Stressors, psycho-genomic pathways and cancers
Identifying psychological, psychosocial, physiological, environmental & genomic
pathways to prevent and treat cancers
The Power Thinking Health Council has been established to encourage and develop
psycho-genomic research in order to explore these links and identify possible
methods of preventing and treating cancer.
Contact details: Theo Richter FPNA, President, Psycho-Genomics Research Institute
research@psycho-genomics.org
Stressors ____________________________________________________________ 1
Physiology and stress __________________________________________________ 2
Emotions & stress views from the Institute of HeartMath® ____________________ 3
Psychological & psychosocial interventions and cancer ______________________ 4
DNA, genes, predisposition & cancer _____________________________________ 6
Conclusion _________________________________________________________ 11
Bibliography ________________________________________________________ 12
Abstract
Various experiments and clinical research have identified links between stressors
and psychological, psychosocial, environmental factors and genes which may
provide a basis for treatment and prevention of cancers. This paper considers
existing research into cancer predisposing genes and the psychological,
psychosocial, and environmental factors which may be involved.
Stressors
The Breast Cancer at the ABC Toowong Queensland: Third Progress Report from
the Independent Review and Scientific Investigation Panel, (2006) (Third Progress
Report) reported on what has been referred to as a review of a cluster of women with
breast cancer in a work place in Queensland noting “Stress and an individual’s
response to it are popularly believed to be important factors in causing cancer.”
(p.29).
The Third Progress Report cautioned, however, that a recent critical review of
psychological factors and cancer development by Garrsen (2004) concluded that:
“…there is not any psychological factor for which an influence on cancer
development has been convincingly demonstrated in a series of studies.” (p.29).
On the other hand, another review, by Butow et al (2000), also referred to in the Third
Progress Report, that focused specifically on breast cancer and commissioned by
Australia’s National Breast Cancer Centre, noted that while research had not
indicated that psychosocial factors played a major role in the development of breast
cancer, “… few studies have been of sufficient quality to state definitively that such a
role does not exist.” (p.29).
While Butow et al (2000) observed that the strongest psychosocial factors associated
with the development of breast cancer are emotional repression (especially
repression of anger) and severely threatening life events such as the death of a
significant other, results from a more recent prospective cohort study with follow up
over 9 years, by White et al (2007) suggested that anger control and negative affect
are not connected with breast cancer, melanoma, or total cancer, although they may
have a small role in the risk of prostate, colorectal and lung cancer. The conclusions
by White et al (2007) noted that although more research is needed to confirm the
latter associations, the results suggested that if affective states are associated with
cancer development, the association may differ for different cancers and argue
against the use of total cancer as an outcome measure for studies in this area.
Physiology and stress
Research over the years has identified the physiological effects of different levels of
stress on various bodily functions. The table below (Melhuish, 1978) summarizes
early research that is still useful today.
Normal
(relaxed)
Under pressure
Acute pressure
Chronic pressure
(stress)
Brain
blood
supply
normal
blood
supply
up
thinks
more
clearly
headaches or
migraines, tremors
and nervous tics
Mood
happy
serious
increased
concentration
anxiety, loss of
sense of humour
Saliva
normal
reduced
reduced
dry mouth, lump
in throat
Muscles
blood supply
normal
blood
supply up
improved
performance
muscular
tension and
pain
Heart
normal rate and increased rate and
hypertension
improved performance
blood pressure blood pressure
and chest pains
Lungs
normal
respiration
Stomach
reduced blood
normal blood
supply and
supply and acid
increased acid
secretion
secretion
Bowels
normal blood
supply and
bowel activity
increased
respiration rate
improved performance
coughs and
asthma
ulcers due to
reduced blood supply
heartburn and
reduces digestion
indigestion.
reduced blood
supply and
increased bowel
activity
reduced blood supply abdominal pain
reduces digestion
and diarrhoea
frequent urination
frequent
frequent urination due
urination,
to increased nervous
prostatic
stimulation
symptoms
Bladder
normal
Sexual
Organs
(m) impotence
(male) normal.
