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A powerful technology that continues to evolve, researchers say, has rekindled interest in liquid biopsies as a way to disrupt tumor progression. The technology, genetic sequencing, is allowing researchers a closer look at the genetic trail tumors leave in the blood as cancer develops. That capability, as these new “liquid” blood tests work their way into clinics, may further a deeper understanding of how tumors alter their molecular masks to defy treatment.
Black women in the United States have about a 41% higher chance of dying from breast cancer than white women. Some of that disparity can be linked to genetics, but the environment, lingering mistrust toward the health care system, and suspicion over prescribed breast cancer treatment also play roles, according to a new study from the Brown School at Washington University in St. Louis.
In recent years, biological sciences have witnessed a surge in the generation of data. This trend is set to continue, heralding an increased need for bioinformatics research. By 2018, sequencing of patient genomes will likely produce one quintillion bytes of data annually – that is a million times a million times a million bytes of data. Much of this data will derive from studies of patients with cancer.
In 1998 the biotech company Genentech launched Herceptin for the treatment of certain types of breast cancer. Herceptin was an example of a ‘therapeutic antibody’ and was the first of its type for cancer treatment. Antibodies are proteins in our immune system that can target abnormal cells (or bacteria, toxins, viruses, etc.) in the body, and on arriving at the target can set in motion a whole set of biological events that in principle can remove or degrade to a non-dangerous state the abnormal cells.
Frequently, antibodies that we should produce as a natural response to cancer cells that may develop in an organ or tissue are somehow either inhibited from forming, or where they do form are poorly effective at destroying the cancer. To combat this ineffectiveness, specific antibodies against targets on the cancer cell can be made in the laboratory and then reintroduced into the human body, causing the cancer cell to ‘self-destruct’, or become sensitized to natural immune processes that aid the cancer cell killing.
In commenting on the efficacy of such antibodies in the treatment of cancer, delivered to an international antibody conference in San Diego in December 2012, Professor Dane Wittrup (MIT) reminded the audience how limited the response rate (~10%) of current antibody therapies has been. While there may be different views on the reasons for this, we can be reasonably certain that it is due, in part, to some or all of the following: the development of tumor resistance after repeated therapy, the presence of side effects serious enough to warrant interruption or even cessation of treatment, or limited antibody efficacy in the real tumor environment. Despite the investment of billions of dollars in antibody research it is clear that the human immune system still retains many secrets, the decoding of which has been, and continues to be, a long and complex process.
Current antibody therapies target specific ‘circuits’ in cancer cells that are important for the growth of the cancer, either shutting down or blocking key points in specific cellular circuitry, thereby reducing the cancer cell viability. Unfortunately, a cancer is a population of cells and as the inhibitory antibodies move into attack mode, biological changes within the cancer cells over time can activate alternative survival circuits that allow the cancer to evade the antibody effects, effectively becoming ‘resistant’. (For example, some breast cancers are known to become resistant over time to repeated treatment with Herceptin.) To counteract this effect, therapeutic modalities have been developed where two antibodies targeting different sites (circuits) within the cells, or an antibody coupled with a highly toxic drug or toxin molecule, are being adopted. While more effective than the single antibody approach, there is still a heavy hitting part of the immune system, the so-called Cytotoxic T-lymphocyte, or CTL (‘T’ for thymus-derived) mediated response, that often stands idle while the antibody arm of the immune system goes about its work. Why might that be?
In the late 1980s and early 1990s, research groups working at research laboratories in Marseille and a pharmaceutical company in Princeton described two new proteins associated with cells of the immune system that appeared to regulate their activity, allowing them to discriminate between normal tissues and abnormal tissues such as cancer cells. These new proteins were named ‘immune checkpoint receptors’ and are now known to be instrumental in deciding whether or not CTLs become active. When CTLs receive the correct activation signal, they are primed to engage an abnormal target with a view to destroying it in what is part of the ‘adaptive immune response’. Within the cells of the immune system, these checkpoint receptors are part of a complex activating and damping signaling system involving a receptor and a second molecule (or ‘ligand’) that interacts with the receptor in a sort of pas de deux. When the two find each other, as in normal tissues, a CTL attack is prevented (if this did not happen, an autoimmune response could be initiated). So, if the same ligand signal is somehow offered by a tumor cell masquerading as a normal cell, the ‘call to attack’ signals will be overridden and a CTL assault will not occur. In many tumors, just such biochemical changes are known to occur that fool the immune system into ‘thinking’ that the tumor consists of normal human cells thus avoiding attack by CTLs.
