[ RadSafe ] Radiation Exposure: Does it Always Cause Cancer?

John Jacobus crispy_bird at yahoo.com
Mon Aug 7 11:38:00 CDT 2006

I am not sure what your question is, if that is what
you mean to say in the subject line.  From what I
read, a defect in BRIT1 may not surpress, or will
result is a weakened surpression of cancers, as noted
in the underexpression in human ovarian, breast and
prostate cancer cell lines.  

They used ionizing radiation to enhance aberrations of
the DNA.  Even without ionizing radiation, there was
aberration of the DNA.  Obviously, the ionizing
radiaton enhanced the effect, which I don't think is

I doubt that this is the "key" factor in cancer
initiation.  There are probably many genes that have
to function properly along the ATM and ATR pathways.

--- ROY HERREN <royherren2005 at yahoo.com> wrote:

>  Public release date: 3-Aug-2006
> Contact: Scott Merville
> sdmervil at mdanderson.org
> 713-792-0661
> University of Texas M. D. Anderson Cancer Center 
>   Researchers identify gene as protector of DNA,
> enemy of tumors    Houston -- A single gene plays a
> pivotal role launching two DNA damage detection and
> repair pathways in the human genome, suggesting that
> it functions as a previously unidentified tumor
> suppressor gene, researchers at The University of
> Texas M. D. Anderson Cancer Center report in Cancer
> Cell.
>   The advance online publication also reports that
> the gene - called BRIT1 - is under-expressed in
> human ovarian, breast and prostate cancer cell
> lines.
>   Defects in BRIT1 seem to be a key pathological
> alteration in cancer initiation and progression, the
> authors note, and further understanding of its
> function may contribute to novel, therapeutic
> approaches to cancer.
>   "Disruption of BRIT1 function abolishes DNA damage
> responses and leads to genomic instability," said
> senior author Shiaw-Yih Lin, Ph.D., assistant
> professor in the Department of Molecular
> Therapeutics at M. D. Anderson. Genomic instability
> fuels the initiation, growth and spread of cancer.
>   A signaling network of molecular checkpoint
> pathways protects the human genome by detecting DNA
> damage, initiating repair and halting division of
> the damaged cell so that it does not replicate.
>   In a series of laboratory experiments, Lin and
> colleagues show that BRIT1 activates two of these
> checkpoint pathways. The ATM pathway springs into
> action in response to damage caused by ionizing
> radiation. The ATR pathway responds to DNA damage
> caused by ultraviolet radiation.
>   By using small interfering RNA (siRNA) to silence
> the BRIT1 gene, the scientists shut down both
> checkpoint pathways in cells exposed to either type
> of radiation.
>   Researchers then used siRNA to silence the gene in
> normal human mammary epithelial cells (HMEC). The
> result: Inactivation of the gene caused chromosomal
> aberrations in 21.2 to 25.6 percent of cells.
> Control group HMEC had no cells with chromosomal
> aberrations. In cells with the gene silenced that
> were then exposed to ionizing radiation, 80 percent
> of cells had chromosomal aberrations. 
>   "We also found that BRIT1 expression is aberrant
> in several forms of human cancer," Lin said. The
> team found reduced expression of the gene in 35 of
> 87 cases of advanced epithelial ovarian cancer. They
> also found reduced expression in breast and prostate
> cancer tissue compared with non-cancerous cells. 
>   Genetic analysis of breast cancer specimens
> revealed a truncated, dysfunctional version of the
> BRIT1 protein in one sample.
>   Loss of the DNA damage checkpoint function and the
> ability to proliferate indefinitely are two cellular
> changes required for the development of cancer. Lin
> and colleagues have now tied the gene to both
> factors. They previously identified BRIT1 as a
> repressor of hTERT, a protein that when reactivated
> immortalizes cells, allowing them to multiply
> indefinitely. 
>     ###
>   Co-authors with Lin are first author Rekha Rai,
> Ph.D., Hui Dai, M.D., John P. Lahad, M.S., Jiyong
> Liang, Ph.D., and Gordon Mills, M.D., Ph.D., all of