(decreased blood
decreased blood
(female) normal
supply) (f) irregular supply
periods etc
periods
Skin
healthy
decreased blood
supply - dry skin
oxygen
normal: oxygen
consumption up,
consumed,
Biochemistry
glucose
glucose and
and fats
fats liberated.
consumption up
decreased blood
supply
(m) impotence.
(f) menstrual
disorders
dryness and
rashes
more energy
rapid tiredness
immediately available
Source: Melhuish, A, Executive Health, London Business Books with extracts from Andy Ellis, Ruskin
College, Oxford, UK, 1978
Emotions & stress views from the Institute of HeartMath®
The Institute of HeartMath is a non-profit organization based in California USA. It
states on its website that it is a recognised global leader in researching the critical
link between emotions, heart-brain communication and cognitive function. For our
discussion purposes, it notes on its website that stress and emotions cannot be
separated. Dr. Rollin McCraty, Director of Research for the Institute of HeartMath, in
an article “Are we resigned to stress “ says, "On-going, low grade stress can do more
harm to the body, mind and emotions than one large stressful event can.”
Further in the HeartMath article, Psychologist Deborah Rozman, Ph.D., founding
partner of HeartMath, says:
The majority of people believe that emotions just happen to them. We haven't
been taught that we can shift out of stressful emotions. But it's important to
understand that stress is accumulated by carrying around unsettled or negative
feelings without resolving them. The lack of understanding about how to address
our emotions is one of the real causes for today's stress epidemic.
Our brain's neural circuitry is designed to create habits to make it easier to perform
tasks without having to think much about them. Each time you repeat a habit,
whether an attitude, behaviour or a repetitive task like driving a car, it becomes more
reinforced and unconscious. According to HeartMath, the same is true with stress.
One way HeartMath says you can stop the negative emotional experiences from
accumulating is to learn to track the more subtle emotional reactions. They suggest
thinking of the emotions as sound effects. Your outer sound effects, such as sighs,
swear words, negative humour and expressions whispered under your breath can
give you clues to the real feelings underneath. Your "inner sonics" like ugh, silent
swear words and feeling that things have "gone south" go on all the time and affect
your next thoughts and choices.
While many people believe that the mind rules, HeartMath says that it is our
emotions that shape much of our thinking and, more often than not, determine
choices and behaviours.
Accumulated stress can actually prevent us from finding the creative solutions that
we need to better deal with stress. Whether an irritation triggered by a relative or coworker, or low-grade anxiety triggered by current news events, HeartMath's research
shows that stress compromises our cognitive abilities. That research notes that we
cannot think as clearly or as creatively and we have a harder time making decisions.
In the study by Maddock & Pariante (2001), when discussing the concept of stress,
the authors noted that stress results when environmental demands exceed a
person’s resources to meet those demands (Lazarus, & Folkman, 1984). They noted
also that stress has various dimensions (Herbertt, & Cohen, 1993). It may be
considered in terms of its duration (acute vs chronic; for example, laboratory stressor
vs incurable disease); quantity (discrete events vs cumulative events; for example,
bereavement vs daily hassles); and quality (interpersonal event vs non-interpersonal;
for example, divorce vs earthquake). The individual’s perception of, and adaptation
to, stressors is accompanied by physiological and behavioural changes.
There is evidence to link stress with the onset of major depression and a poorer
prognosis in cardiovascular disease and cancer. Chronic stress appears to result in
suppression of the immune response, whereas immune activation and suppression
have been associated with acute stress. Inflammatory cytokines, soluble mediators of
the immune response, can result in symptoms of depression, Maddock & Pariante
(2001).
