different cancer types. The only exception was patients with estrogen receptor-negative, progesterone receptor-negative breast cancer. Rural patients with this cancer didn’t live as long as their urban counterparts, a finding the team says could be attributed to a few factors, including timely access to follow-up chemotherapy after their first round of cancer treatment.

“If people diagnosed with cancer, regardless of where they live, receive similar care and have similar outcomes, then a reasonable inference is that the best way to improve outcomes for rural patients is to improve their access to quality care,” Unger said.

Unger noted that the NCI CommunityOncology Research Program (NCORP) – which funded his study—brings clinical trials into community hospitals and clinics, including in rural areas, and represents the community-level outreach that can provide the quality cancer care that may be needed. In 2014, NCI officials broadened NCORP eligibility to include oncology practices that serve large rural populations. Currently, there are NCORP sites in 13 states in which the rural population exceeds 30 percent—Alaska, Ark., Iowa, Ky., Miss., Mont., N.C., N.D., S.C., S.D., Tenn., Wis., and Wyo. The result is that tens of thousands of rural cancer patients can enroll in NCI clinical trials and be cared for right at their local hospital and clinic.

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Better statistical methods to understand gene interactions leading to cancer development

Research led by Hui-Yi Lin, Ph.D., Associate Professor of Biostatistics at LSU Health New Orleans School of Public Health, has developed another novel statistical method for evaluating gene-to-gene interactions associated with cancer and other complex diseases. The Additive-Additive 9 Interaction (AA9int) method is described in a paper published in Bioinformatics.

“This method can identify combinations of genetic variants for predicting cancer risk and prognosis,” notes Dr. Lin, who is also the paper’s lead author.

AA9int is based upon another method Lin developed, SNP Interaction Pattern Identifier (SIPI), to identify interactions between single nucleotide polymorphisms (SNPs). According to the National Institutes of Health, “Single nucleotide polymorphisms, frequently called SNPs (pronounced “snips”), are the most common type of genetic variation among people. Each SNP represents a difference in a single DNA building block, called a nucleotide. Most commonly, these variations are found in the DNA between genes. They can act as biological markers, helping scientists locate genes that are associated with disease. When SNPs occur within a gene or in a regulatory region near a gene, they may play a more direct role in disease by affecting the gene’s function.”

Although SNP-SNP or gene-gene interaction studies have been emerging, the statistical methods for evaluating SNP-SNP interactions are still in their infancy. The conventional approach to test SNP interactions is to use a hierarchical interaction model with two main effects plus their interaction with both SNPs as an additive inheritance mode. However, this approach tests just one specific type of interaction, which can lead to many false negative findings.

SNP Interaction Pattern Identifier (SIPI), the first statistical method to thoroughly search for meaningful SNP-SNP interaction patterns in cancer and other complex diseases, can detect novel SNP interactions that the conventional statistical approach cannot. SIPI evaluates 45 SNP interaction patterns. Its computational demands are large, however, which may not be desirable for large-scale studies. So, Lin and her colleagues sought a smaller version with fewer testing models but with similar power. They showed that a mini version of SIPI—AA9int, which is composed of nine interaction models—used only about 20% of computing time. More efficient and feasible for large-scale studies, AA9int is still more effective than the traditional approach.

“We found that AA9int successfully detected 72-90% of the SIPI-identified SNP pairs,” reports Lin. “Not meant to replace SIPI, but for large-scale studies, AA9int is a powerful tool that can be used alone or as the screening stage of a two-stage approach (AA9int+SIPI) to detect SNP-SNP interactions.”

The research team also studied the impact of inheritance mode and model structure on detecting SNP-SNP interactions. SNP Interaction Pattern Identifier (SIPI) evaluates SNP interaction patterns by considering three major factors: model structure (hierarchical and non- hierarchical model), genetic inheritance mode (dominant, recessive and additive), and mode coding direction. AA9int considers non-hierarchical model structure and the additive mode. They found that non-hierarchical models play a more important role in SNP interaction detection than inheritance modes.

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Diets ‘devoid of vegetable matter’ may cause colon cancer

Researchers from the Francis Crick Institute in London, United Kingdom, found that keeping mice on a diet rich in a compound known as indole-3-carbinol (I3C) — which comes from such vegetables — prevented the animals’ intestines from becoming inflamed and developing colon cancer.

They report the study in a paper now published in the journal Immunity.

“Seeing the profound effect,” says study senior author Dr. Brigitta Stockinger, a group leader at the Francis Crick Institute, “of diet on gut inflammation and colon cancer was very striking.”

Our digestive system produces I3C when we eat vegetables from a “large and diverse group” of plants known as brassicas.

Brassicas include, but are not limited to: broccoli, cabbage, collards, Brussels sprouts, cauliflower, kale, kohlrabi, swede, turnip, bok choi, and mizuna.

Colon cancer typically starts as a growth, or polyp, in the lining of the colon or large intestine. It can take many years for the cancer to develop from a polyp and not all polyps become cancerous.

Cancer of the colon or rectum is the third most commonly diagnosed in both women and men in the United States, not counting skin cancer.

