DRUG WITH POTENTIAL MARKED EPIGENETIC EFFECTS

There are medications of which role or mechanism of action needs clearly further clarification because they may prevent cancer from occuring. One such medication is:  (from mayo site)   Imiquimod.
"Imiquimod topical is used to treat external warts around the genital and rectal areas called condyloma acuminatum. It is not used on warts inside the vagina, penis, or rectum. Imiquimod is also used to treat a skin condition of the face and scalp called actinic keratosis (AK), which is caused by too much sun exposure. Imiquimod may be used to treat certain types of skin cancer called superficial basal cell carcinoma (sBCC).
Imiquimod works on the immune system to help the body fight viruses that cause warts. It does not destroy the viruses directly. It is not known how imiquimod works for actinic keratosis or skin cancer."

Understanding the mode of action of this drug in better detail appears critical for further development of target therapy that may help prevent certain cancers induced by chronic irritation and viral drive!
(another Medication used for same pathology is Podophyllin)
All they say is  "Podophyllin is a cytotoxic agent that has been used topically in the treatment of genital warts. It arrests mitosis in metaphase, an effect it shares with other cytotoxic agents such as the vinca alkaloids⁽²⁾. The active agent is podophyllotoxin, whose concentration varies with the type of podophyllin used; the American source normally containing one-fourth the amount of podophyllotoxin as the Indian source⁽³⁾."

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One thing for sure, viral driven neoplastic diseases can be caused by integral incorporation of the viral genome in that of the host, or induce molecular disturbances changing the course of Metabolism and gene amplification or overexpression of transcription factors by affecting modulator or regulatory genes.  Abnormality of splicing will alter major functional core binding molecules, giving  new patterns to metabolic events, boosting hypertrophy (by loss of sense of cell limits and perturbances at adhesion molecules) and proliferation.   And if the the" foreign" (antigen) sense of the viral presence is not completely suppressed, the cell will be superexcited and the NF-kB on overdrive inducing significant epigenetic events including hyperproduction of Cyclins, Tumor growth factors and disturbances at miRNAs and polymerases (RNA--->DNAs).

All in all significant epigenetic events ensue.  Drugs that will affect epigenetic events must have a role in the control or modulation of these events.  We have to assume that Imiquimod and Podophyllin must have significant tampering effects of epigenetic events.  Indeed Etoposide is known to control these kind of diseases. And it is not because of its topoisomerase II activity and DNA attack, but this drug must have significant epigenetic effects, that is why it can tamper even other epigenetic driven pathologies such as the leukemias.  It is surprising that CPT-11 is not as used as Etoposide.  Pointing to role of heterogeneity in variation of pathologic expression of epigenetic events!

One thing for sure, medications important in control of these epigenetic events have the bad side effects of causing pulmonary fibrosis (Mitomycin). This point to the conclusion that some Cyclins/ TGF (Interleukins in particular) are over expressed leading to fibrosis.  And we still don't screen these Cyclins as biomarkers for detections.  But we know it (pulmonary fibrosis) is dose dependent!  Head in a sand situation again!

(Written on the go at CRBCM...)