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After activation, NF-κB rapidly translocates to the nucleus and binds specifically to target genes, thereby initiating the transcription of Endothelin-1 (ET-1) and inflammatory cytokines, such as tumor necrosis factor (TNF), Interleukin-1β (IL-1β), and Interleukin-6 (IL-6)[17]

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398 AR inhibitors and LHRH antagonists, which have the advantage of bypassing the sex steroid surge observed with LHRH agonists, may offer a greater opportunity for T cell reconstitution

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