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Although ubiquitination was initially characterized as a signal for proteasomal degradation, emerging evidence suggests that ubiquitin-tagged proteins can be routed through proteasomal processing pathways while ultimately being degraded in the lysosome (Alwan et al., 2003)

Until a reliable treatment emerges, it does appear that some of the non-surgical treatments discussed can be used to stabilize the scarring process and may result in some reduction of deformity with improved sexual function

The primary mechanism involves cellular disruption, affecting both malignant and normal cells, resulting in undesirable consequences

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