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Page 20 of 40 Maner et al. J Cancer Metastasis Treat 2020;6:37 I http://dx.doi.org/10.20517/2394-4722.2020.60

A

B

Figure 9. Genetic lineage of BSC. A: activating SHH pathway mutations initially drive formation of BCCs. Acquisition of de novo ARID1A
mutations or other chromatin remodeling mutations under pharmacological SMO inhibition drive cellular plasticity, pushing basal cells
to undergo squamatization and leading to BSC formation; B: within the BCC zone, high levels of SHH signaling, low RAS/MAPK pathway
activity, and high levels of ciliation drive tumor growth. Within the SCC zone, RAS/MAPK signaling increases with a concomitant
reduction in SHH pathway activity and ciliation. Within the transition zone, ce3lls begin to show higher levels of RAS/MAPK pathway
activity while maintaining SHH signaling. The levels of ciliation are unknown. SHH: sonic hedgehog; BCC: basal cell carcinoma; SMO:
Smoothened; BSC: basosquamous cell carcinoma

these genetic pathways, there is a possibility that SCCs could become BCCs and BCCs can become SCCs.
There is a need for further research finding data to address this issue.

Prevention of apoptosis
Strong expression of FasL in both BCC and SCC is believed to allow the tumor to avoid apoptosis. FasL
mediates apoptosis in cells that express Fas receptor and is a member of the tumor necrosis family. FasL
on tumor cells can bind to the Fas receptor on T-cells, macrophages, and natural killer cells which make
these effector cells unable to infiltrate the tumor nodules and trigger the extrinsic apoptotic pathway [139] .
Although there have not been studies confirming that strong expression of FasL is an important mode for
how BSCs prevent apoptosis, BSCs’ genetic similarity to BCC and histopathologic characteristics of both