The human being is a very complex organism, and you are a very
individualistic one too. Your body, or cells rather, are not going to listen
to, or abide by, the statistics and say, "oh, I will only mutate after 15 years
of, or 1,000, chest x-ray exposures".

If you are a bit unlucky, all it takes is a SINGLE shot to cause mutations
of p53, p21 and RAS in a SINGLE cell, override its Hayflick limit, and
start the ball rolling. That's it.

All the talk or literature in the world is not going to make a difference
when that happens.

Cancer is just basically cell immortality.

do you even know wat you're talking about?
first u are worried that ionizing radiation can cause sclc before skin cancers.
and now i'm not sure if u even know wat p53 and p21 are.
p53 deficiency is a very rare autosomal dominant disorder. the patients fate has already been determined from birth.
sure it can be an acquired as well. but thats also very rare, usually induced by long term infection of HPV. and certainly not xrays.
p21 on the other hand plays no role at all in the predisposition to cancer. high levels are found in hiv resistant individuals
lets just stick to the basics.

from what i see, the only risk u have atm for lung cancer would be your tuberculosis infection. it is a predisposing factor, maybe u should be more worried about that than some simple radiographs.

Thank you for the explanation and suggestions incx & valkryie85!

I am well aware of the predisposition to lung cancer from TB.


A search of p21 and cancer turns up 13,780 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term=p21+cancer


p53, cancer, 46,109 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term=p53%2C+cancer


ras, cancer, 22,709 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term=ras%2C+cancer



p21, lung cancer, 1,048 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term...%2C+lung+cancer


p53, lung cancer, 4,108 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term...%2C+lung+cancer


ras, lung cancer, 2,659 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term...%2C+lung+cancer



p21, SCLC, 35 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term=p21%2C+sclc


p53, SCLC, 148 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term=p53%2C+sclc


ras, SCLC, 73 studies.

http://www.ncbi.nlm.nih.gov/m/pubmed/?term=ras%2C+sclc



" p53 mutations are common in lung cancer and range from 33% in adenocarcinomas
to 70% in small cell lung cancers. "

http://p53.free.fr/Database/p53_cancer/p53_Lung.html





p53 accumulation in the organs of low-dose X-ray-irradiated mice.

http://www.ncbi.nlm.nih.gov/m/pubmed/8640750/



Occurrence of mutations in the epidermal growth factor receptor gene
in X-ray-induced rat lung tumors.

http://www.ncbi.nlm.nih.gov/m/pubmed/18271921





SCLC is actually a neuroendocrine cancer. In my American friend Bill's case,
there was some discussion of its hedgehog signalling pathway, and supplements
or herbs to inhibit it, in his thread at that time.

http://www.ncbi.nlm.nih.gov/m/pubmed/21983857



Here is a very lucky long-term survivor, party attributed to topotecan.

" Small cell lung cancer (SCLC) results in death within 1-2 months if left untreated. "


http://www.ncbi.nlm.nih.gov/m/pubmed/18787355/



In most patients however, resistance rapidly sets in after a typically initial good
response to chemotherapy, and the disease relapses in less than two months.

The newer chemo drugs have made hardly any difference to survival.

http://www.ncbi.nlm.nih.gov/m/pubmed/14512193

http://www.ncbi.nlm.nih.gov/m/pubmed/16488055/

http://www.ncbi.nlm.nih.gov/m/pubmed/21918390

http://www.ncbi.nlm.nih.gov/m/pubmed/17285598

http://www.ncbi.nlm.nih.gov/m/pubmed/20871263/

http://www.ncbi.nlm.nih.gov/m/pubmed/20559150


An exception might be the Japanese topoisomerase 2 inhibitor, amrubicin,
which I had urged Bill to get himself enrolled in a Phase 2 trial at that time.

However, his oncologist there turned a blind eye, despite the fact his hospital in Maine
was actually one of those involved in the trial at that time, and chose to treat
him with the 30-year old hopelessly outdated first-line regimen of cisplatin and
etoposide.