The American Cancer Society (ACS) estimate that there will be 97,220 new cases of diagnosed colon cancer in the U.S. in 2018.

‘Concrete evidence’ of hidden mechanism

Despite a lot of evidence about the benefits to our digestive system of a diet rich in vegetables, much of the underlying cell biology remains unknown.

The new findings are the first to give “concrete evidence” of how dietary I3C — through its effect on a cell protein known as aryl hydrocarbon receptor (AhR) — protects the gut from inflammation and cancer.

AhR has several roles, and for it to work properly, it has to be activated by a compound that binds to it uniquely. I3C is such a compound.

One of AhR’s jobs in the gut is to pick up environmental signals and pass them on to immune cells and other cells in the lining. These signals are important for protecting the digestive tract from inflammation-promoting signals that come from the “trillions of bacteria” that live in it.

Another important role that AhR plays is helping stem cells convert into specialized gut lining cells that produce protective mucus and help extract nutrients from food.

When AhR is absent or does not work properly, the stem cells do not convert into working cells in the gut lining but “divide uncontrollably.” Uncontrolled cell division may lead to abnormal growths that can become malignant, or cancerous.

Importance of ‘plant matter’ in diet

Dr. Stockinger and her colleagues saw that normal laboratory mice that ate “purified control diets” developed colon tumors within 10 weeks, while those that ate standard “chow” containing grains and other ingredients did not develop any.

Purified control diets are tightly controlled to include precise amounts of protein, fat, carbohydrate, fiber, minerals, and vitamins. They are designed to exactly match nutritional requirements without including germs, allergens, and other substances that might introduce spurious variables in experiments.

The new study suggests that because purified control diets contain less plant matter, they have fewer compounds that activate AhR, compared with standard chow diets or diets enriched with I3C.

Dr. Chris Schiering, of Imperial College London, remarks that “even without genetic risk factors,” it would seem that “a diet devoid of vegetable matter can lead to colon cancer.”

‘Significantly fewer tumors’

The researchers used mice and organoids, or “mini guts,” grown from mouse stem cells, in their experiments. These revealed that the ability of intestinal epithelial cells to replenish themselves and repair the gut lining after infection or chemical damage was “profoundly influenced” by AhR.

The team also found that genetically engineered mice whose intestinal epithelial cells had no AhR — or could not activate the protein — failed to control an infection from a gut bacterium called Citrobacter rodentium. The animals developed gut inflammation and then colon cancer.

“However, when we fed them a diet enriched with I3C, they did not develop inflammation or cancer,” remarks first author Dr. Amina Metidji, also of the Francis Crick Institute.

Additionally, notes Dr. Metidji, when they switched mice that were already developing colon cancer to a diet rich in I3C, they found that those animals developed “significantly fewer tumors” and that those tumors were less likely to be malignant.

In discussing their results, the researchers raise the issue of whether it is the high fat content or the low consumption of vegetables in high-fat diets that explains the link to colon cancer.

The scientists now expect to continue the work on I3C and AhR with organoids grown from human gut tissue extracted in biopsies. Eventually, they expect the work to lead to human trials.

These findings are a cause for optimism; while we can’t change the genetic factors that increase our risk of cancer, we can probably mitigate these risks by adopting an appropriate diet with plenty of vegetables.”

Dr. Brigitta Stockinger

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Clinical trial suggests new direction for heavy-smoking head and neck cancer patients

Patients with a greater than 10 pack/year history of smoking tend to develop an especially dangerous form of head and neck squamous cell cancer (HNSCC) for which prognosis remains poor and treatments have changed little during the past two decades. However, recent phase 1 clinical trial results by the Head and Neck Cancer Group at University of Colorado Cancer Center suggest a possible new direction for these patients. The first-in-human trial of the oral PARP inhibitor olaparib, with the anti-EGFR drug cetuximab and radiation, led to 72 percent 2-year survival in 16 patients on trial, compared with an expected 2-year survival rate of about 55 percent for standard-of-care treatment.

“Colorado promotes innovation, and this trial was certainly innovative when it was designed by our group,” says David Raben, MD, CU Cancer Center investigator and professor in the CU School of Medicine Department of Radiation Oncology. “Much credit goes to Antonio Jimeno, MD, Ph.D. who was very supportive of this idea and helped move this forward along with Dr. Sana Karam and Dr. Daniel Bowles.”

The drug cetuximab targets EGF receptor signaling (EGFR) and while it earned FDA approval in 2006 for use against head and neck cancers over-expressing EGFR, Raben stated there is significant room for improvement.

“That’s where olaparib and radiation come in,” he says. “Ten years ago, I was on a sabbatical from CU, working for AstraZeneca in England. And I remember taking the train from Manchester to Cambridge to learn about this new drug from a small biotech company called Kudos Pharmaceuticals. It was a PARP-inhibitor, meant to keep cells from repairing damaged DNA. That’s the drug we now call olaparib.”

Early in development, the drug had shown remarkable activity in woman with BRCA mutations, “but we wanted to know if it worked in other diseases where BRCA wasn’t the story,” Raben says.