Psychological & psychosocial interventions and cancers
While the relationship between psychosocial factors and the development of cancer
has not been strongly established, research does demonstrate that addressing
psychological stress as part of treatment programs for cancer patients does have
benefits in facilitating adjustment and in improving survival.
Recently 'Clinical practice guidelines for the psychosocial care of adults with cancer'
were approved by the National Health and Medical Research Council and released
as a National Breast Cancer and National Cancer Control Initiative 2003. It noted at
page 14 that:
Evidence is accumulating that psychological therapies improve emotional
adjustment and social functioning, and reduce both treatment- and diseaserelated distress in patients with cancer. Meta-analyses of randomised controlled
trials demonstrate the efficacy of both supportive and cognitive behavioural
therapies in the treatment of depressive disorders in patients with cancer and the
efficacy of both individual and group therapies.
In a meta-analysis of 45 randomised controlled trials in patients with cancer,
those receiving psychological therapies showed, on average, a significant
improvement of 12% in measures of emotional adjustment, 10% in social
functioning, 14% in treatment and disease-related symptoms, and 14% in overall
improvement in their quality of life, compared with those not receiving
psychological therapies.
A meta-analysis of 116 intervention studies found that patients with cancer
receiving psycho-educational or psychosocial interventions showed much lower
rates of anxiety, depression, mood disorders, nausea, vomiting and pain, and
significantly greater knowledge about disease and treatment, than the control
group.
Psycho-educational programs are defined as programs with both psychological (for
example, supportive group therapy) and educational (for example, coping skills training,
stress management, education about disease and treatment) components (italics added).
Psychosocial intervention programs are defined as treatments that are intended to
address psychological, social and some spiritual needs, while psychosocial support is the
culturally-sensitive provision of psychological, social and spiritual care.(italics added).
While a number of studies discussed below demonstrated that interventions to
reduce psychological stress improve cancer survival, further research is required.
Speigel, Bloom, Kraemer & Gottheil (1989) treated women with metastatic breast
cancer by means of weekly group therapy. The intervention focused on encouraging
a discussion of how to cope with cancer, and the expression of feelings about illness
and its physical consequences. Relationships that developed amongst group
members provided increased social support. A randomized study compared one year
of the psychosocial treatment versus a control group. Both groups received routine
oncology care. After 10 years of follow-up, the survival time of patients in the
intervention group was almost double that of the controls; 36.6 months versus 18.9
months starting from the onset of the intervention. A further randomized prospective
trial by Speidel et al (2007) however was unable to replicate these findings and
concluded:
The earlier finding that longer survival was associated with supportive-expressive
group therapy was not replicated. Although it is possible that psychosocial effects
on survival are relevant to a small sub sample of women who are more refractory
to current hormonal treatments, further research is required to investigate
subgroup differences.
A group therapy intervention approach was utilised in the treatment of patients with
malignant melanoma (Fawzy et al, 2003). The intervention was multifaceted,
consisting of:
(1) health education (eg melanoma, nutrition, exercise, sun exposure);
(2) stress management (eg general stress information, personal stress awareness,
relaxation techniques);
(3) enhancement of coping skills (eg problem solving, general coping alternatives,
theoretical and personal application of solutions); and
(4) psychological support (from group members and staff).
At six months follow-up the intervention group, compared to a randomly selected
control group, exhibited lower levels of psychological distress (Fawzy et al, 1990a).
Furthermore, after 5-6 years of follow-up the psychosocial intervention group had a
lower rate of death and cancer recurrence than controls (Fawzy et al, 1993.) In a 10
year follow-up review the researchers noted that between the 5-6 year follow-up and
the 10 year follow-up, the effects of the intervention had not entirely disappeared
(Fawzy et al, 2003).
In 2000, Stanton et al noted:
Although not yet extended to cancer patients, experimental investigations
provide the most convincing evidence to date that emotional processing and
expression are related causally to positive outcomes.
