MPIP: Melanoma Patients Information Page

The MPIP is the oldest and largest community of people affected by melanoma hosted through the Melanoma Research Foundation. It is designed to provide support and information to caregivers, patients, family and friends. Once you have been touched by melanoma—either as a patient or as a family member or friend of a patient—you become part of a community. It is not a community anyone joins willingly. But if you must be part of this group, you will find no better place to find the tools you need in your journey with this cancer, and the friends who can make that journey more bearable.

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My dad has stage 4 melanoma. Initial diagnosis was found when finding two tumors in his brain - 2 craniotomies, WBR and gamma knife have been his treatment methods so far. They cannot find his original source and as of now do not see any other signs of melanoma in his brain or the rest of his body. Next set of whole body scans scheduled for end of March.

His Dr. gave him the option of taking Temodar as a "preventative" measure. He could either do a strong dose x number of days straight and then take a break or take a lighter dose daily for 30 days. Radiation was really rough on him and he's just now starting to feel better again (although still has trouble with eating due to the taste of food) Although we'd rather he not sit back and just wait for the cancer to show up again, he's hesitant about taking the Temador because he's worried about the side effects and how they will make him feel. For those of you taking/who have taken Temodar, what have your side effects consisted of and how bad? Also, what type of a dosing schedule were you on? Daily for a month straight or larger dose x number of days straight then break?

 Thank you for any feedback - I'd really like him to "try" the Temodar but he's really worried about the potential side effects.

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JerryfromFauq's picture
Replies 1
Last reply 3/8/2012 - 7:26am
Replies by: Bob B.

Daily Low-dose Aspirin Substantially Reduces Deaths From Several Common Cancers

NEW YORK -- December 8, 2010 -- A study published online first and appearing in an upcoming issue of The Lancet is the first to prove that aspirin
reduces death rates from a range of common cancers.

The article is by Peter Rothwell, MD, John Radcliffe Hospital, and University of Oxford, Oxford, United Kingdom, and colleagues.

A previous paper published by Dr. Rothwell and colleagues in October 2010 in The Lancet established that long-term low-dose aspirin (ie 75
mg/day) reduced death rates from colorectal cancer by more than a third. In this new work, the authors studied deaths due to all cancers during and after randomised trials of daily aspirin versus control done originally for prevention of vascular events.

The authors studied 8 eligible trials, that covered 25,570 patients. They showed that allocation to aspirin reduced death due to cancer by 21% during the trials (based on 674 cancer deaths), with benefits apparent after 5 years’ follow-up (death rates after 5 years falling by 34% for all cancers and 54% for gastrointestinal cancers).

By long-term follow-up of patients after the trials (including 1634 cancer deaths) they also showed that the 20-year risk of cancer death remained 20% lower in groups who had previously been allocated aspirin than in the control groups for all solid cancers, and 35% lower for gastrointestinal cancers.

The latent period before an effect on deaths was about 5 years for oesophageal, pancreatic, brain, and lung cancer, about 10 years for stomach and colorectal cancer, and about 15 years for prostate cancer. For lung and oesophageal cancer, benefit was confined to adenocarcinomas. The 20-year risk of death was reduced by about 10% for prostate cancer, 30% for lung cancer, 40% for colorectal cancer, and 60% for oesophageal cancer. The reductions in pancreas, stomach and brain cancers were difficult to quantify exactly because of smaller numbers of deaths. However, the authors noted that treatment with aspirin during the trials lasted for only 4 to 8 years, on average, and so the effects on subsequent risk of deaths due to cancer may well underestimate those that would result from longer-term treatment (ie, from age 50-75 years).

Benefit was unrelated to increasing aspirin dose (75 mg upwards), sex, or smoking, but the absolute effect on 20-year risk of cancer death increased with age. However, Dr. Rothwell said that the increased effect on aspirin on cancer deaths in older people is due to general increased risk of cancer-related death in that age group. He believes that, if people are treated with 20 to 30 years of low-dose aspirin, it would be those starting treatment in their late 40s or 50s who might eventually derive the most benefit.

“These findings provide the first proof in man that aspirin reduces deaths due to several common cancers,” the authors wrote. “Benefit was consistent across the different trial populations, suggesting that the findings are likely to be generalisable.”

Dr. Rothwell noted that “these results do not mean that all adults should immediately start taking aspirin, but they do demonstrate major new benefits that have not previously been factored into guideline recommendations. Previous guidelines have rightly cautioned that in healthy middle aged people the small risk of bleeding on aspirin partly offsets the benefit from prevention of strokes and heart attacks, but the reductions in deaths due to several common cancers will now alter this balance for many people.”

The authors concluded that taking aspirin daily for 5 to 10 years, as in the trials, reduced all-cause mortality (including any fatal bleeds) during that
time by about 10%. Subsequently, there were further delayed reductions in cancer deaths, but no continuing excess risk of bleeding. In terms of
cost-effectiveness, such benefit would exceed that of established initiatives such as screening for breast or prostate cancer, potentially justifying added costs to reduce bleeding complications, such as co-prescription of a proton-pump inhibitor and further development of more effective derivatives of aspirin.