Figure 1 by Anthony R. Rees
As with many aspects of biological systems, the adaptive immune system is a balancing act between allowing effective immune responses to alien agents, such as bacteria, viruses, toxic molecules, and the like, and at the same time avoiding mounting similar responses to our own tissues, organs, and cells that could lead to ‘autoimmunity’. Immunologists use the term ‘tolerance’ to describe this protection that self-tissues and organs experience as the immune system goes about its work. Lupus erythematosus and multiple sclerosis are two examples of autoimmune responses where the normal regulatory controls have been interrupted and immune antibodies or cells have attacked normal, healthy tissues with often debilitating effects. It is currently thought that checkpoint receptors and their partner ligands play an important role in maintaining this tolerance state in normal healthy persons, preventing unwanted autoimmune responses.
But what if antibodies could be targeted to these checkpoint receptors, blocking the ability of the tumor cell to interact with the receptors on CTLs, and hijacking their deceptive “I am normal” signal? (see Figure 1). This would mean, of course, that in theory, any cell, normal or abnormal, could be a target for CTL killing since both types of cell would have their “I am normal” signal blocked. Dangerous? Possibly, if not controlled. Desirable? If a tumor is so aggressive (e.g. melanoma, pancreatic cancer, etc.) that some autoimmune side effects could be tolerated or clinically managed in order to rid the body of the cancer, perhaps the therapeutic modality would be justified.
Well, we can do better than ‘in theory’. In a recent study of patients with advanced melanoma, one of the most aggressive tumors known and refractory to most therapeutic regimes, two different antibodies against each of the two most characterized immune checkpoint receptors showed spectacular results. In summary, the Phase I/II clinical trial results showed that 40% of patients treated with the combined antibody therapy experienced tumor shrinkage, and 65% of patients experienced shrinkage or stable disease. While these results truly are impressive we cannot yet declare that the war against cancer is approaching resolution, despite the claims of some enthusiasts.
As I noted above, immune checkpoint receptors are important in avoiding immune responses to our own tissues and organs. If their regulatory role is undermined by antibody blockade then autoimmune effects could be anticipated. In fact, in all clinical trials so far conducted with antibodies against these targets, autoimmune responses have been seen, including colitis, dermatitis, hypophysitis, pneumonitis, and hepatitis. These are classes of side effects the clinical community is not accustomed to seeing during antibody therapy, and will require stringent observation during treatment while improved therapeutic regimes are developed that manage these autoimmune effects.
Despite the embryonic nature of this approach, we have truly entered a new age for antibody therapy. As with all checkpoints, two way traffic is ever present, and while in one direction there may be freedom, in the other may lie painful experiences that have to be managed. The key for the future success of this approach will be the development of immune strategies that allow the benefits of immune checkpoint inhibition in cancer treatment to be counterbalanced by clever therapy designs that avoid, or at least minimize, the associated disadvantages.
Header image: Breast cancer cell. Public domain via Wikimedia Commons.
Receiving a cancer diagnosis is emotional and overwhelming for patients. While initially patients may appropriately focus on understanding their disease and what their treatment options are, supportive care should begin at diagnosis and is a vital part of care across the continuum of the cancer experience. Symptom management, as a part of supportive care, is aimed at preventing the side effects of the cancer and its treatment. Appropriately managing these side effects will help enable patients to maintain their quality of life through their cancer journey.
