Primary conjunctival
melanomas.
Patient profile
• 7 patients.
5 females ; 2 males.
The female age range was 39-77 (median age 62).
The males were aged 44 and 74.
All patients had unilateral disease.
4 right eyes and 3 left eyes were affected.
14 primary
invasive
melanomas
in 7 patients
4 patients
Solitary mm
2 juxta-limbal
bulbar conjunctiva;
2 inferior fornix
and
inferior tarsal conjunctiva.
3 patients
Multiple mm
1 juxta-limbal bulbar,
1 juxtalimbal bulbar and non-bulbar
1 juxtalimbal bulbar and plica involvement.
Melanoma thickness
• 0.1mm to 1.4 mm
• pT1a to pT2b
• All cases associated with in-situ MM
• One case had vascular invasion.
What’s the big deal?
18 months later………………
8 months later………………
2002
2010
19 nodules overall
7 patients
4 patients solitary
3 patients multiple
1-synchronous
2-metachronous
Location of nodules
1 patient
presented
with nodule
6 patients
nodules
after primary
Conj mm diag.
19 nodules
in 7 patients
8 BULBAR
11 NON-BULBAR
Nodule size range 3-9mm
Median-5mm
Nodules
3-102 months
after first primary
Conj mm
(median 10m)
Systemic mets
8-37 m after
First nodule
7 patients
5 free of systemic
mets
2 developed
systemic mets
Alive
level 1 and 2
neck lymph nodes
intra-parotid lymph node
lung.
Dead
Bone
Liver
Brain
Histology of these nodules?
Local conjunctival metastases
(LCM)
Evidence that nodules are
Local METS?
2 cases
Developed
Systemic mets
Well defined
Cannon ball
1 nodulenecrosis
Eg. Skin mm
In-transits
Well defined Grenz
zone
No overlying insitu MM
Multiple
and synchronous
Nodules-behaviour
like mets.
Argument against mets.
•
New primaries with once-existent in-situ melanoma, with
the latter regressed in response to Mitomycin C and the
nodule having been ‘carved out’
Unlikely
1. In one case, the LCM was the presenting feature with no history of
prior topical chemotherapy or surgery.
2. Further primary tumours developed in some cases, while on topical
chemotherapy and none of these further primary tumours exhibited
a well-defined, nodular morphology.
3. One case, the LCM developed 8 years after the primary tumour had
been treated and never received MMC.
Odd distribution of LCMs?
• Local factors that promote arrest and growth of the
LCMs.
• Surgery scarring and inflammation -damming up of
tumour cells-possible but in 1 case, LCM at presentation
and some cases LCM remote from surgery site.
• Seeding by surgery? But 1 case presentation with LCM
with no prior surgery history and no nodules at edge of
dissection lines.
• Dormant micromets that disseminate early…grow..?
• Circulating stem cells that find niche and expand ?
• All of the LCM extravascular,
• Always extravascular, or whether once
intravascular and have exited?
• Intrinsic blood supply
• Associated with a lymphocyte cap. Host
reaction?
LCM selected a pre-existing lymphoid niche?
• LCM associated with lymphatic vessels some
cases. Intraymphatic spread?
Lymphangiogenesis?
Systemic mets.
• 2 cases.
• Is LCM a proxy measure for what is happening
systemically?
• Indication for sentinel LN biopsy?
• Should LCMs be regarded as ‘N’ status in
pathological TNM classification (like large bowel
adenoca)?
Thanks