Olaparib inhibits the action of an enzyme known as PARP, which is important for DNA repair. HNSCC in heavy smokers already tends to carry a heavy load of DNA damage. And radiation creates additional DNA damage. When olaparib nixes the ability of these cancers’ to repair DNA, it can push cancer cells past the tipping point of damage and into cell death. In this way, PARP inhibition and radiation may be synthetically lethal, meaning that together they exploit deficiencies in gene defects that leads to enhanced cell death.

In fact, lab work by Raben and CU Cancer Center colleagues including Xiao-Jing Wang MD, Ph.D., Barb Frederick, Ph.D., and Ariel Hernandez, among others, shows that PARP inhibitors like olaparib may also amplify the effects of anti-EGFR drugs like cetuximab.

“The traditional approach against this kind of cancer uses cisplatin chemotherapy along with radiation. I had seen data suggesting that the combination of cisplatin and olaparib might be too toxic on patients’ blood counts. So our team explored this alternative approach that we hoped would offer a more targeted treatment in this poor prognosis group,” Raben says.

In addition to promising survival results, the trial reinforces earlier work showing that cancer patients who continue to smoke while receiving treatment tend to fare worse than those who quit.

“We didn’t cherry pick our patients for this trial. All were heavy smokers, many were heavy drinkers, advanced T-stages, and some continued to smoke during the treatment. People who continued smoking were the ones who did the worst,” Raben says.

However, the trial’s survival benefit came with additional side effects, some of which appeared relatively late in the course of the trial (demonstrating the importance of long-term follow-up for patients in radiation Phase I studies).

“We did see an increase in skin toxicity, which wasn’t unexpected, and we learned that when you combine olaparib with radiation, you need perhaps one tenth the dose that you would when using olaparib alone,” Raben says. Most common side effects included dermatitis (39 percent) and mucositis (69 percent). Several patients experienced increased long-term fibrosis and one showed carotid stenosis, though Raben points out that some side effects could be due to the continued influence of smoking, as well.

“The question now is whether we should move this combination into a randomized phase II trial or use what we’ve learned to design new combinations,” Raben says. For example, “There is tremendous enthusiasm in the oncology community to combine DNA damage repair inhibitors like olaparib with immune enabling drugs, and this may reduce overall toxicity further when combined with or used after radiation,” he says.

Or, Raben suggests that targeted therapies and immunotherapies could be used earlier in the course of treatment, pointing to a forthcoming clinical trial by collaborator Sana Karam, MD, Ph.D., that will test the ability of radiation and immunotherapy to shrink head and neck cancer tumors before surgery.

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Compound in kale, cabbage and broccoli protects against bowel cancer

Compound in kale, cabbage and broccoli protects against bowel cancer 

Another reason to eat your greens! Compound in kale, cabbage and broccoli protects against bowel cancer

  • When green vegetables are digested, a protein is activated
  • This protein reduces gut inflammation and prevents colon cancer forming
  • It repairs damaged gut cells, allowing them to absorb nutrients and make mucus
  • Damaged cells go on to divide uncontrollably, which can lead to bowel cancer
  • Researchers say the ’cause for optimism’ helps people reduce their cancer risk 
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Kale, cabbage and broccoli protect against bowel cancer, new research suggests.

When green vegetables are digested a protein is activated that reduces gut inflammation and prevents the colon form of the disease, a study found today.

The protein, known as aryl hydrocarbon receptor (AhR), repairs damaged gut cells that would otherwise be unable to absorb nutrients or secrete protective mucus, the research adds. 

Damaged cells go on to divide uncontrollably, which can lead to bowel cancer, the study found. 

Study author Dr Gitta Stockinger, from the Francis Crick Institute, London, said: ‘These findings are a cause for optimism; while we can’t change the genetic factors that increase our risk of cancer, we can mitigate these risks by adopting a diet with plenty of vegetables.’


Kale, cabbage and broccoli protect against bowel cancer, new research suggests (stock)

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DO WALNUTS PREVENT HEART DISEASE AND BOWEL CANCER?

A handful of walnuts a day may prevent heart disease and bowel cancer, research suggested in May 2018.

Eating just a third of a cup of walnuts for six weeks significantly reduces the production of excess bile acids, as well as lowering ‘bad’ cholesterol levels, a study found.

Previous research has linked such bile acids to bowel cancer, while lower cholesterol levels are associated with a reduced risk of heart disease.

Researchers believe walnuts’ high-fibre content encourages the growth of ‘good’ bacteria in the gut, which benefits people’s heart and colon health.

The scientists also found that despite walnuts being relatively high in calories, with around 28 per nut, only 80 per cent of them are absorbed, with gut bacteria using up the remaining 20 per cent.

Results further suggest people who eat a handful of walnuts a day produce less secondary bile acids, which are made in the bowel rather than the liver like their primary counterparts.

Lead author Professor Hannah Holscher, from the University of Illinois, said: ‘Secondary bile acids have been shown to be higher in individuals with higher rates of colorectal cancer.

‘Secondary bile acids can be damaging to cells within the GI tract and microbes make those secondary bile acids.

‘If we can reduce secondary bile acids in the gut, it may also help with human health.’

