Intended for healthcare professionals

Rapid response to:

Analysis And Comment Cancer genetics

Common susceptibility genes for cancer: search for the end of the rainbow

BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.332.7550.1150 (Published 11 May 2006) Cite this as: BMJ 2006;332:1150

Rapid Response:

Failure of cancer genetics; Are we ready to accept the argument for transfer of resources to observational and experimental research in cancer biology ?

Editor,

Baker and Kaprio have reviewed the status of clinical benefit from
cancer genetics(1). We would like to congratulate them for demonstrating
the fallacies of this approach in a systematic manner. This is quite
obvious also at common sense level. But genetics appears to catch both
professional and lay imagination like nothing else in cancer biology. This
situation is like use of Lasers in medicine. The mere words like genes and
lasers have profound effect. The vast amount of resources are spent year
after on cancer genetics without clear long term broad objectives. It is
no surprise that a month after Baker and Caprio’s paper in BMJ there is an
article in a national newspaper perpetuating the myths of value of cancer
genetics(2)There is clear desire here to simplify a complexity as Mr
Wishart has tried to explain.

We believe that more emphasis needs to be given to the the fact that
a cancer is a dynamic process( made up of several very well co ordinated
sub processes). These processes are being dealt with mostly in a clinical
setting. There are structural changes within the host of a cancer and in
the cancer itself which are used as clinical, investigational and
laboratory signs. Cancer genetics is study of one important aspect of the
structural changes and will always be of the value for what it is worth
under such complex circumstances.

Various structural attributes of a cancer e.g. histology, and grades,
tumour stage; clinical and imaging information, serological estimation of
tumour activity only give us a cross section or snapshot information
regarding a cancer. Trillions of dollars and pounds have been wasted in
the reductionist approach in cancer research. Common susceptibilty gene
approach is an example of this misguided direction of research. This
approach grossly underestimates the environmental infulences. The
separtion of the two in a practical world will remain improbable until we
have at least few starting reliable and reproducible equations. At present
unfortunately we have none.

What we have not explored is treating each cancer as an individual
process using the biological or observational approach(3). This may
involve more respect for the cancerous phenomenon than is being given at
present. For example we may have to visualise a cancer as an organism
within an organism with at least some autonomy. For example carrying out
serial MRI spectroscopy, PSAs and serial targeted biopsies in prostate
cancer over a peroid of time will help us to assess the individual
behaviour of a cancer.. That will be one type of such assessment.
Additionally provocative in vitro assessment is possible using the
stimulus and response model. In vitro response to various investigations
and treatments may give us information which may have more value than the
static tests. The information so gained will be akin to a multimedia file
compared to the snap shots assessment which are carried out at present.
What is not being appreciated is that time is a compulsory variable which
is being omitted too often to simplify various equations Omission of time
leads to making imperfect impressions about a dynamic process which leads
to n number of probabilities and rarely concludes to a certainty. Bringing
time back into these equations will pose problem. There will be obvious
ethical questions in an assessment where time is allowed to elapse after
diagnosis without treatment. Applying thinner slices of time using ultra
sensitive measurments and using examples of slow growing cancers e.g.
prostate cancer may provide some answers to these ethical dilemmas.
Relating the audio-video file. of each patient with their genotype and and
their environment may open newer avenues of cancer research. As clinicans
we use this approach every day processing real time information on our
patients, but our measurements tools are rather crude. And we do not
record what we measure all the time. Refining these tools may lead us to
insights regarding hard facts not yet imagined by us. But for present we
should focus resources in clinical research and slow down on orthodox
cancer genetics.

References:

1. “COMMON SUSCEPTIBILITY GENES FOR CANCER: SEARCH FOR THE END OF THE
RAINBOW” Stuart G Baker, Jaakko Kaprio BMJ 2006;332:1150-1152,

2. “A CURE FOR CANCER” lead story, Nigel Hawkes and Adam Wishart, The
Times, Times2 l No 68728, Friday June 16 2006; 4-5.

3. "POST-BIOPSY RISE IN SERUM PSA: A POTENTIAL TOOL FOR DYNAMIC
EVALUATION OF PROSTATE CANCER/PROSTATIC INTRAEPITHELIAL NEOPLASIA" (PIN)
Shiv Bhanot, R. Gopalakrishnan, R.T.D. Oliver. Cancer Biology &
Therapy 2.1,59-62,Jan/Feb 2003

Competing interests:
None declared

Competing interests: No competing interests

18 June 2006
Shiv Mohan Bhanot
Consultant Urologist
IG3 8YB
King George Hospital, Barley Lane