Can anyone summarise in laymans terms please!
Discussion
I'm interested in finding out what I can with regard to cannabinoids and Chronic Lymphocytic Leukemia.
I understand that 'induction of apoptosis' is positive:
"We and others (1, 2) have previously observed an overexpression of CNR1 and 2 and induction of apoptosis upon incubation with cannabinoids in hematologic malignancies, including chronic lymphocytic leukemia (CLL). These data led us to more thoroughly evaluate the role of the two receptors in CLL."
However the rest of the text is well outside of my grasp. Could anyone possibly give a brief summary of the the following please. It's not a huge paper, eight paragraphs - I'd just like to understand what I can.
If anyone can help I would appreciate it.
http://www.mecfsforums.com/index.php?topic=14351.0
I understand that 'induction of apoptosis' is positive:
"We and others (1, 2) have previously observed an overexpression of CNR1 and 2 and induction of apoptosis upon incubation with cannabinoids in hematologic malignancies, including chronic lymphocytic leukemia (CLL). These data led us to more thoroughly evaluate the role of the two receptors in CLL."
However the rest of the text is well outside of my grasp. Could anyone possibly give a brief summary of the the following please. It's not a huge paper, eight paragraphs - I'd just like to understand what I can.
If anyone can help I would appreciate it.
http://www.mecfsforums.com/index.php?topic=14351.0
Just to get back on track, does the following statement "we provide data that mRNA expression of CNR1 but not CNR2 is of prognostic value in CLL" mean that mRNA expression from CNR1 is desirable and is provoked by the cannabinoid?
So those particular cannabinoids are the key, CNR1 is the lock and this messenger RNA is the golden goose?
I mean, if mRNA can be made to be expressed in decent amounts, is this good? If so, are there any other ways of getting it out of CNR1?
So those particular cannabinoids are the key, CNR1 is the lock and this messenger RNA is the golden goose?
I mean, if mRNA can be made to be expressed in decent amounts, is this good? If so, are there any other ways of getting it out of CNR1?
Edited by ReaderScars on Wednesday 19th November 22:45
You've only posted a link to the abstract, not the full paper and without seeing it all, it is difficult to critique in full but the conclusion is clear from the authors last paragraph:
"Although some cannabinoids reduce viability in neoplastic cells considerably independent of CNR expression, also healthy cells are affected, indicating a poor therapeutic ratio in chronic lymphocytic leukemia."
"Although some cannabinoids reduce viability in neoplastic cells considerably independent of CNR expression, also healthy cells are affected, indicating a poor therapeutic ratio in chronic lymphocytic leukemia."
HughS47 said:
the conclusion is clear from the authors last paragraph:
"Although some cannabinoids reduce viability in neoplastic cells considerably independent of CNR expression, also healthy cells are affected, indicating a poor therapeutic ratio in chronic lymphocytic leukemia."
Clear to you, perhaps - I've just had to look up another medical term!"Although some cannabinoids reduce viability in neoplastic cells considerably independent of CNR expression, also healthy cells are affected, indicating a poor therapeutic ratio in chronic lymphocytic leukemia."
But what I don't understand clearly from the last para is, 'independent of CNR expression' - ie, what are the cannabinoids doing apart from provoking CNR?
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