Although Israeli researchers were not involved in groundbreaking research
presented over the weekend by the American Association for Cancer Research, the
population here – exposed on a daily basis to the stress of security dangers,
economic and family pressures and tension at the workplace – would be well
advised to take note.
For the first time, a direct link between stress
and damage to the chromosomes in every cell has been shown, with the ends –
called telomeres – shortening as people are more exposed to chronic emotional
Although telomere length generally shortens as one ages,
lifestyle and not only genetic differences can make these structures longer or
shorter and thus affect one’s risk and timing of diseases from cancer to
cardiovascular disease and stroke to diabetes.RELATED:Breaking barriers through water research2 leading Israeli scientists to get Canada Gairdner awards‘Thinking’ white cells go from place to place, as needed
Two pieces of research
related to telomeres were unveiled at a Saturday press conference at the AACR’s
102nd annual meeting, in Florida, that aroused much interest around the
The studies were simultaneously published in Cancer Prevention
In the first, a study led by Prof. Edward Nelson, division
chief of the department of hematology/oncology at the University of California,
Irvine, lent credence to the idea that improving quality of life affects
stress-related biological markers and possibly the health of cancer
Until now, there was only epidemiological but not direct
evidence that stress and not only aging can affect telomere length.
are trying to understand the interconnections between the mind and the body;
that is, how does the diagnosis and treatment of cancer impact patients not only
psychologically, but also physiologically and how can we improve their
Cancer drives a chronic stress response in some patients,” said
Telomeres have been described like the plastic or metal ends of
shoelaces that prevent them from unraveling or fraying. They protect the
chromosome from deteriorating, breaking apart or joining with other chromosomes,
which can lead to mutations.
Chromosomal rearrangements are seen in
cancers and provided a biological reason to investigate this link, said
“For this study, we wanted to know if chronic stress was
associated with accelerated telomere shortening in cancer patients, and if a
psychosocial intervention that modulates the stress response could also modulate
telomere length,” he said.
In this retrospective study, the researchers
took biological samples from 31 women with cervical cancer who had been
randomized to one of two groups – those who received six counseling sessions by
telephone and those who received usual care without counseling.
sessions consisted of a quality of life and psychosocial profile, managing
stress and emotions, enhancing health and wellness, addressing relational and
sexual concerns, and integrating and summarizing the information.
enrollment and after four months, the researchers obtained biological samples
from both groups and investigated changes over time to see if psychological
counseling had any physical effects.
“Improved quality of life and
reduced stress response was associated with changes in telomere length,” Nelson
Nelson’s study was the first study of telomere length and chronic
stress in a cancer population, and the first longitudinal analysis of whether
changes in quality of life and changes in the stress response would be
associated with modulating the telomere length, he said. Giving backing to the
mind/body approach in cancer treatment, he said there is “no doubt that offering
psychological services has the potential to improve quality of life and outcomes
of patients, but “whether we can draw conclusions or make recommendations about
the capacity of a behavioral intervention to modulate telomere length remains an
AACR president and 2009 Nobel Prize laureate biologist
and physiologist Elizabeth Blackburn of the University of California, San
Francisco, wrote an editorial in the AACR journal.
“[The study] has shed
light on the biology of early cancers and their initiating events.
advances now create unprecedented opportunities for novel approaches directed at
prevention and early interception of cancer’s deadly trajectory,” Blackburn
Although she stressed that the effect of interventions to lengthen
telomeres would need to be tested in prospective studies, she said the finding
was a major research advancement.
The other published study was written
by University of Texas epidemiologist Prof. Jian Gu, who with his team linked
both longer telomeres on the chromosome and a 19-percent reduction in the risk
of bladder cancer.
Of some 300,000 SNPs – DNA sequence variations – in
459 healthy participants, it was found that 15,120 of them were associated with
telomere length. The team also found that smoking especially augmented the risk
of bladder cancer in those people having the other genetic variant, which was
associated with shorter telomeres. Gu said that a common genetic variation links
to both bladder cancer risk and to the length of protective caps found on the
ends of chromosomes.
Although not part of the studies, Tel Aviv
University Sackler School of Medicine cancer researcher Prof. Yosef Shiloh was
highly honored by receiving the G.H.A.
Clowes Memorial Award at the
Florida conference for his work on damage response and the rare genomic
instability syndrome ataxiatelangiectasia (A-T).
AACR chief executive
Margaret Foti said that the Israeli’s discovery, “along with his
subsequent work, has played a critical role in increasing our understanding of
DNA damage response and repair, which has important implications for cancer and
Dr. Shiloh is a truly exceptional scientist, and we
congratulate him on receiving the G.H.A. Clowes Memorial Award.”
with A-T exhibit progressive neurodegeneration, immunodeficiency, striking
cancer predisposition and chromosomal fragility.
The disease is caused by
a profound defect in a major mechanism that maintains genomic stability – the
cellular response to DNA double strand breaks.
Shiloh, who spoke to The
Jerusalem Post before leaving for Orlando, has for three decades been
investigating AT and the defect in the DNA damage response that leads to this
disease. He changed the field when his lab identified the A-T gene in 1995 and
successfully cloned it.
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