Dr. Rothwell and colleagues noted that more research is required. Effects of aspirin on incidence of cancer must be determined, both for cancers that are less commonly fatal and to determine whether the latent period before an effect is shorter than for death. More trial data are required for the effect of aspirin on risk of breast and other cancers of women. Follow-up beyond 20 years is necessary to identify any late rebound in cancer deaths. Dr. Rothwell and his study group hope to report the answers to these and other questions with new research during 2011.

“Perhaps the most important finding for the longer-term is the proof of principle that cancers can be prevented by simple compounds like aspirin and
that ‘chemoprevention’ is therefore a realistic goal for future research with other compounds,” said Dr. Rothwell.

SOURCE: The Lancet

I'm me, not a statistic. Praying to not be one for years yet.

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Lucassi's picture
Replies 7
Last reply 6/16/2012 - 2:14pm

Mike had a CT scan on 2/21/12 that showed a 12 mm pulmonary nodule in the upper left lobe.  The CT report states that it is highly suspicious for metastatic disease.  The oncologist has ordered a PET scan for next week.  Although there is a chance that it is not cancer, I am very concerned that the melanoma has spread.  Has anyone else had pulmonary nodules that ended up not being metastatic disease? 

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ElaineLinn's picture
Replies 5
Last reply 3/21/2012 - 3:56pm

I ha ve done so well with the first IFFi injection. Blood work was all great on my 2nd dose apptntment. Sob the dr. gave me my second dose on March 1sr and all went well. UNTIL March 2nd just got my kids to bed around 8 , my oldest son was there with me when I went into convultions. So a quit trip to close hospital and was transferedd 3 hours away to columbus Ohio where my doctor is . I find tha they think that I have some lesions on my brain causing it to swell. So today I have been put throught the ringers MRI, 6 different drawing of the blood, so many different anti sezeisure meds that I for got what they were.  Has anyone else been trought this.   I am asking for all the prayers I can get!

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Anonymous's picture
Anonymous
Replies 9
Last reply 8/27/2013 - 1:39pm
 
Over the course of 12 months, I have had several moles removed.   Four were mildly dysplastic and 1 was moderate and required further extraction.   Right now, I do not think I have any other dysplastic nevi.  I did not know about dysplastic nevi prior to this year and I am becoming very frantic.
I have a few questions.
First, what is the risk of melanoma for someone with five dysplastic nevi?
Second, is it possible that I do not develop anymore of these moles?
Have you personally known someone with numerous dysplastic nevi that never developed melanoma?
My doctor said I will have six month follow ups for two years, does this mean I am most at risk for the next two years and if I did not develop anymore in the next two years, my risk factors for skin cancer go down? 

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carolyn.k's picture
Replies 6
Last reply 3/4/2012 - 10:34pm

My husband was diagnosed with stage 4 in April 2011, with mets in both lungs, liver, spleen and femur.  His original primary was on his back, and excised 11 years prior.  He was NED for 11 years; then an unrelated screening showed stage 4 disease.  He presented with just a little nausea and fatigue.  Since there are no melanoma specialists in Sacramento, we traveled to San Francisco and interviewed doctors at UCSF, NCMC and CPMC, and ended up enrolling in a clinical trial at UCSF with Dr. Daud.  Since Thomas is BRAF/NRAS/CKIT  negative, and was 72 at the time of diagnosis, our options were somewhat limited to either Yervoy or the clinical trial.  We chose the clinical trial, which is axitinib + carboplatin + paclitaxel.  He endured 8 rounds of chemo, and has since been on a continuous, maintenance dose of axitinib since November 22, 2011.  His last 5 PET/CT scans show "stable disease" although we do not consider this a victory, as his quality of life is horrible.  On a nausea scale of 1 - 10, with 1 being very mild and 10 meaning vomiting, his nausea usually hovers around a 2 - 3, but has escalated recently, even though he is considered stable.  For the past few weeks, his nausea maintains at about a "5", and he gets little relief from all the usual anti-emetics.  To date, he has tried:  zofram, Emend, compazine, phenergan, reglan, ativan, benadryl, scopolamine patch, Sancuso patch, medical marijuana, acupuncture, fresh ginger tea, candied ginger, licorice root tea, acupressure wrist bands.  Some of these worked to alleviate the post-chemo nausea, but the only thing that gives him any relief at the moment is a combination of ativan+reglan+benadryl.  However, he keeps building up a tolerance to the drugs and we increase the dose (per Doctor's orders) which gives him a little relief.  Dr. Daud believes that most of the nausea is due to his liver disesase:  approximately 50% of his liver is involved and it is not detoxifying his food properly, resulting in the nausea.  I feed him almost exclusively a very healthy, 95% organic diet, to keep pesticides and additives out of his system.  Direct liver intervention, via chemo embolization, or other treatments isn't an option because of the size of his liver mets; it would require a lot of chemo which could damage the remaining healthy liver tissue.  We are considering switching to a PD1 trial, but as it hasn't opened up yet at UCSF, we are waiting.  Does anyone have any other remedies for persistent nausea that we haven't tried?  Any and all ideas, both conventional and alternative, would be welcomed.