It is well-known that, unfortunately, many cancer treatments (mainly chemotherapy) will cause nausea and vomiting. Fortunately, decades of research have improved our understanding of chemotherapy-induced nausea and vomiting (CINV) and have led to the development of very effective and safe drugs to prevent and manage these bothersome and potentially debilitating side effects. Research has also shown us that often combinations of two or three drugs taken together, sometimes over multiple days, offers the best CINV prevention with certain chemotherapies. With the appropriate use of these “antiemetic” drugs, CINV can now be prevented in the majority of patients. However, 20-30% of patients may still suffer from these side effects. Some of these patients are refractory in that the recommended antiemetic prophylactic treatments, for whatever reason, do not prevent the nausea and/or vomiting. Other patients, unfortunately, are incorrectly managed and are not given the appropriate preventative treatments. This is indefensible and not representative of an optimal patient-centered approach to cancer management. Physicians should be approaching symptom management in the same manner as they approach cancer therapeutics, utilizing the best and most appropriate treatments available.
Chemotherapy bottles, National Cancer Institute. Public domain via Wikimedia Commons.
With the goal of making prevention of CINV simpler and more convenient, the first antiemetic combination product has recently been developed, combining two drugs in a single pill that only needs to be taken right before chemotherapy is administered along with a single dose of dexamethasone. This new product (called NEPA or Akynzeo®) was recently approved by the US Food and Drug Administration (and is under review in Europe) after years of development. The combination not only comprises two drugs from two classes, an NK1 receptor antagonist (RA) and a 5-HT3 receptor antagonist, representing the current standard-of-care. The NK1 RA (netupitant) and the 5-HT3 RA (palonosetron), however, are long-acting, and palonosetron is recommended by many guidelines committees as the preferred 5-HT3 RA.
Three of the pivotal studies conducted to establish the efficacy and safety of NEPA were recently published in Annals of Oncology. These selected articles convincingly show efficacy with the NEPA combination, superior prevention of CINV compared with that of oral palonosetron, and maintenance of efficacy when given over multiple cycles of chemotherapy known to result in nausea and vomiting.
NEPA appears to be a promising new agent with the potential to address some of the barriers interfering with physicians’ administration of recommended antiemetics. This is accomplished by conveniently packaging effective and appropriate antiemetic prophylaxis in a single, oral dose that is taken only once per chemotherapy cycle, along with a single dose of dexamethasone.
Hopefully this will help, because preventing the symptoms has to be as important as treating the disease.
Heading image: Cancer cells by Dr. Cecil Fox (Photographer) for the National Cancer Institute. Public domain via Wikimedia Commons.
Each year there are 1,800 people killed on the roads in Britain, but over the same period there are around four times as many deaths from cancers that were caused by hazardous agents at work, and many more cases of occupational cancer where the person is cured. There are similar statistics on workplace cancer from most countries; this is a global problem. Occupational cancer accounts for 5 percent of all cancer deaths in Britain, and around one in seven cases of lung cancer in men are attributable to asbestos, diesel engine exhaust, crystalline silica dust or one of 18 other carcinogens found in the workplace. All of these deaths could have been prevented, and in the future we can stop this unnecessary death toll if we take the right action now.
In 2009, I set out some simple steps to reduce occupational exposure to chemical carcinogens. The basis was the recognition that the overwhelming majority of workplace cancers from dusts, gases and vapours are caused by exposure to just ten agents or work circumstances, such as welding and painting (see chart). Focusing our efforts on this relatively short priority list could have a major impact.
Many of these exposures are associated with the construction industry. Almost all are generated as part of a process and are not being manufactured for industrial or consumer uses, e.g. diesel engine exhaust and the dust from construction materials that contain sand (crystalline silica).
The strategies to control exposure to these agents are well understood and so there is no need to invent new technological solutions for this problem. Use of containment, localized ventilation targeted at the source of exposure and other engineering methods can be used to reduce the exposures. If further control is needed then workers can wear personal protective devices, such as respirators, to filter out contaminants before they enter the body.