Green vegetables reduce tumours in cancer sufferers 

The researchers analysed genetically modified mice that could not produce or activate AhR in their guts.

The rodents developed gut inflammation that progressed to bowel cancer. 

Yet, the animals fed a diet rich in green vegetables developed neither inflammation nor cancer.

Lead author Dr Amina Metidji said: ‘Interestingly, when mice whose cancer was already developing were switched to the [green vegetable]-enriched diet, they ended up with significantly fewer tumours which were also more benign.’ 

‘It’s not just fibre in vegetables that reduces the risk of bowel cancer’

Professor Tim Key, from Cancer Research UK, who was not involved in the research, said: ‘This study suggests it’s not just the fibre in vegetables like broccoli and cabbage that help reduce the risk of bowel cancer, but also molecules found in these vegetables too.

‘This adds to the evidence that a healthy diet, rich in vegetables, is important.’ 

Dr Stockinger added: ‘We often think of colon cancer as a disease promoted by a Western diet rich in fat and poor in vegetable content, and our results suggest a mechanism behind this observation. 

‘Many vegetables produce chemicals that keep AhR stimulated in the gut. We found that AhR-promoting chemicals in the diet can correct defects caused by insufficient AhR stimulation. 

‘This can restore cell differentiation, offering resistance to intestinal infections and preventing colon cancer.’

The researchers hope to analyse the effects of green vegetables on human colon cells in the lab and eventually in people.

Dr Stockinger added: ‘There is very little literature on which vegetables are the most beneficial or why. 

‘Now that we’ve demonstrated the mechanistic basis for this in mice, we’re going to investigate these effects in human cells and people. In the meantime, there’s certainly no harm in eating more vegetables!’ 

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Large collection of brain cancer data now easily, freely accessible to global researchers

A valuable cache of brain cancer biomedical data has been made freely available to researchers worldwide, say researchers at Georgetown Lombardi Comprehensive Cancer Center. The dataset, REMBRANDT (REpository for Molecular BRAin Neoplasia DaTa) hosted and supported by Georgetown, is one of only two such large collections in the country.

Information about the brain cancer data collection, which contains information on 671 adult patients collected from 14 contributing institutions, is detailed in Scientific Data, an open-access journal (Nature). Already, thousands of researchers in the U.S. and internationally log on to the data site on a daily basis, and word about the resource is expected to increase its use, says Subha Madhavan, Ph.D., chief data scientist at Georgetown University Medical Center and director of the Innovation Center for Biomedical Informatics (ICBI) at Georgetown Lombardi.

The Georgetown data resource is unique in several ways. One is that it contains genomic information, collected from volunteer patients who allowed their tumors to be sampled, as well as diagnostic (including brain scans), treatment and outcomes data. Most collections contain either one or the other.

Additionally, the data collection interface is extraordinarily easy to use, Madhavan says.

“It sits on Amazon Web Services, and has a simple web interface access to data and analysis tools. All a researcher needs is a computer and an internet connection to log onto this interface to select, filter, analyze and visualize the brain tumor datasets.

“We want this data to be widely used by the broadest audience—the entire biomedical research community—so that imagination and discovery is maximized,” says first author on the paper Yuriy Gusev, Ph.D., associate professor and a faculty member of the ICBI. “Our common goal is to tease apart the clues hidden within this biomedical and clinical information in order to find ways that advance diagnostic and clinical outcomes for these patients.”

“We are just beginning to understand the science of how these cancers evolve and how best to treat them, and datasets like this will likely be very helpful,” Madhavan says.

The REMBRANDT dataset was originally created at the National Cancer Institute and funded by Glioma Molecular Diagnostic Initiative led by co-authors Howard Fine, MD, from New York Presbyterian Hospital, and Jean-Claude Zenklusen, Ph.D., from the National Cancer Institute. They collected the data from 2004-2006.

The NCI transferred the data to Georgetown in 2015, and it is now physically located on the Georgetown Database of Cancer (G-DOC), a cancer data integration and sharing platform for hosting alongside other cancer studies. G-DOC investigators, led by Madhavan, developed novel analytical tools to process the information anew.

The genomic data includes the specific genes within individual tumors that are either over-expressed or under-expressed as well as the number of times that gene is repeated within a chromosome.

“We inherit two copies of a gene—one from Mom and one from Dad—but in cancer cells, DNA segments containing important tumor suppressor or onco- genes can be entirely deleted or amplified. It isn’t unusual to see a chromosome within a tumor that has 11 copies of a gene, each of which may be producing a toxic protein that helps the cancer grow uncontrollably,” she says.

The data collection also includes information on RNA, which is produced by genes (DNA) and can be measured to assess genes that are dysregulated.

Researchers can search their gene of interest, check their expression and amplification status and link that to clinical outcomes, Madhavan says. They can save their findings to their workspace on the G-DOC site and share with their collaborators. Given the approximately 20,000 protein coding genes in the human genome, and the variety of brain cancer tumor types, “it will take a big village—really a vast metro area—of investigators to understand the bases of these tumors and to effectively develop treatments that target them.”