The study by Stanton et al (2000) tested the hypothesis of coping through emotional
approach and its impacts on enhancing adjustment and health status for breast
cancer patients. The authors noted evidence suggesting that coping through
emotional approaches, i.e. coping through actively processing and expressing
emotion, may enhance adjustment in cancer patients.
In the Stanton et al (2000) study, the authors referred to previous randomized,
controlled studies of psychological interventions, in which one intervention
component was the facilitation of emotional expression. These studies provided
evidence that in groups with cancers such as metastatic breast cancer and malignant
melanoma such interventions can enhance psychological adjustment (Fawzy et al,
1990; Spiegel, Bloom, & Yalom, 1981), improve immune function (Fawzy et al, 1990),
and perhaps promote longer survival (Fawzy et al, 1993; Spiegel, Bloom, Kraemer, &
Gottheil, 1989).
Further in the Stanton et al (2000) study, the authors referred to other studies of
adjustment to cancer that indicated that coping through cognitive and behavioural
avoidance is detrimental to adjustment (Carver et al, 1993; Friedman, Nelson, Baer,
Lane, & Smith, 1990; Stanton, & Snider, 1993) and perhaps to health status (EppingJordan, Compas, & Howell, 1994; Jensen, 1987).
DNA, genes, predisposition & cancer
It is important to note that genes themselves do not cause disease – gene-based
disorders are caused by mutations that make a gene function improperly. For
example, when people say that someone has “the cystic fibrosis gene”, they are
usually referring to a mutated version of the CFTR gene which causes the disease
(Genomics Home reference – Your Guide to Understanding Genetic Conditions, US
National Library of Medicine, National Institute of Health website).
A mutation occurs when a DNA gene is damaged or changed in such a way as to
alter the message carried by that gene. Once a gene is damaged or changed, the
mRNA transcribed from that gene will now carry an altered message. Since genes
are composed of DNA, nearly anything that can change the structural composition,
sequence, physical integrity or length of a DNA molecule can cause mutations.
Further, mutations can occur by what are described in the field as missense,
nonsense, insertion, deletion, duplication, frameshift or repeated expansion.
Cancers develop due to alterations (mutations) in genes that when working properly,
promote normal, controlled cell growth. Only a small percentage of cancers involve
inherited mutations that are passed from generation to generation (genetic). The
majority of cancers can be attributed to acquired mutations. "Acquired" means that
the mutations occur only in the tissue that is affected by cancer (for example, colon
cancer cells), and are not passed to children. These changes occur at the cellular
level after birth, as a result of environmental exposures (such as smoking, working
with asbestos), lifestyle behaviours (such as eating poorly or not exercising), or
chance alone. Mutations in a person's DNA accumulate over time. If mutations affect
genes that control cell growth this may cause a cell to grow out of control, and to
ultimately become a cancer cell (All About Cancers, description of genetics, Health
Topics, University of Virginia Health System, website).
How does our mind potentially modulate our genes? This question is explored in a
book by E L Rossi (2003), The Psychobiology of Gene Expression:
Neuroscience and Neurogenesis in Hypnosis and the Healing Art. Rossi
explains that genes can be affected by thoughts and emotions. Ewin, D M, American
Journal of Clinical Hypnosis, 2003 referring to an extract of the book, notes:
’Gene expression’ is the technical word for a gene that is activated into producing
a particular protein. Some of these in turn, generate new neurons and
connections in our brain. Since a thought or emotion can cause gene expression,
there is now a true psycho-biology awaiting our understanding. We have millions
of genes that can toggle ‘on’ or ‘off’ when we find the right switches in our
thoughts and feelings.
A Japanese study (Irie et al, 2001) using a sample of healthy adults, not only
provided evidence of a stress-cancer linkage, but also suggested possible sex
differences in the mechanisms of stress-related cancer initiation. This study noted
that gene alterations, which are important in the pathogenesis of cancer, have
scarcely been investigated in relation to psychosocial factors. It examined the
relationship between psychosocial factors and cancer-predisposing gene alterations
simultaneously in order to assess the stress-cancer linkage, particularly with respect
to cancer initiation. Very limited issues, such as poorer repair of DNA damage, an
increase of sister chromatid exchange and alterations in apoptosis, have been
reported to be linked causatively with stress.
