Cancer research questions, so many it is mind troubling!

1.Can disruption of the Nuclear CAP be used as therapeutic intervention in dividing cell?
lewis et al:
"The defects in splicing and U1 snRNP binding caused by CBC depletion can be specifically reversed by recombinant CBC. In summary, efficient recognition of the cap-proximal 5' splice site by U1 snRNP is facilitated by CBC in what may be one of the earliest steps in pre-mRNA recognition. Data in Colot et al. (this issue) indicate that this function of CBC is conserved in humans and yeast."

It is a conserved process for a reason! CAN INTERFERING WITH SPLICING BE USED IN CANCER THERAPY?

2. Could blocking Transportins (1,2) or A1 be a novel therapeutic approach in Breast cancers since levels of Molecule transfer seems of importance in this disease.
Can these molecules (transporters in general) be biomarkers of cellular activities in breast cancers.  What is the role of targeting the poly tail (A) of RNA, should that limit the movement of these RNA

3. Should BH3 domains, presence of BNIP3 activation,  BCL2, NOTCH activation,  be surrogates for anti-apoptosis in cancer biology? what about SHC1


4. Should presence of activity at CD47 be consider a biomarker of BCL-2 activity? Anti-apoptosis?
CD47 (IAP).
wikipedia:"By blocking TSP1 from binding to its cell surface receptor (CD47) normal tissue becomes nearly immune to cancer radiation therapy and assists in tumor death."

5.GIPC 1 could turn out to be an important Target in Ovarian cancers! because of DAB2 and LRP interactions.

So many things to test, it is mind "troubling" or is it "mind buggling",they say!