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Woman had two days to live after dismissing her cancer as stress

The woman given just two days to live after dismissing her cancer symptoms as divorce stress

Woman, 32, who dismissed her exhaustion and headaches for divorce stress was horrified to discover they were signs of blood cancer and she had just 48 HOURS to live

  • Kate Stallard thought her headaches were down to her adapting to single life 
  • Became concerned after collapsing in the bathroom in the middle of the night
  • Cancer had weakened her immune system, leaving her with deadly sepsis
  • Forced to start treatment immediately with no time to freeze her eggs
  • After entering remission, her cancer returned in her central nervous system  
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A woman discovered she had just two days to live after she mistook symptoms of leukaemia for signs of divorce stress.

Kate Stallard, 32, who separated from her husband of 18 months in the summer of 2016, thought her headaches and exhaustion were the result of her adapting to single life until she collapsed in the middle of the night.

After being diagnosed with acute promyelocytic leukaemia, Ms Stallard was told the cancer had weakened her immune system so much she had developed life-threatening sepsis and would die within days unless she started chemotherapy.

Kate Stallard’s condition was so severe she did not have time to freeze her eggs before initiating treatment, which has left her infertile, forcing her to give up her hopes of being a mother.

After enduring three rounds of chemotherapy that left her hospitalised for six weeks, Ms Stallard was told she was in remission, only to discover the cancer had returned to her central nervous system, forcing her to undergo a further 17 weeks of chemo.

Although happy to now be cancer free, Ms Stallard, from Worcestershire, has revealed she is grieving the loss of ever having children of her own.

She is now speaking out to raise awareness of the symptoms of leukemia.   


Kate Stallard (pictured before she became unwell) was given just two days to live after she dismissed her exhaustion and headaches as being down to the stress of her divorce


After being diagnosed with acute promyelocytic leukaemia, Ms Stallard was told she would die within two days unless she started chemotherapy (pictured during treatment)


Ms Stallard underwent cranial radiotherapy to prevent her cancer entering her brain (pictured during treatment), however, after entering remission, the disease returned to her central nervous system. She was then forced to endure 17 more weeks of chemotherapy

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WHAT IS ACUTE PROMYELOCYTIC LEUKAEMIA?

Leukaemia is cancer of the white blood cells. Acute leukaemia means the condition progresses rapidly and aggressively, requiring immediate treatment.

Acute promyelocytic leukaemia (APML) is a rare form of the Acute Myeloid Leukaemia (AML), the form of the disease which affects the myeloid cells.

APML accounts for around 10 -15 per cent of all cases of AML.

The myleloid cells perform a number of different functions, such as fighting bacterial infections, defending the body against parasites and preventing the spread of tissue damage.

In APML a change in a specific chromosome leads to a changes in white blood cells called Promyelocyte cells, which means they do not progress to maturity.

This leads to a bleeding disorder due to abnormal clotting.

The symptoms include pale skin, tiredness, breathlessness, frequent infections, and unusual and frequent bleeding, such as bleeding gums or nosebleeds.

The main treatment for AML is chemotherapy, which is used to kill as many leukaemia cells in your body as possible and reduce the risk of the condition coming back (relapsing).

In some cases, intensive chemotherapy and radiotherapy may be needed, in combination with a bone marrow or stem cell transplant, to achieve a cure.

Studies have shown that people with acute promyeloid leukaemia (APML), around 85 per cent will live for at least five years with treatment.

Source: NHS Choices

‘I put it down to the emotional toll of the divorce’  

Speaking of her separation, Ms Stallard said: ‘It was a really stressful time, and very difficult to try and survive it all.’

Determined to stay positive, Ms Stallard, who had been in a relationship with her husband for 10 years, began going to the gym more often in an attempt to boost her energy levels and improve her mood.

Yet despite her best efforts, Ms Stallard constantly felt exhausted and even needed breaks while walking her dogs, saying: ‘For two months, I put it down to the emotional toll of the divorce. 

‘I started getting throbbing headaches too, where I could literally hear my heartbeat.

‘I was working out a lot, but so tired that I wasn’t getting any fitter no matter how much I trained. I put a lot of it down to divorce stress.’

Then, in September 2016, just days before her diagnosis, Ms Stallard started her period, which was unusually heavy.

She said: ‘It just wouldn’t stop. It was almost like a haemorrhage.’

Beginning to panic, Ms Stallard visited a doctor, saying: ‘I’d spoken with a relative who’d had aplastic anaemia, a rare bone marrow disease, so I thought it’d be something like that, or perhaps even a virus. 

‘I assumed I’d go to the doctor and be sent off with some antibiotics.’

After being checked over, Ms Stallard asked if she could have a blood test, just to be sure.

Yet, due to her being classed as a non-urgent case, she was told she would need to wait a week for an appointment to become available.


Ms Stallard (pictured before) began exercising to help her cope with the stress of separation and therefore thought unexplained bruises were down to her bumping against gym equipment


Ms Stallard (pictured before) became concerned when her period was exceptionally heavy 

Told to go to A&E urgently        

Just two days later, Ms Stallard rapidly went downhill, as she recalls crawling up the stairs to her bathroom. 

