The risk of serious adverse effects on the blood status and bone marrow of patients during chemotherapy can be predicted by a model developed at Linköping University, Sweden. This research may make it possible to use genetic analysis to identify patients with a high probability of side effects. 

It is often difficult during cancer treatment to achieve a balance between getting rid of as many tumour cells as possible, while at the same time not causing serious side effects.

One of the common properties of tumour cells is that they grow rapidly and in an uncontrolled manner. The chemotherapy drugs that are used to treat cancer have for this reason been designed to kill rapidly growing cells. But the treatment also kills normal cells that grow rapidly. One of the more sensitive tissues is the bone marrow, where various types of blood cell are formed at a rapid rate. Approximately 25% of lung cancer patients who receive combination treatment with the drugs gemcitabine and carboplatin experience life-threatening side effects on the bone marrow during standard treatment. In many cases, the treatment must be discontinued.

We know that genetic factors play a role in the response of an individual to these treatments. Complicated interactions between many genes are probably involved. The scientists who carried out the study have therefore investigated whether genetic signatures exist that can be used to identify the patients at a high risk of experiencing severe side effects from the treatment. This would enable them to adapt treatment to the individual more accurately from the start: those with a low risk of side effects can be given higher doses, with a stronger effect on the cancer, while those with highest risk can be given another treatment. 
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The study, published in npj Systems Biology and Applications, is a collaboration between researchers in pharmacogenetics and bioinformatics. They determined the complete DNA sequences of 96 patients with non-small cell lung cancer who had been treated with gemcitabine/carboplatin. Sequencing of the whole genome in this way provides information about millions of genetic variants that may be interesting. The researchers wanted to see whether they could find in this huge amount of data functional groups of genes that were linked to the degree of toxicity that the treatment had had on the bone marrow of the different patients

It is not biology, but access to health care that is causing Black Non-Hispanic patients with squamous cell cancer of the head and neck to have lower survival rates

Studies have long reported that Black cancer patients have poorer outcomes than their white counterparts. But two University of Colorado Cancer Center researchers decided to investigate the data further and figure out why. What they found was that the outcome disparity was caused not by biology, but simply by differences in access to health care.

The researchers, Jessica McDermott, MD, an assistant professor in the Department of Medical Oncology, and Sana Karam, MD, PhD, an associate professor in the Department of Radiation Oncology, examined Medicare data for individuals suffering squamous cell cancer of the head and neck. All 13,117 patients in this study were diagnosed with their first and only malignant tumor at age 66 or older sometime between 2006 and 2015.

The data confirmed what has been widely reported for years -- that the Black head and neck cancer patients had worse outcomes than the white cancer patients.

"But then when we controlled for access to care, those differences suddenly disappeared," says McDermott. "When you closely examine the data, it becomes clear what is going on."
Their findings were published this week in the Journal of the National Comprehensive Cancer Network. The physicians hope their research will catch the attention of those who can help narrow those disparate outcomes.

McDermott and Karam identified two major differences for Black patients: first, they presented at later stages of cancer, and second, they were less likely to receive treatment.

"This is an interesting finding," says McDermott. "A lot of the reasons driving the disparate outcomes came down to socially related things - they were less likely to be married, lived in poor areas, had comorbidities [presence of two or more chronic diseases], were less likely to see a primary care provider in the year leading up to the diagnosis, and were more likely to present in the emergency room."

For most cancers, where and when a patient first presents can make a large difference both in the care received and in the outcome.

"Just a reminder that we are talking about a curable disease, a disease that, if treated properly, can be eradicated with a high degree of certainty," says Karam. "I hope that more targeted interventions can be developed as a result of our findings. The problem lies not so much in biological differences, but access. If Black patients get the treatment, they do just as well."

Women who have been treated for breast cancer may have a higher risk of developing cardiovascular disease and in some groups the risk of dying from cardiovascular disease is higher than the risk of dying from breast cancer. The new study shows that it is possible to spot those at the greatest risk using computer analysis of the CT scans that are taken for planning cancer treatments. Researchers say that identifying patients most at risk of cardiovascular disease could allow steps to be taken to lower the risk.

The research was presented by Professor Helena Verkooijen, from the Division of Imaging and Oncology at the University Medical Center Utrecht in The Netherlands. She said: "We've seen great improvement in breast cancer survival, thanks in part to better treatment. However, treatments have side effects and some treatments - such as radiotherapy and certain types of cancer drug - can increase the risk of cardiovascular disease. In my opinion, treating breast cancer means finding the right balance between maximising chances of tackling the tumour, while minimising the risks of side effects, including the risk of cardiovascular disease."

The study included around 14,000 breast cancer patient who were treated with radiotherapy in three large hospitals in The Netherlands between 2005 and 2016.Professor Verkooijen and her colleagues used a measure called coronary artery calcium (CAC) score. This is a calculation of the amount of calcium in the walls of the heart's arteries and it is known to be strong risk factor in cardiovascular disease because calcifications can lead to narrowing or blocking of the blood vessels.