There are also robust regulations to ensure employers understand their obligations to employees, contractors and members of the public, both in Britain through the Control of Substances Hazardous to Health (COSHH) Regulations and in the rest of Europe via the Carcinogens and Mutagens Directive.
We know that as time goes on, most exposures in the workplace are decreasing by between about 5% and 10% each year. This seems to be true for many dusts, fibres, gases and vapours, and it is a worldwide trend. There is every reason to believe this is also true for the carcinogenic exposures we are discussing. This means that over a ten-year period the risk of future cancer deaths is may drop by about half. If we could increase the rate of decrease in exposure to 20% per annum then after 10 years the risk of future disease should have decreased by about 90%.
However, during the five years since my article was published, very little has been done to improve controls for carcinogens at work. Recent evidence from the Health and Safety Executive (HSE), the regulator in Britain, shows widespread non-compliance at worksites where there is exposure to respirable crystalline silica. Most people are still unaware of the cancer risks associated with being a painter or a welder and so no effective controls are generally put in place. There have been no effective steps taken to reduce exposure to diesel engine exhaust, or most of the other “top ten” workplace carcinogens. What is the barrier preventing change?
In my opinion, the main issue is that we don’t perceive most of these agents or situations as likely to cause cancer. For example, airborne dust on construction sites, which often contains crystalline silica and may contain other carcinogenic substances, is considered the norm. Diesel soot is ubiquitous in our cities and we all accept it even though it is categorized as a human carcinogen. In my paper I complained that there were ‘no steps taken to reduce the risk from diesel exhaust particulate emission for most exposed groups and no particular priority given to this by regulatory authorities.’ Nothing has changed in this respect. We need an agreed commitment from regulators, employers and workers to change for the better. Perhaps we need to consider requiring traffic wardens to wear facemasks and encourage painters to work in safer healthier ways. At least we should take a fresh look at what can reasonably be done to protect people.
We know that since 2008 the number of road traffic deaths in the United Kingdom has decreased by about a third and downward time trend seems relentless. Road traffic campaigners have envisaged a future of zero harm from motor vehicles. Similarly we know that the level of exposure to most workplace carcinogenic substances is decreasing. Can we not also consider a future world where we have eliminated occupational cancer or at least reduced the health consequences to a tiny fraction of today’s death toll? It will be a future that our children or their children will inhabit because of the long lag between exposure to the carcinogens and the development of the disease, but unless we act the danger is that we never see an end to the problem.
As a first step we need to have en effective campaign to raise awareness of the problem of workplace cancers and to start to change attitudes to the most pernicious workplace carcinogens.
John Cherrie is Research Director at the Institute of Occupational Medicine (IOM) in Edinburgh, UK, and Honorary Professor at the University of Aberdeen. He has been involved in several studies to estimate the health impact from carcinogens in the workplace. He is currently Principal Investigator for a study that will estimate the occupational cancer and chronic non-malignant respiratory disease burden in the constructions sector in Singapore. In 2014 he was awarded the Bedford Medal for outstanding contributions to the discipline of occupational hygiene. He is the author of the paper ‘Reducing occupational exposure to chemical carcinogens‘, which is published in the journal Occupational Medicine.
Occupational Medicine is an international peer-reviewed journal, providing vital information for the promotion of workplace health and safety. Topics covered include work-related injury and illness, accident and illness prevention, health promotion, occupational disease, health education, the establishment and implementation of health and safety standards, monitoring of the work environment, and the management of recognised hazards.
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Image credit: Graph provided by the author. Do not reproduce without permission.
With the WHO Executive Board recently adopting the resolution ‘Strengthening of palliative care as a component of integrated treatment within the continuum of care’, which is to be referred to the World Health Assembly for ratification in May, Nathan Cherny puts the current global situation in perspective and lays out the next steps needed in this crucial campaign to end suffering to millions.