Terrified she would pass out with nobody to find her, Ms Stallard called NHS 111, which organised for her to have an emergency appointment in the middle of the night.

She said: ‘I got there about 1am. They took one look at me and knew something was really wrong. 

‘They examined all my bruises and took more bloods, which they sent off to be urgently tested.

‘I went home to wait for the results, and around two hours later, my phone rang again with the doctor telling me I was seriously ill and needed to get to A&E fast.’

‘My world fell apart’ 

From there, Ms Stallard’s sister Lindsay, 37, drove her to Worcestershire Royal Hospital, where a team of doctors and nurses were waiting.

Taken straight into isolation, she was given a blood transfusion while they ran further tests, including a bone marrow biopsy.

A few hours later, doctors broke the news she had leukaemia and sepsis. 

Ms Stallard said: ‘I’d been panicking, realising something was very wrong, but I still never thought it could be cancer. Being diagnosed was absolutely terrifying. My world fell apart.

‘After the night I went to hospital, I didn’t leave for six weeks. Doctors told me if I hadn’t started treatment right away, I would have only had a couple of days left to live.’

Speaking of her sepsis diagnosis, Ms Stallard added: ‘Where my immune system was so weakened by the cancer, I must have picked up other bugs, which had then developed into a type of sepsis as my body attacked itself.’

Due to her requiring urgent care, Ms Stallard was unable to go home, with her remaining in hospital while doctors ensured she was strong enough to begin chemotherapy in two days’ time.

She said: ‘I was told the type of chemotherapy drug I was to have can affect fertility. One of my first questions was, “can I freeze my eggs?”

‘But doctors told me that the process takes a few weeks and I wouldn’t survive it. It was devastating.

‘I held on to the hope that the chemotherapy may not do that much damage, but I have since gone for fertility tests and it wasn’t possible to harvest any eggs.

‘That’s been one of the hardest parts and most horrific side effects for me. I know adoption and so on is an option, and that I had to have the treatment to stay alive, but I still need to grieve.

‘One of the things that helped get me through my divorce was that I’m still young, so there was time to meet someone else and start a family.’ 


After collapsing in the night and finally being diagnosed, Ms Stallard started treatment immediately, with her enduring three rounds of chemotherapy during a six week hospital stay 


Treatment needed to start straight away, with her having no time to freeze her eggs. Due to chemo reducing a patient’s fertility, Ms Stallard’s hopes of being a mother were dashed 


After entering remission, Ms Stallard was forced to endure chemotherapy all over again when her eyesight became blurred, with tests showing she had cancer of the central nervous system


Ms Stallard had a further 17 weeks of chemo, as well as a stem cell transplant


She has been in remission since August 2017, with her undergoing scans every three months

‘The cancer had returned and was in my central nervous system’ 

Ms Stallard endured three rounds of chemotherapy before being told she was in remission.

Yet, the good news was short lived, with her health declining again in February last year.

She said: ‘I was suffering with double vision, and my right eye began to turn in on itself.

‘It transpired the cancer had returned and was in my central nervous system.’

This time Ms Stallard endured 17 weeks of chemotherapy, where drugs were injected into her spinal fluid via a lumbar puncture, followed by a stem cell transplant.

She has been in remission since August last year, with her undergoing scans every three months. 

Ms Stallard is working closely with the charity Leukaemia Care’s ‘Spot Leukaemia’ campaign to raise awareness of the signs of the disease via special symptoms cards, which can be ordered from their website and shown to doctors.

She said: ‘Leukaemia Care are a fantastic charity and together we want to let people know of the symptoms to watch out for.

‘If you’re experiencing anything at all that doesn’t feel right – breathlessness, unexplained bruising, night sweats, bleeding or persistent infections – don’t be afraid to be open and honest with your doctor, and push for a blood test.’ 

Find more information or order a symptoms card here.   


Ms Stallard (pictured this summer) is grieving the loss of ever having children of her own 


She claims loosing her fertility was the hardest side effect and will consider adoption 

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Ministers bow to pressure to lower bowel cancer screening age to 50

Delight as health ministers finally bow to pressure to lower the bowel cancer screening age to 50

Health ministers finally bow to pressure to lower the bowel cancer screening age to 50 in England in move that will save thousands of lives

  • Under current guidelines, patients aged 60 to 74 are offered a home testing kit
  • But new plans, accepted by officials, will bring down the threshold by a decade
  • Charities have expressed their delight over the move, after years of campaigns
  • They hope that it will detect bowel cancer much earlier in thousands of patients
  • Scotland already offers patients their first home testing kit when they turn 50 
  • Officials in Wales and Northern Ireland are expected to make similar moves 
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BBC newsreader George Alagiah is among those who have called for an earlier screening programme for the disease

Everyone aged over 50 will be screened for bowel cancer in England as ministers today finally bowed to pressure to lower the age.

Under current guidelines, patients aged between 60 and 74 are offered a home testing kit for the killer disease every two years.

But new plans, accepted by both the Department of Health and Social Care and Public Health England, will bring down the threshold by a decade.  

Charities today expressed their delight over the bold move, following years of campaigning to bring England in line with Scotland.