The researchers developed a deep learning algorithm that could gauge the presence and extent of coronary artery calcifications from the CT scans that were already being carried out to help plan each woman's radiotherapy treatment. This allowed them to automate the measurement of CAC for all the women with only minimal extra workload.

Is increased coffee consumption associated with improved survival in patients with advanced or metastatic colorectal cancer?

In a study of 1171 patients with advanced or metastatic colorectal cancer, increased coffee consumption  was associated with lower risk of disease progression and death. Significant associations were noted for both caffeinated and decaffeinated coffee.

Among patients with advanced or metastatic colorectal cancer, the study found that increased coffee intake was associated with lower risk of disease progression and death.

Mackintosh et al. Association of Coffee Intake With Survival in Patients With Advanced or Metastatic Colorectal Cancer. JAMA Oncol, 2020. doi:10.1001/jamaoncol.2020.3938 [Article]

Scientists at Huntsman Cancer Institute (HCI) at the University of Utah (U of U) report today the development of new models to study molecular characteristics of tumors of the lung and pancreas that are driven by mutations in a gene named NTRK1. 

In healthy bodies, NTRK1 has critical functions in the development of nerve cells, particularly those that send signals to the brain about pain, temperature, and touch. In some cancers, these powerful genes malfunction to send signals to cells, instructing them to grow constantly.

The study, published in the journal Cell Reports, was led by Martin McMahon, PhD, senior director of preclinical translation at HCI and professor of dermatology at the U of U, and Aria Vaishnavi, PhD, a postdoctoral fellow in McMahon's lab. McMahon's team focuses on cell-cell communication, like the signaling promoted in some cancers by NTRK1.

One way to examine this experimentally is to devise a way to model human cancers in mice. This process produces a new tool, a "mouse model," which allows scientists to analyze in a laboratory setting how a cancer develops, how it behaves over time, and to test potential new drugs and treatment targets. The researchers hope the new NTRK1 mouse models reported today will accelerate progress toward finding more effective treatments for patients with NTRK1-driven lung and pancreas cancers.

A conversation with Ignacio Garrido-Laguna, MD, PhD, a physician-scientist at HCI, associate professor of internal medicine at the U of U, and director of the HCI Phase I Clinical Research Program, inspired the idea for this study. Garrido-Laguna was caring for a pancreatic cancer patient who was participating in a clinical trial at HCI (NCT02568267). The patient's tumor had a mutation in NTRK1 and then had a remarkable response to the NTRK1 inhibitor drug being evaluated. Hence, it made sense to Garrido-Laguna and McMahon that the response might be related to inhibition of the mutated NTRK1.

McMahon posited that if NTRK1 signaling was responsible, disruption of that signaling might be beneficial. "Pancreatic cancers have proven to be a particularly recalcitrant to treatments, so we wanted to thoroughly evaluate such a dramatic response as we work to identify new potential treatments for this disease," said McMahon. Moreover, since the responses to the NTRK1 inhibitors are often short-lived, McMahon and colleagues wanted to design new combination therapies that prevented the onset of lethal drug resistance.

Breast Cancer patients are 60 percent more likely to die of cancer after surviving a heart attack, a new study finds.

Led by researchers at NYU Grossman School of Medicine, the study shows how heart attacks, by blocking blood flow through arteries, trigger a specific, pro-cancer immune reaction.

Designed by evolution to attack invading bacteria and viruses, the immune system also recognizes cancer cells as abnormal and worthy of attack, say the study authors. But heart attack, along with other blood flow-reducing events like stroke and heart failure - were found to come with changes to immune cells that rendered them less able to respond to tumors.

Published online in Nature Medicine, the analysis of more than 1700 early-stage breast cancer patients found that those who also experienced heart attack, stroke, or heart failure had a greater risk than those that did not of cancer recurrence, cancer spread, and of dying from breast cancer.

The new work also found that mice with breast cancer saw a two-fold increase in tumor volume over 20 days after ligation (cutting off) of blood flow in the coronary artery, which simulated a heart-attack, when compared to mice with cancer but normal blood flow.

"By blunting the immune system's assault on cancer cells, a heart attack appears to provide an environment that enables tumor growth," says corresponding author Kathryn Moore, PhD, the Jean and David Blechman Professor of Cardiology, and Director of the Cardiovascular Research Center at NYU Langone Health. "While further studies will be needed, our results provide support for the aggressive clinical management of cardiovascular risk factors, not only to reduce risk of cardiovascular disease, but possibly breast cancer progression."

As one in eight American women will develop breast cancer during their lifetimes, and with nearly three million breast cancer survivors in the United States, the need for a better understanding the interplay between cancer and cardiovascular disease is urgent, adds Moore.

Patients who already used opioids, sedatives or antidepressants prior to colorectal surgery may experience significantly more complications post-surgery.  The study examined 1,201 patients 18 years of age and older who underwent colorectal resection for any indication other than trauma at UK HealthCare. Of these patients, roughly 30% used opioids, 28% used antidepressants and 18% used sedatives, all legally prescribed by a doctor pre-operatively.

