yes, there are papers but not quoted as such, this was my observation in last 3 years of my research but not getting any clue to begain for the reason...
The problem is that gastric pH is yet from 0 to 1 ; so there is no changes that could be caused by a bacteria. Probably explaination could be due to other causes
hi renu, what i think is helicobacter releases enzyme urease which is responsible to neutralize the acidic enviornment around it, once the initial part i.e invasion is possible through the neutralization step, once the cell is transformed there is no further requirment of the bacteria & hence not found in the later stages of the cancer development. or another possible way is that once the cell is transformed, its clone are formed, some substances are secreted by these cells which might inhibit the growth of helicobacter& hence not found in the later stages.
hi raghav yes this may be one of the reasons but ur first comment that once the cell is transformed there is no further requirement of bacteria is little confusing as our body resist any infection and we till now treat H. pylori as pathogen.... for ur kind attention if this is regarded one of the reasons then h. pylori should be treated as commensal helping in lipid digestion in stomach as researches suggest it was preasent in aboout 90% population about 100 years ago. today also it is inhabiting very large low cancer rich population....
I am not a specialist (gastro-enterologist) , but I thought that H. Pilory favoured gastric ulcer first; and chronic ulcer favours gastric cancer (as often hte case during chronic inflammation).
I am not uptodate with refrences on the subject, but is there direct proofs that this bacteria promotes directecly cancer (and by which way ?). If not, the presence or not (or persistance) of the bacteria at different stages of gastric cancer could be a consequence and not linked as cause or favouring factor of cancer.
yes true but it is geography dependent eg it is high in cancer risk population like japan and coloumbia but there are population where incidences of infection are higher but there is low incidences of gastric cancer one among such is our country India here the incidences of infection seen are as high as 70% in healthy population... there is perhaps difference in the strain or host genetic make up for such difference.....
yes true but it is geography dependent eg it is high in cancer risk population like japan and coloumbia but there are population where incidences of infection are higher but there is low incidences of gastric cancer one among such is our country India here the incidences of infection seen are as high as 70% in healthy population in some regions... there is perhaps difference in the strain or host genetic make up for such difference....
As far as I am concerned, all I can say is that H Pylori causes chronic inflammation of the mucosal lining of the GIT because of its capacity to secrete cytotoxins which pave the foundation stone for other cellular activities ..... which in acute infection leads to aberration of key tumor suppressor genes ... these aberration in turn cause the transformation of cells to tumorous ones