The "anticancer potential" is a very theoretical meaning because the fact of killing cancer cells does not mean that your extract will be clinically developed.
An extract is a mixture of a myriad of compounds.
So to "validate" the "anticancer potential" of a plant extract, you should perform bioguided assays (using for example the MTT colorimetric one) in order to identify the compound(s) responsible for the "in vitro anticancer activity".
You can work with cancer cells only at the begining.
The bioselectivity between normal and cancer cells should be addressed later.
I am not sure that my responses will reach your expectations. I am however providing you here in attached files some articles that we published and that relate to the field of your question(s).
I agree with you that one should do screening first. but my question is that if the extract kills the cancer cells equally like it kills the primary cells then we cannot consider the extract(as whole not the isolated compounds) as anticancer ? and we should not proceed with it ?
Because when you dig in to the literature for this type of question you may not find a huge data supporting this fact that an extract should be screened on primary cells as well to validate its cytotoxicity for anticancer properties if it possess some. Not even the isolated compounds are often tested for the primary cell lines to establish the fact that they kill only cancer cells and are completely safe for the primary cells. and how many drugs available in the market for the treatment of cancer are completely safe for the primary cells or vice versa ?
You have no proof that there are the same compound(s) in your extract that (will) kill normal versus cancer cells.
As you wrote in your precedent message, most (> 99%) of the compounds used by oncologists to treat cancer patients also kill normal cells in vitro.
So, if your plant has not been "heavily" studied, you should try to identify the compound(s) that kill the cancer cells.
If the compound is "very" known, end of the story.
If the compound is not known, but kills cancer cell through very classical pathways of cell death, then a publication.
If the compound is not know and kills the cancer cells in an actual new cell death pathway (I mean by "new" not a classical pro-apoptotic one), then it is the begining of a very interesting story.
A very interesting story for your compound should be for it to hit one of the non-apoptotic cell death pathways described in the two attached article.
At the end, if your (very) interesting compound(s) also kill(s) normal cells, it will always be possible to make derivatization (camptotecin ==> irinotecan; podophylotoxin ==> etoposide; etc..) or using more or less sophisticated delivery system(s) to the cancer in vivo.
Thank you for such an elaborate answer. But the thought behind is if its kills normal cells as well do we still need to go for mechanistic studies for cellular targets of the extract ? because if it kills both cancer cells and normal cells then according to pharmacologists it does not lie in therapeutic window. And if something doesnt lie in therapeutic window then its as simple as if we choose detergent to kill cells. and making delivery system for detergent will make no sense. Do you support this view ?
And did cells ever recover from pyknosis ? and what mechanism might be involved in the case where at lower concentrations of the drug cells undergo apoptosis but at higher concentrations of the drug cells stay at pyknosis despite of the fact that all cells were seeded at the same phase of cell cycle.