Patients on any of these medications showed an increase in several common complications post-surgery, including infections, prolonged intubation, longer length of stay, readmissions, respiratory failure and even mortality. These problems were particularly pronounced in patients who regularly used opioids prior to surgery.

The preoperative use of opioids, sedatives and antidepressants is on the rise in the U.S. Though the current opioid crisis has raised awareness for limiting opioid use, many patients still receive opioids for pain management, and finding the right balance of medication is an ongoing issue for many patients and doctors. Patients with anxiety disorders or other mental health issues often receive sedatives or antidepressants.

As people age, cancer becomes an increasing health concern. Solid cancer tumors are cancers that don't affect the blood and instead form tumors, or growths of abnormal cells in certain parts of the body. These solid cancer tumors mainly impact people who are 65 and older.

If you or an older loved one is diagnosed with cancer, many different factors come into play to guide treatment choices. However, leading geriatric oncologists (specialists who treat cancer in older adults) say that, perhaps surprisingly, age is not necessarily one of them. Recently, leaders in the field emphasized that being older, on its own, does not necessarily mean that surgical treatment is not an option for you.

Older patients with cancer may not receive the same treatment as younger adults. The reasons for this are unclear and may include the fact that surgical oncologists fear a higher risk of poor outcomes for older cancer patients following surgery. They may be uncertain about how surgery will affect an older patient's survival and quality of life. But since long-term outcomes after surgery for older adults with cancer have not been well-studied, we don't know whether such concerns are justified.
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Fortunately, a screening tool exists that may help surgical oncologists and other physicians decide which patients might face complications after surgery. The "Preoperative Risk Estimation for Onco-Geriatric Patients" (or PREOP) risk score uses several easy-to-administer tests and can be given to people before surgery. The risk score includes a nutritional risk score to make sure you aren't malnourished and a test called Timed Get Up and Go (TUG). In this simple test, you are timed getting out of a chair, walking 10 feet, and sitting back down again.

Cancer care and management is a stressful and distressing time for patients and families at the best of times - with COVID-19 the challenges become even more monumental.  However, over the years we have come across the most remarkable stories of cancer patients who have overcome adversity to continue full and active lives. Below is a list of links for advice on cancer care during the pandemic that we hope you will find useful.
 
Cancer and Coronavirus (COVID-19). MacMillan Cancer Support

Coronavirus and COVID-19: What People With Cancer Need to Know. Cancer.Net 
 
Managing Cancer Care During the COVID-19 Pandemic: Agility and Collaboration Toward a Common Goal. National Comprehensive Cancer Network  
 
Cancer guidelines during the COVID-19 pandemic. The Lancet, Oncology 
 

One of the most frequent problems when treating cancer is that the tumours develop resistance to therapies, that is to say, at some point, treatments cease to be effective in stopping tumour growth. This is especially relevant in patients with aggressive diseases such as pancreatic cancer or patient with metastases, who for this reason often undergo frequent changes in treatment. Now, a study led by the Spanish National Cancer Research Centre (CNIO) in collaboration with researchers from the Weill Cornell Medicine Center and Pfizer Inc. (United States), proposes a novel combined approach to avoid pancreatic cancer resistance to chemotherapy, and thus achieve the elimination of these tumour cells effectively. The work will be published in the journal Cancer Cell.

Effective therapies in breast cancer
One of the characteristics of cancer is the alteration of the cell cycle, that is, the alteration of normal activity related to cell growth, maturation and death. The molecules CDK4 and CDK6 are involved in the uncontrolled cell growth, which ends up generating a tumour mass.

In recent years, drugs have been developed that inhibit the action of CDK4 and CDK6 and are very effective in stopping the growth of advanced breast cancer. Their clinical use, in combination with hormone therapy, has been approved in the United States since 2015 and in Europe since 2017 for patients with this type of cancer. The success of this combination has made it the standard treatment for these patients. However, until now it was not clear if these benefits could be extended to other types of cancer.

"A problem with CDK4/6 inhibitors is a consequence of their mechanism of action that prevents tumour cells from multiplying," explains Marcos Malumbres, Head of the CNIO Cell Division and Cancer Group and principal investigator of the project. "Most of the current chemotherapies -involving, for example, platinum or taxol derivatives-, act only on tumour cells that are dividing. Therefore, if we inhibit CDK4/6 and thus prevent these cells from dividing, we prevent chemotherapies from working properly. For this reason, until now it was believed that we could not combine CDK4/6 inhibitors with classical chemotherapy."
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Not at the same time, but after
During her predoctoral work at the CNIO, researcher Beatriz Salvador decided to design a new strategy in which CDK4/6 inhibitors would be used not at the same time as chemotherapy, but after chemotherapy to prevent the recovery of tumour cells. The results of the study show that administering CDK4/6 inhibitors after the drugs commonly used against various metastatic tumours prevents tumour cells from resisting these treatments and growing again after chemotherapy.