By Nathan Cherny
In the curious trail that has been my life thus far, some would say that there was a certain inevitability that I would end up working for cancer patients’ right to access medication for adequate relief of their suffering. As a medical student I suffered terrible cancer-related pain from a thoracotomy to remove lung metastases for testicular cancer. As an oncologist and palliative care physician in the Middle East, my current work allows me to look after both Israeli and Palestinian patients. My profession has also taken me to caring for many “medical tourists” from Eastern Europe as well as foreign workers from Thailand, India, Nepal, and the Philippines. Oh, and I was born on Human Rights Day, 10 December 1958!
I hate pain. I am appalled by the global scope of untreated and unrelieved cancer pain. At the initiative of its Palliative Care Working Group, the European Society for Medical Oncology (ESMO) has taken this on board as a global priority issue. ESMO facilitated the first comprehensive study to evaluate the barriers to pain relief in Europe, which highlighted the distressing situation in many Eastern European counties.
The GOPI studied opioid availability and accessibility for cancer patients in Africa, Asia, the Middle East, Latin America, and the Caribbean. The results were published in a special supplement of the Annals of Oncology in December 2013. The seven manuscripts in the special issue highlighted the global problem of excessively restrictive regulations regarding the prescribing and dispensing of opioids — ‘catastrophe born out of good intentions’.
In order to prevent abuse and diversion, most patients with genuine need to relieve severe cancer pain cannot access the appropriate medication. Millions of people around the world end their lives racked in pain, harming not only the patients but also their families who bear witness to this torturous tragedy.
On 23 January 2014, the WHO Executive Board adopted a stand-alone resolution on palliative care which will be referred to the World Health Assembly for ratification in May 2014. This is great news for all those campaigning to improve access to medication to end suffering to millions. There is still much to be done on this long, winding road, yet we can still be proud. Thanks to our united efforts and the evidence provided by the GOPI data, our voices are being heard.
Overregulation of opioids is not the only problem impeding global relief of cancer pain. In many places around the world there is major need to: educate clinicians in the assessment and management of pain; educate the public regarding the effectiveness and safety of opioid analgesia in the management of cancer pain; and secure supplies of affordable medications.
The next steps: The GOPI Collaborative Group is now writing to Ministers of Health in the many countries where we have identified major over-regulation with a 10 point plan to help redress the problem, covering education, restrictions, limits, professional standards, monitoring, and prescription.
Tell us what actions you can take to incorporate these next steps in your country. Can you contact your Ministry of Health? What could be inspirational for others to know? We make more noise if we all shout together.
Annals of Oncology is a multidisciplinary journal that publishes articles addressing medical oncology, surgery, radiotherapy, paediatric oncology, basic research and the comprehensive management of patients with malignant diseases. Follow them on Twitter at @Annals_Oncology.
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Image credits: (1) Photo of Nathan Cherny, via ESMO; (2) GOPI banner, via Global Opioid Policy Initiative/ESMO
Oncologists have long known that one patient is not the same as another. Indeed one patient’s cancer is not the same as another’s. Regardless of apparent clinical similarities, doctors witness huge variations in rates of cancer progression and patients’ response to treatment. There is increasing understanding of the need to investigate the multiple molecular differences between cancers, which may predict differences in patterns of growth and spread, and assist in the selection of the most effective treatments, whilst avoiding treatment in those unlikely to benefit. These molecular differences can evolve during the course of a patient’s disease, so that the cancer from which a patient might die may be very different to the one with which they were originally diagnosed. Exciting as these advances are, they bring into stark relief just how difficult the challenges faced by the patient and their oncologist are: how to develop treatments to which the individual’s particular cancer is likely to respond, and how to mount a re-challenge should it evolve.