Irie et al, (2001) undertook a study to investigate the relationships between the levels
of 8-OH-dG in peripheral blood leukocytes and various psychosocial factors that may
be associated with oxidative DNA damage. The study considered such psychosocial
factors as emotions, stress-coping behaviours, social support, working conditions,
and lifestyle factors in workers during usual stressful conditions. The relationships
were examined adjusting for age, body mass index (BMI), cigarette smoking and
alcohol drinking habits, because these factors have been reported to have
associations with carcinogenicity and the formation of 8-OH-dG.
In an article on current directions in cancer research, Antoni and Lutgendorf (2007)
state that psychosocial factors such as stress, personality, and social support relate
to differences in disease progression in cancer patients. Neuroendocrine substances
associated with psychosocial factors may regulate immune responses to cancer as
well as regulate the activity of oncogenic (cancer-causing) viruses, DNA-repair
processes, and the expression in tumor cells of genes that may affect the tumor's
growth and metastasis. Biobehavioral oncology research seeks to understand how
these psychosocial factors, and interventions designed to modify them, become
neurohormonal changes that alter cell signaling and tumor growth, viral oncogenesis,
and immune responses. Antoni and Lutgendorf (2007) reviewed the empirical basis
for psychosocial factors and biobehavioral processes in cancer progression and
suggest future research.
Lutgendorf et al, (2005) examined the relationships between distress, social support
and natural killer (NK) cell activity in ovarian cancer patients in peripheral-blood
mononuclear cells (PBMC), ascetic fluid and tumor-infiltrating lymphocytes (TIL). The
researchers found that psychosocial stress was related to impaired immunity in
cancer patients. However, the extent to which these relationships exist in immune
cells in the tumor microenvironment in humans was not explored. In Lutgendorf et al
(2005) research, patients awaiting surgery for a pelvic mass suspected of being
ovarian cancer completed psychological questionnaires and gave a pre-surgical
sample of peripheral blood. Samples of tumor and ascites were taken during surgery,
lymphocytes were then isolated, and NK cytotoxicity and percentage were
determined. The final sample, which was confirmed by surgical diagnosis, included 42
patients with epithelial ovarian cancer and 23 patients with benign masses.
The results of the research by Lutgendorf et al (2005) noted that peripheral NK cell
activity was significantly lower among ovarian cancer patients than in patients with
benign masses. It noted, among ovarian cancer patients, NK cytotoxicity in TIL was
significantly lower than in PBMC or ascitic fluid. Social support was related to higher
NK cytotoxicity in PBMC and TIL, adjusting for stage. Distress was related to lower
NK cytotoxicity in TIL. A multivariate model indicated independent associations of
both distress and social support with NK cell activity in TIL. In other words, the
research by Lutgendorf et al (2005) concluded that psychosocial factors, such as
social support and distress, are associated with changes in the cellular immune
response, not only in peripheral blood, but also at the tumor level. These relationships
were more robust in TIL. These findings supported the presence of stress influences
in the tumor microenvironment.
An earlier study on vascular endothelial growth factor (VEGF) by Lutgendorf et al
(2002) also contributes to our understanding of the biological basis for the link
between social support and cancer prognosis. Pre-surgical levels of VEGF, a
cytokine that stimulates tumor angiogenesis, were lower in patients with ovarian
cancer who had higher levels of social well-being.
Barclay (2002) observed that research is providing evidence that psychosocial
factors can affect immunological responses of cancer patients. He discussed
particularly one study conducted in Iowa, and noted from that research:
Growing evidence has indicated that psychological factors, such as stress,
depression, and social support, are able to modulate many of the immunologic
activities relevant to patients with malignant disease.