Amrubicin had already been used extensively in Japan for years before that.

http://www.ncbi.nlm.nih.gov/m/pubmed/17135647

ok.. any1 can just put a blind search of 2 keywords.
ur first link p21 and cancer. the first study itself shows this

"Taken together, these results suggested that neuronal differentiation of EC cells induced by lidamycin was associated with the inhibition of Oct4 expression and the activation of p21 transcription. Our results have provided a novel mechanism, in which lidamycin led to cancer cell differentiation"

the content suggested nothing to predisposition to cancer of any sort.
it is just a blind search of 2 keywords. take a look yourself. it leads to cancer cell differentiation. it means that it improves the prognosis. poorly differentiated cancer cells are the one we are worried about.

and as for p53. i never denied that it leads to a high risk of cancer.
please scroll up and read. i merely mentioned that it is rare and mostly hereditary and almost 0 chance for u to contract it from x-rays.

ur third link. regarding the Ras gene
its just another blind search. there is almost nothing related to ras there.
however once again, i have never denied that the RAS subfammily is a common oncogen. its just that the etiology of its inappropriate activation is poorly understood at the moment. it has merely been found in about 1/4 of all human tumours.

and ur blind search of p21, lung cancer
once again. so many irrelevant results. kidney cancer , prostate cancer are thrown into the mix of results there. once again i'll take the first link.


"transcription factors and the genes p21/CDKN1A and Myc, which have previously been implicated in NSCLC development, were revealed by a combination of pathway analysis and microarray meta-analysis. These findings suggest that neuroendocrine-related genes, potentially driven through p21/CDKN1A and Myc, are closely linked to whether or not a NSCLC patient will have poor clinical outcome"

here, it is mentioned that p21 have previously been implicated in NSCLC.
however, there is no study which claim so and a good look at this show that its a study conducted by the "School of Computer Science, The University of Manchester, Manchester, UK." however it is irrelevant once again as the study itself is to predict the clinical outcome. it doesn't proves anything regarding p21 and its predisposition to cancer.

as for this [" Small cell lung cancer (SCLC) results in death within 1-2 months if left untreated. "]


http://www.ncbi.nlm.nih.gov/m/pubmed/18787355/

fine, however its just 1 study claim against the statistics once again.
sclc can be divided into limited and extensive disease which both have different survival rates.

as for the other links i'll go through it later wheni get some free time.

More cancer developments. What about hereditary?

SINGAPORE: A study by the National Cancer Centre Singapore (NCCS) has shown that family history of breast cancer is a strong indicator of breast cancer risk among local women.

A history of at least one affected immediate relative (for example, a mother, daughter or sister) is twice as important for breast cancer risk in Singapore women relative to Western women.

The study also showed that the Gail Model - a standard model used in Western populations to predict individual risk of breast cancer - was inaccurate in the local population.

Dr Chay Wen Yee, one of the researchers said: "Our study showed that the Gail Model over-estimated the risk of breast cancer among local women. This shows that methods used to predict risk of breast cancer in the West do not provide accurate estimates in our setting."

http://www.channelnewsasia.com/stories/sin...1193963/1/.html

hello. i got hydrosis. my palms and my feets sweat all the times. And i easily sweat anywhere anytime. Eg : When i was queue buying cinema ticket, sometime only me that gt sweat, evry1 was looking at me weirdly, as the environment is cold due to the aircon. Any tips ?

well the hereditary etiological factor in breast cancer is well established .
it is also established that the incidence is higher among white western women.

Lung cancer also perhaps?