In recent years, cancer immunotherapy has returned to the forefront of cancer research. This aims to exploit the power and targeted response of the patient’s own immune system to fight their cancer. Resurgence in interest has been prompted particularly by developments in the management of malignant melanoma, a type of skin cancer as well as kidney cancers, along with exciting clinical trial data in patients with lung cancer. Many patients with a diagnosis of secondary melanoma now routinely have access to the anti-cancer treatment ipilimumab, an antibody which triggers a specific response from a sub-group of the patient’s own white blood cells (called cytotoxic T-cells). One role of these T-cells is to recognise and kill cancerous cells, but to protect the rest of the body from unnecessary attack, this response is usually dampened down. Ipilimumab ‘releases the brakes’ from the immune system, speeding up the reaction time and growth of the T-cells. For a small minority of patients with secondary melanoma this can result in control of their tumour, sometimes lasting years, offering a tantalising insight into the potential of the immune system to eliminate cancerous cells. But the majority of patients derive no benefit, yet may suffer the multi-organ side-effects of the drug and the average survival with secondary melanoma continues to be measured in months.
How then to provoke the immune system more consistently and more specifically? Following successes with vaccinations against infectious diseases, there has been inevitable long-standing interest in the concept of vaccination to provoke a useful reaction against established cancers. Despite numerous avenues of research, little has translated into clinical practice. A solitary ‘therapeutic cancer vaccine’ currently approved by the US Food and Drug Administration for use in asymptomatic patients with hormone-resistant secondary prostate cancer has yet to find its place in the routine management of this disease.
Particular recent research focus has been on the role of the dendritic cell within the immune system, a cell derived from the bone marrow which captures ‘foreign’ material and is highly efficient at presenting it to T-cells, effectively launching the immune system to target the ‘foreign’ material. Earlier this year the BBC reported on a clinical trial underway in patients with glioblastoma, a brain tumour typically with a dismal prognosis and a low chance of responding to standard treatment options. There are over ten published small-scale studies performed along similar lines which, collectively, hint sufficiently at improved outcomes to justify expanding recruitment to several hundred patients. A sample of each patient’s tumour has been mixed with a sample of their own dendritic cells, before re-injection at intervals over a two year period. Each patient’s injection is a unique blend of their own cancer and their own immune cells, reintroduced to their immune system in the hope of educating it both to recognize their cancer as a target for destruction — and to remember that cancer, should it re-emerge in the future.
Results of this individualised cancer vaccine in patients with brain tumours are awaited, but the drive for evidence-based personalised cancer therapy has already advanced routine oncology practice. For instance, a patient’s breast cancer can be risk-stratified by analysis of a panel of mainly cancer-related genes. This can help the patient decide with their oncologist whether chemotherapy is the right treatment for them.
Future years will see rapid expansion in the concept of personalised cancer care, likely to encompass all aspects of the patient’s pathway, from diagnosis to treatment. The latest emerging concept is the ‘Mouse Avatar’ – the implanting of a sample of a patient’s cancer into an immunodeficient mouse to provide a personalized, living and reproducing model of that patient’s unique cancer. In theory this could enable oncologists to offer treatment to patients for which there is evidence of response in ‘their’ mouse. In reality, this technology remains in the earliest stages of development and multiple hurdles can be anticipated; scientific, financial and even ethical. Huge leaps are required before there is any prospect of it becoming a reality for the vast numbers of cancer patients requiring treatment each year.
But we have begun the journey towards the goal of personalised cancer care. Just as doctors should endeavour to treat each patient as unique, it seems possible that one day oncologists may be able to treat each patient’s cancer as unique too.
Miranda Payne is a Locum Consultant in Medical Oncology at the Oxford University Hospitals NHS Trust, specializing in the treatment of malignant melanoma, gynaecological and breast cancers. She took a first in Physiological Sciences at Oxford University and obtained her DPhil in Medical Oncology from Oxford University in 2010. Along with Jim Cassidy, Donald Bissett, and Roy Spence, she has been editor of the Oxford Handbook of Oncology for ten years and more recently, the Oxford American Handbook of Oncology (with Gary Lyman).
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Image credit: cancer cell – closeup. Image by Eraxion, iStockphoto.
Psychological treatment studies that did not measure the maturity of psychological adaptive mechanisms in cancer patients have reported conflicting cancer survival results. Widely publicized studies noted increased survival rates among cancer patients who underwent psychotherapeutic treatment. However, more recent multicenter study could not replicate improved survival after behavioral treatment, and other studies have reported similarly conflicting results. Since published reports suggest that patients likely to benefit from psychotherapies are generally those with the most psychological maturity, it seems possible that the underlying health of psychological adaptive mechanisms may be related to cancer survival.
