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2017 ; 36
(1
): 109-140
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The biology of uveal melanoma
#MMPMID28229253
Amaro A
; Gangemi R
; Piaggio F
; Angelini G
; Barisione G
; Ferrini S
; Pfeffer U
Cancer Metastasis Rev
2017[Mar]; 36
(1
): 109-140
PMID28229253
show ga
Uveal melanoma (UM), a rare cancer of the eye, is distinct from cutaneous
melanoma by its etiology, the mutation frequency and profile, and its clinical
behavior including resistance to targeted therapy and immune checkpoint blockers.
Primary disease is efficiently controlled by surgery or radiation therapy, but
about half of UMs develop distant metastasis mostly to the liver. Survival of
patients with metastasis is below 1 year and has not improved in decades. Recent
years have brought a deep understanding of UM biology characterized by initiating
mutations in the G proteins GNAQ and GNA11. Cytogenetic alterations, in
particular monosomy of chromosome 3 and amplification of the long arm of
chromosome 8, and mutation of the BRCA1-associated protein 1, BAP1, a tumor
suppressor gene, or the splicing factor SF3B1 determine UM metastasis.
Cytogenetic and molecular profiling allow for a very precise prognostication that
is still not matched by efficacious adjuvant therapies. G protein signaling has
been shown to activate the YAP/TAZ pathway independent of HIPPO, and conventional
signaling via the mitogen-activated kinase pathway probably also contributes to
UM development and progression. Several lines of evidence indicate that
inflammation and macrophages play a pro-tumor role in UM and in its hepatic
metastases. UM cells benefit from the immune privilege in the eye and may adopt
several mechanisms involved in this privilege for tumor escape that act even
after leaving the niche. Here, we review the current knowledge of the biology of
UM and discuss recent approaches to UM treatment.
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