My family is good at it.

perhaps, however unlike breast or ovarian cancer. it is still just a claim and further studies on the subject has to be done.
incidence of lung cancer is indeed higher to a minor degree in patients with positive family history. however it may also be due to a common environment. *eg: second hand smoke from a family member, or even air pollution in the neighbourhood.

edit : spelling mistake

This post has been edited by tjinn: Apr 9 2012, 03:56 PM

^ do bother reading what u are quoting before hand? from the links alone all i can see is that u just search for the 2 terms and in case u dunno, keyword searches aren't tat good for research papers... the ones u are quoting is totally out of the context of the discussion

dude, tham~
how many xrays have you got in the past 12 months?

Four. At least two more to go. I never knew that Tung Shin's Shimadzu
machine was firing at 100 kilovolts, even if for just 2 milliseconds. . That's
quite a shot of gamma rays.

I think I'll go over to Damai Service Hospital next round.




Yes, I know those are blind searches. They were meant to be, largely
to show the countless studies showing the association between tumor
suppressor/oncogenes and cancer, particularly p21, since Tjinn maintained
that there was no link whatsoever between this gene and cancer.


The searches were than progressively narrowed down from "cancer" to "lung cancer"
and finally "SCLC", to show the association between these genes and SCLC. Maybe
I should have searched with them in parathenses, since that would reduce the number
of hits further.

The final two studies and the French p53 site were meant to show the possibility
of low-dose x-rays causing mutations in these genes, particularly p53, thus
predisposing us to cancer, including that of the lung, since Tjinn noted that the "patient's
fate has already been determined from birth".

http://p53.free.fr/Database/p53_cancer/p53_Lung.html

http://www.ncbi.nlm.nih.gov/m/pubmed/8640750/

http://www.ncbi.nlm.nih.gov/m/pubmed/18271921


I am familiar with p53, p21 and ras - I come from this site and their forum below.

http://www.imminst.org

http://www.longecity.org/forum/


Around half of the posts so far in these two threads are mine.
(I am not in the medical field, not do I even have any degree. I'm
just an ordinarly lowly-paid penpushing layman.)

http://www.longecity.org/forum/topic/25952-cancer-knowledge/

http://www.longecity.org/forum/topic/23093...imers-research/


I joined Bill's extensively long thread a bit late in his advanced SCLC, though.

http://www.longecity.org/forum/topic/23038...ighting-cancer/


SCLC is a very complex cancer with many genetic deletions/mutations (the Immortality
Institute's members are far more familiar with this than me) as the disease progresses,
which is why it relapses so rapidly after an initial good response to chemo.


I am also familiar with some of the other genetic/signalling pathways in cancer -
Bax, Bcl2, caspase 3, PKA, PKC, AKT, PI3K, PPAR gamma, CXCR4, CCR5, etc.


This was the main reason why Bill took high dose resveratrol. Unfortunately, we
didn't realize at that time that resveratrol's bioavailability, at least in humans, is
very poor and disappointing against cancer in vivo (seems to work very well in
dog cancer).

http://www.longecity.org/forum/topic/23038.../page__st__2580

http://www.longecity.org/forum/topic/23038...230#entry283230


I mentioned the Chinese herbs, Scutellaria baicalensis and barbata, to him right from
the start when I joined his thread, but somehow it didn't really get thru him, I guess
mainly because he was unfamiliar with Chinese cancer-fighting herbs.



I believe that one of the main reasons why cancer patients deteriorate rapidly
when the cancer relapses, with the cancer refractory to second or third-line
chemotherapy regimens, is because the first-line chemo has cleaved their
p53 beyond repair, leaving the patient virtually defenceless. The cancer comes
back and "steamrolls" over them. Our first-line genetic defence against cancer
is, I believe, p53.