They hope it will detect bowel cancer earlier in thousands of patients, boosting their chances of survival dramatically. 

Officials in Wales and Northern Ireland are expected to make similar moves, on the back of the UK-wide recommendations, but have yet to confirm.

BBC newsreader George Alagiah and former health secretary Andrew Lansley are among those who have called for earlier screening for the disease.

Mr Alagiah, 62, who is currently receiving treatment for bowel cancer for the second time, previously said it could have been caught sooner if over-50s were screened in England.

Lord Lansley, announcing he was also being treated for the disease in April, urged the Government to cut the age ‘in line with international best practice’.

Bowel cancer strikes 41,000 each year in UK and kills 16,000, making it the second deadliest cancer – behind only lung cancer.

Survival rates are notoriously poor, as fewer than a tenth of patients survive for five years when it is diagnosed late, compared to 90 per cent if spotted early. 

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The UK National Screening Committee recommended a lower age for screening, following its review of all available evidence. 

They say the faecal immunochemical home testing kit (FIT), easier to use than the current faecal occult blood test, should be rolled out in the UK. 

Studies show the FIT, which needs only one stool sample compared to the six needed in the FOB test, is more accurate in detecting potential bowel cancer. 

GEORGE ALAGIAH’S BATTLE WITH BOWEL CANCER

George Alagiah said in March that he believes his bowel cancer could have been picked up sooner if he lived in Scotland, where earlier screenings are offered.

The BBC newsreader was first diagnosed in 2014 and underwent 17 rounds of chemotherapy and five operations on the cancer, which had spread to his liver and lymph nodes.

After getting the all-clear in 2015, the father-of-two was given the devastating news last December that it had returned. Hours later he went on to present the news that day as normal.

Mr Alagiah, 62, who has been the face of the BBC’s News at Six since 2007, said that while he knows his cancer can no longer be cured, it could have been a different story had he lived in Scotland.

Men and women are offered bowel cancer screening every two years in Scotland from the age of 50. In England, bowel cancer screening often starts at 60, although in recent years one type of test has become available at 55 in some areas. 

The Sri Lankan-born journalist said: ‘Had I been screened, I could have been picked up. Had they had screening at 50, like they do in Scotland… I would have been screened at least three times and possibly four by the time I was 58 and this would have been caught at the stage of a little polyp: snip, snip…

‘We know that if you catch bowel cancer early, survival rates are tremendous. I have thought: why have the Scots got it and we don’t?’

Mr Alagiah has stage 4 bowel cancer, meaning his chance of surviving at least five years is 10 per cent. But the chance of surviving stage 1 bowel cancer for at least five years is almost 100 per cent.

He said the disappointment of the cancer coming back was ‘almost worse than the shock of finding out in the first place’.

Speaking to The Sunday Times, he said: ‘The first time you are just stunned and shocked. But somehow, when you think you have made it well, I might still make it … The disappointment was pretty bad.’

Mr Alagiah was diagnosed with bowel cancer in April 2014 after noticing blood in his stools. He returned to the BBC in November 2015 after being cleared of the disease.

Health and Social Care Secretary Matt Hancock and Public Health Minister Steve Brine agreed to the recommendations by the independent body.

FIT is already due to be rolled out in the autumn and will initially be offered to those aged 60 to 74 years old.

It is expected to be gradually rolled out to over-55s, followed by over-50s, but no official timetable has yet been given.

Men and women in England and Wales are currently offered a one-off bowel scope at the age of 55, if it’s available in their area.

The procedure is expected to be maintained until the new home test is rolled out to this age group.

Public health minister Steve Brine said: ‘We are determined to make our cancer survival rates the best in the world.’

He described it as a ‘much more convenient and reliable test’, which gives them a ‘real opportunity’ to detect thousands of patients earlier.

NHS England and Public Health England will now consider how to move towards lowering the age of screening.

Simon Stevens, chief executive of NHS England, revealed the plans will be included in its goal of reshaping cancer care in the next decade.

Professor Anne Mackie, director of screening at PHE, said: ‘The risk of bowel cancer rises steeply from around age 50-54 and rates are significantly higher among males than females.

‘Starting screening 10 years earlier at 50 will help spot more abnormalities at an early stage that could develop into bowel cancer if not detected.

‘The committee recognises that this change will take time but wants the FIT test to be offered to all aged 60 and over as soon as possible, and options considered for a roll-out plan where screening can be offered at 55 and eventually to all aged 50 – ensuring we have the best bowel screening programme possible.’

Sara Hiom, director of early diagnosis at Cancer Research UK, welcomed the move, arguing more cancers will be spotted earlier, ‘saving lives’.

She said: ‘We’re delighted that the Government has committed to lowering the age that bowel screening can start from 60 to 50. 

‘When bowel cancer is diagnosed at an early stage, nine in 10 people survive but when it is detected in the late stages, survival falls to one in 10.’

However, Ms Hiom argued the staffing crisis in the NHS must be dealt with urgently to ensure that a lower screening age is never threatened.

Deborah Alsina MBE, chief executive of Bowel Cancer UK, announced the charity was also delighted to hear the screening age will be lowered.