To our knowledge, prior to our 2006 report, psychological adaptive mechanism maturity had not been considered as affecting cancer survival either in behavioral-treatment studies or in trials of antidepressants. In that report we used measures of both depression symptom frequency and psychological adaptive mechanism maturity to assess what, if any, relationship each bore on survival probability in cancer patients. On the basis of previous studies of depression and ego-adaptation, we believed that “Immature” adaptive styles and frequent depression symptoms would independently predict lower survival rates. Then we studied 86 consecutive, mostly late-stage, cancer outpatients for up to 5 years; their survival data were analyzed in relation to the Beck Depression Inventory (BDI) and the Defense Style Questionnaire (DSQ) scores at study entry. Cumulative survival probability curves contrasted the extreme cases: the most (N = 15) to the least (N = 21) depressed, and the “immature” (N = 14) to the “mature” (N = 16) adaptors. Depression did not separate the groups until 30 months after diagnosis. (Figure 1)
Figure 1: Five-Year Cumulative Survival Probability by Maturity of Adaptive Styles
Psychological adaptive mechanism (ego defense) style separated them at 8 months; by 18 months, the Immature survival probability had dropped to 50%, versus 87% for the Mature. At 36 months, survival probabilities were 19% and 57%, respectively. This study suggested further clinical attention toward psychological adaptive mechanism maturity and immaturity as a potentially strong indicator of distress and lowered survival in cancer patients. It also indicated that the maturity of adaptive mechanisms must be taken into account in both medicinal and behavioral treatment trials of cancer patients since underlying difficulty may be more related to poor adaptation rather than traditional psychopathological constructs like depression.
Figure 2: Algorithm for the Assessment of Psychological Adaptive Mechanisms
While human psychological adaptation has been studied in various forms, including such terms as coping or ego defense mechanisms, this concept has yet to reach clinical use owing largely to the absence of a replicable clinical format that can allow reliable recognition of psychological adaptive mechanisms in the clinical, one-on-one setting. The Principal Investigator (PI) has developed a decision tree recognition algorithm for the purpose of assessing individual adaptive behaviors in the diagnostic and treatment settings. (Figure 2)
While previous methods, such as the DSQ, offer a relative convenience, they are crude measures of these complex phenomena and can only be used in studies that compare groups of individuals in contrast to each other. The recognition algorithm approach aims at a specific assessment of respective individuals in a here-and-now setting. This approach can be used both in clinical assessment and treatment as well as in research studies that seek to characterize groups of patients, such as those presenting with use of Immature adaptive mechanisms who present with much lower likelihoods of cancer survival.
Other research indicates that psychological adaptive mechanisms occur naturally in graded steps that reflect increasing brain development from birth through early adulthood. Conversely, however, complex behaviors of this kind that utilize many brain tracts, including frontal lobe functions, may theoretically be lost when brain function decreases or when stress is overwhelming, as may be the case of the stress of cancer illness in the setting of the less flexible mechanisms. Neurodegenerative changes following radiation treatment of neoplasms in the brain, for example, may result in impaired functioning modulated by the fronto-subcortical tracts, including judgment, motivation, and executive planning functions. Alternatively, overwhelming stress reactions can result in lowered adaptive mechanism maturity, such as that seen in some cases of Post-Traumatic Stress Disorder. Much remains to be learned in the interaction between humans and the illnesses that they encounter; the psychological adaptation model offers one new approach to both clinical and empirical understanding.
Dr. Thomas P. Beresford is Professor of Psychiatry at the University of Colorado School of Medicine and the author of Psychological Adaptive Mechanisms: Ego Defense Recognition in Practice and Research. Trained in psychiatry at The Cambridge Hospital/Harvard Medical School, he has focused his clinical and scientific career on the psychiatric problems that medical and surgical patients encounter, whether in adjusting to illness or in returning to normal brain functioning.