---

Added on April 10, 2012, 4:22 am

" For B-cell ALL, even one X-ray was enough to moderately increase the risk. "

http://newscenter.berkeley.edu/2010/10/04/x-ray/


http://www.dailymail.co.uk/health/article-...isk-cancer.html

http://articles.mercola.com/sites/articles...y-part-one.aspx




X-Rays, Cancer and Heart Disease


" The inability of human cells, to repair correctly every type of radiation-induced
chromosomal damage, has been demonstrated in nuclear workers (who received
their extra low-dose radiation at minimal dose-rates) and in numerous studies of
x-ray-irradiated human cells at low doses. "

" Besides demonstrating non-repair or imperfect repair, such studies have established
that x-rays have an extremely low doubling-dose for structural chromosomal mutations. "

" X-rays are capable of causing virtually every known kind of mutation — from the
very common types to the very complex types, from deletions of single nucleotides, to
chromosomal deletions of every size and position, and chromosomal rearrangements
of every type. When such mutations are not cell-lethal, they endure and accumulate
with each additional exposure to x-rays or other ionizing radiation. "



\
" Ionizing radiation is firmly established by epidemiologic evidence as a
proven cause of almost every major type of human cancer. Some of the
strongest evidence comes from the study of medical patients exposed to
x-rays — even at minimal dose-levels per exposure. "



http://www.drheise.com/xrays.htm




John Gofman's book -

Radiation from Medical Procedures in the Pathogenesis of
Cancer and Ischemic Heart Disease :
Dose-Response Studies with Physicians per 100,000 Population

http://www.ratical.org/radiation/CNR/RMP/index.html

http://www.ratical.org/radiation/CNR/RMP/chp1F.html





This post has been edited by Tham: Apr 10 2012, 05:28 AM

WASHINGTON: Hundreds of novel genes that are mutated in stomach cancer, the second-most lethal cancer worldwide, have been identified.

The finding by an international team of scientists, led by researchers from the Duke-NUS Graduate Medical School (Duke-NUS) in Singapore and National Cancer Centre of Singapore, paves the way for treatments tailored to the genetic make-up of individual stomach tumours.

Stomach cancer is the second leading cause of cancer death globally with more than 700,000 deaths each year, and is particularly common in East Asia.

Treatment of this deadly disease is often difficult and unsuccessful because of late detection of tumours and a poor understanding of the causes. In the United States, less than a quarter of patients survive more than five years after diagnosis, even after treatment.

http://timesofindia.indiatimes.com/home/sc...ow/12593360.cms

your meant to be blind searches showed alot of irrelavent information. it would be better if u could link it to a proper article or research paper so we can have a better discussion going on.

alright. currently there is no established proof that p21 supression predisposes to carcinoma.
studies have been done before with p21 knock out mice. most of them have not yielded satisfactory responses.

and as for p53 i maintain what i said.
it is rare and most commonly seen as Li-fraumeni syndrome which is an autosomal dominant disorder.
in which it will be inherited to the off spring regardless. thus his fate has been determined since birth.

i also did mention that it can be acquired. more so commonly by long term hpv infection. for xrays it takes many years. 15 - 20 years
of constant exposure.

i'm very interested to see what are behind those links. but please forgive my short reply. i'll go through it after work.

Even dental xray can kena brain tumour. Scary right?

WASHINGTON: People who get regular dental X-rays are more likely to suffer a common type of brain tumour, US researchers said on Tuesday, suggesting that yearly exams may not be best for most patients.

The study in the US journal Cancer showed people diagnosed with meningioma who reported having a yearly bitewing exam were 1.4 times to 1.9 times as likely as a healthy control group to have developed such tumours.

A bitewing exam involves an X-ray film being held in place by a tab between the teeth.

Also, people who reported getting a yearly panorex exam -- in which an X-ray is taken outside the mouth and shows all the teeth on one film -- were 2.7 to three times more likely to develop cancer, said the study.

http://www.channelnewsasia.com/stories/hea...1194192/1/.html

Taking 200 to 400 mcg of selenium a day will drastically
reduce a woman's risk of breast and ovarian cancer.

Increased rates of chromosome breakage in BRCA1 carriers
are normalized by oral selenium supplementation.

http://cebp.aacrjournals.org/cgi/pmidlooku...g&pmid=15894690



BRCA1 is apparently also vital to heart function and remodelling.
Thus selenium should also cut down the chances of heart failure with age.