> the Department of Molecular Therapeutics; Asha S.
> Multani, Ph.D., Department of Cancer Genetics at
> M.D. Anderson; Funda Meric-Bernstam, M.D.,
> Department of Surgical Oncology, M. D. Anderson;
> Kaiyi Li, Ph.D., Department of Surgery at Baylor
> College of Medicine; and Koei Chin, M.D., Ph.D., and
> Joe Gray, Ph.D., of the Life Sciences Division,
> Lawrence Berkeley National Laboratory, Berkeley,
> Calif.
> ---------------------------------
> "George J. Vargo" <vargo at physicist.net> wrote:  Seen
> at:
> George J. Vargo, Ph.D., CHP
> Senior Scientist
> MJW Corporation, Inc.
> http://www.mjwcorp.com
> 610-925-3377
> 610-925-5545 (fax)
> vargo at physicist.net
> Reported August 2, 2006 
> Radiation Exposure: Does it Always Cause Cancer?
> By Vivian Richardson, Ivanhoe Health Correspondent
> ORLANDO, Fla. (Ivanhoe Newswire) -- The survivors of
> the atomic bomb blasts
> in Japan during World War II all developed cancer,
> right?
> No. Many did, and suffered terribly, but the fact
> that a large number of the
> survivors have not yet developed cancer is just one
> part of the mystery
> around radiation exposure and cancer.
> "I think there is no doubt that radiation is, in
> fact, carcinogenic," said
> Herman Suit, M.D., Ph.D., Sc.D., a radiation
> oncologist from Harvard
> University, today at the 48th Annual Meeting of The
> American Association of
> Physicists in Medicine in Orlando, Florida.
> Scientists following 86,611 survivors of the 1945
> atomic bomb blasts found
> only 4.7 percent of the 10,127 cancer deaths could
> be clearly attributed to
> radiation exposure, said Dr. Suit. These deaths
> didn't happen right away --
> 35 percent of the radiation cancer deaths occurred
> between 42 years and 52
> years after the explosions.
> "These cancer deaths keep occurring," said Dr. Suit.
> This reinforces the
> need to very carefully study how cancer patients
> today are affected by the
> radiation used to treat their cancers, especially in
> light of higher
> survival rates and life expectancies of these
> patients.
> One of the most perplexing aspects of this area of
> study is how big a role
> genetics seem to play. Dr. Suit explained many
> studies show that cancer
> occurrence increases with increased cancer exposure.
> In several mouse
> studies, however, the rate at which the cancer risk
> increased varied widely
> between different genetic strains of mice. Also,
> certain types of cancer
> seem to be more likely to be caused by radiation
> exposure than others. He
> reported that data from 14 studies show an increased
> risk for cancers of the
> stomach and pancreas while there was no evident
> increased risk of bladder or
> rectal cancer.
> "It appears we have made some inroads, but not
> enough," said Dr. Suit. What
> scientists need to know now is the genetic
> characteristics of specific
> patients and how those genes react when exposed to
> radiation.
> This article was reported by Ivanhoe.com, who offers
> Medical Alerts by
> e-mail every day of the week. To subscribe, go to:
> http://www.ivanhoe.com/newsalert/.
> SOURCE: Vivian Richardson at the 48th Annual Meeting
> of The American
> Association of Physicists in Medicine in Orlando,
> Fla., July 30-August 3,
> 2006
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> Roy Herren
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=== message truncated ===

>From an article about physicians doing clinical studies: 

"It was just before an early morning meeting, and I was really trying to get to the bagels, but I couldn't help overhearing a conversation between one of my statistical colleagues and a surgeon.

Statistician: "Oh, so you have already calculated the P value?"

Surgeon: "Yes, I used multinomial logistic regression."

Statistician: "Really? How did you come up with that?"

Surgeon: "Well, I tried each analysis on the SPSS drop-down menus, and that was the one that gave the smallest P value"."

-- John
John Jacobus, MS
Certified Health Physicist
e-mail:  crispy_bird at yahoo.com

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