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One of the things that has always puzzled me is the number of palliative care services that have the word ‘pain’ in the title. Why do we concentrate so much on that one, admittedly unpleasant, symptom? Why ‘Pain and Palliative Care Services’ rather than, for example, ‘Vomiting and Palliative Care Service’ , ‘Dyspnoea and Palliative Care Service’, or even ‘Sadness, Anger, Existential Anguish and Palliative Care Service’?
That’s the problem with trying to describe palliative care. The whole point of palliative care is that it is holistic – a word that has acquired a certain flakiness, but which in reality simply refers to looking at the wholeness of a person, rather than focusing on only one domain (such as physical symptoms), or even one specific symptom (such as pain). But the purpose of a definition, by definition, is to set limits around a concept. There is a sense in which defining something as holistic is a contradiction in terms. Yet that is what we have to do in palliative care, if we are to communicate some sense of the task of caring for children and adults with life-limiting conditions; a sense that encompasses both the idea that it is holistic and that it is specialist (there are some things you need to learn to do to do it well).
The clue to the nature of palliative care is in the name: ‘care’. It is a care whose aim is not cure. In the United Kingdom, we have recently seen the results of misunderstanding what palliative care is all about. As in most countries that are resource-rich (or, at least, would have considered themselves as such before the global recession), the United Kingdom sometimes struggles to avoid the temptation to over-intervene. Even where it is overwhelmingly unlikely that an intervention will help – such as when death is inevitable – we in resource-rich countries can’t help ourselves. Sometimes we have to do something even if we know it is more likely to damage a patient – considered holistically – than it is to help them. That is not because anyone is trying to be cruel, but simply because if you are a doctor faced with a very sick patient, it is hard not to intervene, even when the latter option would truly be the right thing to do.
So, if you want to improve the lives of people who are close to death, one really good way to do it is to offer doctors more support in doing less, and in doing it well. The Liverpool Care Pathway for the Dying Patient (LCP) was designed to do exactly that. Its sole purpose has been to protect dying patients from the pain and indignity of useless interventions around the end of their life. Sadly, holding back on those interventions that will harm people can sometimes look, at least to the untutored eye, very like deliberately killing them. Even some philosophers find it tricky to admit that killing someone is not at all the same thing as refusing to try to prevent their inevitable death. So perhaps it is not surprising to find that, in trying to see who were the baddies here, the Daily Mail crashed clumsily down on the wrong side, screaming that babies were being euthanised using the Liverpool Care Pathway. But it isn’t true.
The Liverpool Care Pathway hasn’t really found its way into children’s care, despite the Daily Mail‘s assertions. That’s because it was designed for adults, mainly with cancer, rather than for children and the much larger range of conditions that can cause their death. There’s nothing wrong with the concept. As in adults, the art and science of palliative care in children is to preserve wellbeing as far as possible, using all the tools at our disposal. To do that often means introducing some interventions – some medication, perhaps, or the opportunity to talk about fears, or the chance to decide where you or your child should die. But improving wellbeing can equally mean withholding interventions that would be likely to cause an overall damage to it. Good paediatric palliative care must mean knowing what procedures to leave out, as well as knowing which ones to introduce. Whatever some moral philosophers say, there is a big difference between actively hastening someone’s death, and not trying fruitlessly to prevent death when to do so would mean making life worse. And whatever the Daily Mail may confidently claim, putting a patient on the Liverpool Care Pathway is not the same as euthanasia. Care pathways are pointers to the best way to avoid careless and harmful over-intervention. Properly used, palliation and pathways do exactly what they say on the tin; they care.
Dr Richard Hain is Consultant and Lead Clinician at the Wales Managed Clinical Network in Paediatric Palliative Care Children’s Hospital, and Visiting Professor at the University of Glamorgan, and Honorary Senior Lecturer at Bangor University. He is co-editor of the Oxford Textbook of Palliative Care for Children, Second Edition (OUP, 2012), with Ann Goldman and Stephen Liben.
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