" BRCA1 mutation carriers, in addition to risk of breast and ovarian cancer,
may be at a previously unrecognized risk of cardiac failure. "

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3247816/

finally got some time to myself. so here goes.

hi tham i've gone through your links.
with exception to the thread regarding your friend bill.

your first link http://newscenter.berkeley.edu/2010/10/04/x-ray/

u say 1 xray may moderately increase the risk for B-Cell ALL

something new like this in the field of medicine is very unexpected.
if even a single xray predisposes a child to leukemia, just imagine what a mri or ct scan would do.

so i looked up for the original research paper. u can view it here at.

http://ije.oxfordjournals.org/content/earl...yPe&keytype=ref

"post-natal diagnostic X-ray exposures in childhood, early studies reported greater exposure among cases than controls, but studies from the past 20 years have produced inconsistent results. Several found no increased risk associated with post-natal X-rays, even for multiple exposures, or among different study populations. Conversely, others found a slightly elevated risk for childhood ALL, specifically pre-B-cell ALL, associated with exposure to two or more X-rays. To our knowledge, only one study has assessed risk of childhood AML associated with post-natal diagnostic X-ray exposures, and no increased risk was observed."


The results suggest that exposure to post-natal diagnostic X-rays is associated with increased risk of childhood ALL, specifically B-cell ALL, but not AML or T-cell ALL. Given the imprecise measures of self-reported X-ray exposure, the results of this analysis should be interpreted with caution and warrant further investigation."

thus. to sum it up.. it is still inconclusive.

on your second link

http://www.dailymail.co.uk/health/article-...isk-cancer.html

i never trust the daily mail. so i headed over to the lancet which is of course a very well established medical journal.
and found this.

http://www.thelancet.com/journals/lancet/a...5433-0/abstract

"We provide detailed estimates of the cancer risk from diagnostic X-rays. The calculations involved a number of assumptions and so are inevitably subject to considerable uncertainty. The possibility that we have overestimated the risks cannot be ruled out, but that we have underestimated them substantially seems unlikely."

so there is some considerable amount of bias on the part of the researcher.

i'll go through the third link after dinner/supper .

*after supper*

well i was going through Dr Gofman's book via the link posted below.
and it seems the study was conducted with taking into account radiographic procedures including ct scans and fluoroscopy?
which is significantly more potent than a simple xray.
note : in fluoroscopy it is a active procedure where the beam is constantly on to obtain a real time image.
the exposure here is alot higher. depending on the procedure being carried out.
for instance : in an orthopedic surgery where nailing has to be done.
but thanks to medical advancement. there are other alternatives now such as image intensifiers which delivers the radiation in pulses.
which shows picture by picture and holds it on screen.
in addition to that.. its an old book, with data from a time when the radiation doses were significantly higher than what is being used today.
however he does in fact prove the point that prolonged exposure to ionising radiation "like i mentioned before" predisposes to cancer.
note that i never said ionizing radiation doesn't predispose to cancer. i merely said that if that u require prolonged exposure to low dose radiation to contract it.
and bashing that technician was uncalled for.

*edit : gone through 3rd link*

This post has been edited by tjinn: Apr 10 2012, 11:33 PM

Asking on behalf of a friend.

Started with itching, followed by scratching, and formation of these (picture in spoiler below).

As of now, itching is sporadic, not a problem. The red part is raised from normal skin, for approx 0.6 mm. Localised only on upper thigh of one leg.

Could it be dermatographic urticaria? Any precautionary measures?



This post has been edited by entryman: May 6 2012, 10:44 PM

i have a family member who eats 3 meals per day...oats and wholemeal bread+milk & lunch of rice+meat+vege. no beef, no red meat, no skin fat. drink milks everyday and eat lots of vege.

...and exercise at least 3 times a week, 1 hour each time..doing aerobic and some light strength training.

his health result: high glucose, high cholesterol, high lymphocyte, low calcium.

any idea why?