She said: ‘We want to see every eligible person in the UK have access to the most effective screening methods. 

‘Today’s recommendation to offer FIT from the age of 50 every two years… is a significant step towards achieving this.

‘We have campaigned strongly for the screening age to be lowered to 50, in line with Scotland and the rest of the world, for some time now.’

Ms Alsina repeated calls for ensuring the over-stretched NHS has enough staff and resources to deal with the increase in demand by lowering the screening age.

WHAT IS BOWEL CANCER?

Bowel, or colorectal, cancer affects the large bowel, which is made up of the colon and rectum.

Such tumours usually develop from pre-cancerous growths, called polyps.

Symptoms include:

  • Bleeding from the bottom
  • Blood in stools
  • A change in bowel habits lasting at least three weeks
  • Unexplained weight loss
  • Extreme, unexplained tiredness
  • Abdominal pain

Most cases have no clear cause, however, people are more at risk if they: 

  • Are over 50
  • Have a family history of the condition
  • Have a personal history of polyps in their bowel
  • Suffer from inflammatory bowel disease, such as Crohn’s disease
  • Lead an unhealthy lifestyle  

Treatment usually involves surgery, and chemo- and radiotherapy.

More than nine out of 10 people with stage one bowel cancer survive five years or more after their diagnosis.

This drops significantly if it is diagnosed in later stages. 

According to Bowel Cancer UK figures, more than 41,200 people are diagnosed with bowel cancer every year in the UK. 

It affects around 40 per 100,000 adults per year in the US, according to the National Cancer Institute.

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Common skin cancer can signal increased risk of other cancers

People who develop abnormally frequent cases of a skin cancer known as basal cell carcinoma appear to be at significantly increased risk for the development of other cancers, including blood, breast, colon and prostate cancers, according to a preliminary study by researchers at the Stanford University School of Medicine.

The increased susceptibility is likely caused by mutations in a panel of proteins responsible for repairing DNA damage, the researchers found.

“We discovered that people who develop six or more basal cell carcinomas during a 10-year period are about three times more likely than the general population to develop other, unrelated cancers,” said Kavita Sarin, MD, PhD, assistant professor of dermatology. “We’re hopeful that this finding could be a way to identify people at an increased risk for a life-threatening malignancy before those cancers develop.”

Sarin is the senior author of the study, which will be published online Aug. 9 in JCI Insight. Medical student Hyunje Cho is the lead author.

Largest organ

The skin is the largest organ of the body and the most vulnerable to DNA damage caused by the sun’s ultraviolet rays. Try as one might, it’s just not possible to completely avoid sun exposure, which is why proteins that repair DNA damage are important to prevent skin cancers like basal cell carcinoma.

Most of the time this system works well. But sometimes the repair team can’t keep up. Basal cell carcinomas are common — more than 3 million cases a year are diagnosed in the United States alone — and usually highly treatable.

Sarin and Cho wondered whether the skin could serve as a kind of canary in the coal mine to reveal an individual’s overall cancer susceptibility. “The skin is basically a walking mutagenesis experiment,” Sarin said. “It’s the best organ to detect genetic problems that could lead to cancers.”

Sarin and Cho studied 61 people treated at Stanford Health Care for unusually frequent basal cell carcinomas — an average of 11 per patient over a 10-year period. They investigated whether these people may have mutations in 29 genes that code for DNA-damage-repair proteins.

“We found that about 20 percent of the people with frequent basal cell carcinomas have a mutation in one of the genes responsible for repairing DNA damage, versus about 3 percent of the general population. That’s shockingly high,” Sarin said.

Furthermore, 21 of the 61 people reported a history of additional cancers, including blood cancer, melanoma, prostate cancer, breast cancer and colon cancer — a prevalence that suggests the frequent basal cell carcinoma patients are three times more likely than the general population to develop cancers.

‘A strong correlation’

To confirm the findings, the researchers applied a similar analysis to a large medical insurance claims database. Over 13,000 people in the database had six or more basal cell carcinomas; these people also were over three times more likely to have developed other cancers, including colon, melanoma and blood cancers. Finally, the researchers identified an upward trend: the more basal cell carcinomas an individual reported, the more likely that person was to have had other cancers as well.

“I was surprised to see such a strong correlation,” Sarin said. “But it’s also very gratifying. Now we can ask patients with repeated basal cell carcinomas whether they have family members with other types of cancers, and perhaps suggest that they consider genetic testing and increased screening.”

The researchers are continuing to enroll Stanford patients in the study, which is ongoing, to learn whether particular mutations in genes responsible for repairing DNA damage are linked to the development of specific malignancies. They’d also like to conduct a similar study in patients with frequent melanomas. But they emphasized that there’s no reason for people with occasional basal cell carcinomas to worry.

“About 1 in 3 Caucasians will develop basal cell carcinoma at some point in their lifetime,” Sarin said. “That doesn’t mean that you have an increased risk of other cancers. If, however, you’ve been diagnosed with several basal cell carcinomas within a few years, you may want to speak with your doctor about whether you should undergo increased or more intensive cancer screening.”

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