Of 24 women with ovarian carcinoma who were recruited at the pre-surgical clinic
visit, those who reported higher levels of social well-being on the Functional
Assessment of Cancer Therapy Quality of Life survey and the Profile of Mood
States had lower levels of VEGF (P=.005). Specific perceptions linked to lower
VEGF levels were greater support from friends and neighbours (P=.005) and less
distance from friends (P=.04). Although depression as a whole was not related to
VEGF levels, feelings of helplessness (P=.03) or worthlessness (P=.08) predicted
higher VEGF levels.
In light of study limitations including the cross-sectional nature of the data and
use of a quality-of-life instrument measuring only limited aspects of social
support, they recommend further research before drawing any causal inferences.
They (sic the researchers) suggested that these findings suggest a novel
mechanism by which bio-behavioural factors may be associated with the
progression of ovarian carcinoma. They concluded that understanding the
mechanisms of such interactions and the type and magnitude of their potential
effects is an important goal of future research.
In a more recent study by Sharma, Sharp, Greenman, Monson, & Walker (2007), the
authors questioned if VEGF was related to psychosocial factors in patients with
colorectal cancer. They reported that:
Various psychosocial factors, particularly cancer-related concerns and
depression, appear to be related to pre-operative and post-operative VEGF level
in patients with colorectal cancer. Future prognostic studies involving VEGF
should assess psychosocial variables and include these in a multivariate analysis
of outcomes.
In another link to the capacity of our immune system to have a positive effect on
cancer outcomes Koebel et al (2007) presented their research findings that
suggested “when cancer cannot be killed, it may be possible to find ways to use the
immune system to contain it”. Co–author Prof Mark Smyth, Head of the Peter
MacCallum Cancer Immunology Program in Melbourne, suggested that the next step
would be to mobilise the immune system to suppress cancer and prevent it from
spreading (Kelly, 2007).
In research of another possible predisposition gene marker, Wu et al (2003) provided
support to their hypothesis that telomere dysfunction impairs chromosomal stability
and is associated with an increased risk of various cancers. These results (using two
different methods to measure telomere length) demonstrated that telomere length
was statistically significantly shorter in lymphocytes from case patients with head and
neck cancer, bladder, lung, or renal cell carcinoma than in control subjects. It also
provided evidence of an increasing risk for head and neck, lung, and renal cancer
associated with progressively shorter telomeres, indicating that telomere dysfunction
may be a risk factor for cancer at these sites and possibly for cancer in general.
A stress hypothesis, including the epigenetic alterations, was investigated in a study
that reported sustained stress environment (SSE) investigations, noted in the table
below, by different natures of stress impacts (Karpinets, & Foy, 2005). The table
below summarizes the links between epigenetic alterations, the relationships with the
nature of stress (environmental) and the tissues and organisms reviewed.
Epigenetic alterations induced by SSE in mammalian cells
Epigenetic alterations
Nature of stress
Tissue/organisms
Ref.
