For patients without comorbidities, the overall cure rate was 73%. For these patients, the cure rates were 85.7% for superficial and nodular BCC, 88% for superficial BCC, 57% for Bowen's disease, 50% for nodular BCC, and 50% for aggressive BCC.
For patients without comorbidities, our study revealed good cure rates for superficial BCC and superficial/nodular BCC (88% and 85%, respectively). Nodular and aggressive BCC and Bowen's disease exhibited lower cure rates (50%, 50%, and 57%, respectively). I
For patients without comorbidities, our study revealed good cure rates for superficial BCC and superficial/nodular BCC (88% and 85%, respectively). Nodular and aggressive BCC and Bowen's disease exhibited lower cure rates (50%, 50%, and 57%, respectively). I
PDF, Free full text article... We found that 5% imiquimod cream is aneffective treatment option for superficial and nodularbasal cell carcinomas, giving a clearance rate of89.5% at an average of 39 months of follow up.
Dr Yin Vun, Siller Medical, 9th Floor, SilvertonPlace, 101 Wickham Terrace, Brisbane, Qld 4000, Australia.
For patients without comorbidities, our study revealed good cure rates for superficial BCC and superficial/nodular BCC (88% and 85%, respectively). Nodular and aggressive BCC and Bowen's disease exhibited lower cure rates (50%, 50%, and 57%, respectively). I
The precise mechanism of the anti-tumor effect of imiquimod in BCC is not known. It has been postulated that ultraviolet radiation induces mutations in the tumor-suppressor genes and alters the immuno-surveillance, so that tumor cells escape from cytotoxic T cells and apoptosis.[1] Th-2 cytokines, that downregulate tumor surveillance, are raised in BCC.[1],[5] Imiquimod acts on toll-like receptor-7 (TLR-7) present on dendritic cells, macrophages and monocytes and induces expression of interferons, Th-1 cytokines (IL-1, IL-6, IL-10 and IL-12), tumor necrosis factor-a and G-CSF, thereby counteracting Th2 cytokines and promoting tumor surveillance.[1],[5] It also enhances the activity of natural killer cells and epidermal Langerhans' cells. The tumor regression is achieved probably by induction of Fas receptors on the tumor cells resulting in their apoptosis.[10]
Raasch B. Clinical, Cosmetic and Investigational Dermatology. 9 June 2009.
There is reasonable evidence that the use of imiquimod for small (<2 cm) superficial BCC that occur other than on the face provides
outcomes only marginally less satisfactory t
There is reasonable evidence that the use of imiquimod for small (<2 cm) superficial BCC that occur other than on the face provides outcomes only marginally less satisfactory than surgery. There would be a place for imiquimod in treating patients with frequent multiple primary lesions when access to surgery is difficult or where clinical judgment may be influenced by patient factors as reported in some of the studies, eg, where patients may have contraindications to surgery. It was noted that if recurrences occurred in this study they mostly occurred during the first 9 months after the end of treatment. The initial response was therefore predictive of long-term outcome so these authors recommend and encourage continued monitoring of skin lesions.
To date one long-term study indicates a treatment success rate of 78%-81% and that initial response is a predictor of long-term outcome. Recurrences tend to occur within the first year after treatment. Future research will compare this preparation to the gold standard treatment for superficial BCC - surgical excision.
Clinical clearance rate at 1, 2 and 3 years were 94, 76 and 70%, respectively. We conclude that imiquimod seems to be an appropriate therapeutic alternative for the treatment of recurrent BCC in patients with associated co-morbidities.
Topical 5% imiquimod cream is well tolerated and most effective in treating nodular BCC when applied once daily for 7 days per week for either 12 or 6 weeks.