primary treatment for conjunctival melanoma typically involves complete excision with surgical margins of 3 to 5 mm when possible
Current Treatment for conjunctival tumors
technique 2 (Brachytherapy)
adjuvant treatment following excision
ophthalmic radiation therapy
goal is to eradicate tumor burden in a manner that maintains visual function and preserves surrounding sensitive ocular tissues
three usages: 1. curative therapy
2. adjuvant treatment following surgical excision 3. palliative therapy for advanced cases
adjuvant treatments following surgery
1. cryotherapy to the surgical margins and/or tumor bed. 2. absolute alcohol epitheliectomy for corneal and limbal involvement
adjuvant treatments following surgery, specifically, radiation therapy
in general, conjunctival melanoma is not radiosensitive, and therefore radiation should not be used as a sole therapy.
radiation therapy may be indicated for certain circumstances including
1. deep scleral invasion detected by pathology following primary excision 2. recurrent disease unresponsive to other therapy 3. palliation for extensive disease which is not surgically excisable 4 . patients who cannot tolerate surgery
technique 1 (EBRT)
EBRT (External Beam Radiation Therapy)
EBRT has been used as adjuvant radiation therapy (total dose of 60 Gy) in tumors with high risk features like increased thickness or close margins of resection
proton beam radiation has been investigated as an alternative to exenteration for diffuse and multifocal patterns of conjunctival melanoma which are not treatable with standard eye-sparing methods.
VERY GOOD INFO
MicroRNAs (miRs) play a key role in cancer etiology by coordinately repressing
numerous target genes involved in cell proliferation, migration and invasion.
The
genomic region in chromosome 9p21 that encompasses miR-31 is frequently deleted
in solid cancers including melanoma; however the expression and functional role
of miR-31 has not been previously studied in melanoma.
Here, we queried the
expression status and performed functional characterization of miR-31 in melanoma
tissues and cell lines.
We found that down-regulation of miR-31 was a common event
in melanoma tumors and cell lines and was associated with genomic loss in a subset of
samples.
Down-regulation of miR-31 gene expression was also a result of epigenetic
silencing by DNA methylation, and via EZH2-mediated histone methylation. Ectopic
overexpression of miR-31 in various melanoma cell lines inhibited cell migration and
invasion. miR-31 targets include oncogenic kinases such as SRC, MET, NIK (MAP3K14)
and the melanoma specific oncogene RAB27a. Furthermore, miR-31 overexpression
resulted in down-regulation of EZH2 and a de-repression of its target gene rap1GAP;
increased expression of EZH2 was associated with melanoma progression and overall
patient survival. Taken together, our study supports a tumor suppressor role for miR-
31 in melanoma and identifies novel therapeutic targets.