Hypermethylation of tumor
suppressor genes (p16, APC) and
decrease in the mean methylation
index
Tobacco smoke exposure
Lung tissue of long-time
smokers
59
Hypermethylation of tumor
suppressor gene p16
Exposure with cadmium
(potent carcinogen)
Cell culture (BALB/c-3T3
cells)
60
Hypermethylation and
transcriptional silencing of p16 and
p53
Exposure with dioxin (an Primary human
ubiquitous environmental keratinocytes
contaminant and a highly
potent carcinogen)
61
Hypomethylation including rafgene
Phenobarbital's exposure
Rodent liver tissue
62
Upregulation and hypomethylation
of c-myc and c-jun
Exposure with
carcinogens (arsenite,
dichloroacetic acid and
trichloroacetic acid)
Variety of tissues, including 63,
64
the liver
Hypomethylation of the genome
Exposure with cadmium
Rat liver cells (TRL1215)
65
Decondensation of the
heterochromatin
Exposure with nickel
Chinese hamster embryo
cells
66,
67
Dose-dependent hypomethylation
Gamma radiation
Four non-malignant
cultured cell lines
68
Dose-dependent hypomethylation
Ultraviolet radiation
(UVB 280–340 nm)
Rat liver
69
Induction of Alu elements (short
interspersed elements)
Genotoxic stress induced
by a variety of DNA
damaging agents
Mouse cells
70
Induction of long interspersed
nuclear element-1 (LINE-1)
Endogenous oxidative
stress
Glucose 6-phosphate
dehydrogenase deficient
mice
71
Induction of VL30 elements (a
Anoxia (may accompany
multigene family within the class of wound healing)
retroviruses and retrotransposons)
Rat fibroblasts
72
Hypermethylation of mismatch
repair genes and microsatellite
instability
Chronic inflammation
(chronic ulcerative
colitis)
Non-neoplastic mucosa
73
Epigenetic silencing of imprinted
genes that are usually induced by
Proliferation under stress
(cell culturing)
Primary mouse embryonic
fibroblasts
74
tumorigenesis
Progressive aberrant methylation of SV40 virus infection
protooncogenes (RASSF1A, HPP1,
DcR1, TMS1, CRBP1, HIC-1 and
RRAD) methylated in malignant
mesothelioma
Human mesothelial cells
Hypermethylation of p16 promoter
Hepatitis B virus and
hepatitis C virus infection
in liver with chronic
inflammation
Liver tissue specimens of
human hepatocellular
carcinoma with or without
hepatitis virus infection
Epstein–Barr virusassociated gastric
carcinoma
Epstein–Barr virusassociated and negative
gastric carcinoma
Specific high-density methylation
of cyclin-dependent kinase
inhibitors p14 and p16
75
76
77
NB: the references are to
those in the original article
Source: Karpinets, & Foy (2005)
Part of the commentary to this table noted that tumorigenesis is considered a
process of the adaptation of mammalian cells to SSE (sustained stress environment)
by means of EA (epigenetic alterations) of the genome, subsequent mutations
matched to EA and natural selection of originated mutant cells via apoptosis (Figure
1, replicated schematic below in this article). The process of adaptation to SSE
involves the emergence of senescent epigenetically reprogrammed (ER) cells with
specific tumor related EA in the genome. The EA prime the cells for error prone
replications and provide epigenetic tags in the genome for beneficial mutations to
arise.
The authors (Karpinets, & Foy, 2005) further hypothesized that tumor related EA
occur before mutations and reprogram the genome for their origin. The initiation
event for these EA is long-term exposure of cell tissue to SSE that induces
continuing replication of some cells in the tissue. Persistent proliferative and stressrelated survival signals in the environment induce in these proliferating cells a stable
activation of biological processes related to promotion of replication and stress
response. On the other hand, processes related to inhibition of proliferation,
activation of cell-cycle arrest and apoptosis, and DNA repair pathways will be
constantly suppressed in these cells.
Source: Karpinets, & Foy (2005)
Conclusion
The evidence presented demonstrates some relationships across psychological,
psychosocial, environmental and gene pathways and cancer. While not determinative,
the evidence provides opportunities for further high quality research in what is a psychogenomic structure.
Research streams that form part of psycho-genomics include cancer, psychology,
emotional expression & processing, psychosocial, environmental, physiology, DNA
genes and genomics.
Power Thinking Health Council aims to undertake that research and will:



identify gene expression and gene mutation marker differentials between cancer and
non-cancer population;
undertake a study over several years looking for blood markers of cellular
dysfunctions which predispose to cancer, i.e. a step before the current screening
phase, and
identify psychological/psychosocial intervention affects on those blood markers over
time in order to treat cancers to increase survivorship and prevent initiation of
cancers.
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