Never give up.

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94z28joe's picture
Replies 15
Last reply 3/5/2012 - 6:05pm

My doctor just called me and told me he had my results. He said that he took 26 lymph nodes and saliva gland. He said that everything came back negative. Wow! Such a sigh of relief I can a least breath a little bit easier for now. I know I will have to constantly be vigil and be aware of what's going on with my body, but it's such I great feeling getting the all clear after your life's been completely turned upside down by finding out you have stage 3b melanoma. Thanks everyone ont this board for your support and stories they are such a huge help!

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justlittleoleme's picture
Replies 3
Last reply 3/2/2012 - 9:45pm

Thought I would update you all on what has been happening with my hubby.

He finished Ipi infusion #4 on 2/6/12.  Admitted to hospital on 2/17/12 with ipi induced colitis.  Five day hospital visit.

Wednesday we visited with a liver specialist as his liver enzymes continue to escalate.

Fast forward to today.  Hospital admission #2.  Liver biopsy performed an hour ago.  Likely he has ipi induced hepatoxicity.

CT scans from a week ago now show 5 hot spots on spine and right pelvic region.  We are planning to do a bone biopsy once they get the liver functioning properly.  Dr. all but assured us that there is no more immunotherapy for him.  If the spots show up as melanoma, pretty sure it is chemotherapy.  What at this point I don't know.

I am at a loss.  The spots weren't there in November when he did his scans to get into the ipi trial.  That concerns his dr.

Pray that we have a short hospital stay.  Our youngest son's 9th birthday is tomorrow and we are in the hospital 3 1/2 hours away.

barb

We don't know how strong we are until being strong is the only choice we have.

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boot2aboot's picture
Replies 11
Last reply 3/5/2012 - 4:33pm

If anyone is like me, very low on money and can't afford airfare, and incredibly frustrated with the lack of help american cancer society offers -what a joke- i want to share this information with you:

http://www.swamedia.com/releases/6146f9bf-d192-41f8-9872-0c3213ebb718

Southwest has a program that will fly you to your cancer treatments

you do have to be able to walk unassisted , but if you can...Here is the info

Call Amanda  Raneri at:

516-300-1660

 

tell them boots sent you

don't back up, don't back down

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Havent posted in a little while, but I normally check the site daily but don't have much to add as I'm fairly new to this horrendous cancer. I went on Tuesday to have my saliva gland removed and approximately 20 lymph nodes removed from my face and neck after I had a positive SLNB. Hoping this set comes back clear, but so far I haven't been so lucky even having a melanoma of .93 it managed to make it to my SNLB. My face on that side is a little sunken in and I'm having a hard to eating anything of substance as my face is still numb and not moving very well on that side. I'm suppose to go and have my drain tube taken out next week. I'm hoping to get my facial movement back after the swelling goes down. I will post up the results when I get them. Thanks for everyone the post on this board as I always find really good information and your stories of survival give me great hope!

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Birdwatch's picture
Replies 3
Last reply 3/2/2012 - 7:39pm

I was diagnosed in April 2011 with melanoma on my arch of my left foot.  Diagnosed at stage II.  I don't understand all of this and have read several postings.  I had surgery to remove and had lemph nodes tested.  Nodes all came back negative.  I have continued seeing dematologist and a cancer specialist.  They infomed my that they got it all.  How can you rest ones mind.  I lost a sister 15 years ago with melanoma as well.  Yesterday I found a bump, lump to the left of my sternum.  How would you proceed and what do you think I should do?

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lhaley's picture
Replies 8
Last reply 3/2/2012 - 5:11pm

I am so excited! Just took the last dex that I have been weaning!  Started Oct 4th or 5th.   I am getting around much  better but have a far way to go, today was a big step!

My eyes are very slinty from all of the swelling and yesterday I was exercising .... noticed right afterwards that there is now blood in the white area.  Like I said there is still a far way to go. They are starting me today on mild Lasix so I can get some of this swelling down. Pants are so tight on my waist but fall down off of my hips and legs!  That will all solve itself.

I've worked hard on being able to get to the floor and getting back up. Savannah (2 year old granddaughter) is coming for the weekend. This will be the first time I've actually been able to play with her since before Christmas.  This is a weekend of celebration for us.

Linda

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gtown's picture
Replies 8
Last reply 3/5/2012 - 4:33pm
Replies by: gtown, Janner, DonW

went down to Penn for checkup today. No tests or anything (had clear lung X-rays 2 months ago). The doctor who was filling in for my doctor mentioned that the lack of inflamation found around the excision site was not a great sign, she said it showed the body's immune system when fighting cancer would show inflamation. She said this after being pressed by me (I ask ALOT of questions). Has anyone else ever heard of this before? I guess like many of you, I get anxiety ridden when I go for tests, checkups etc. I have  real up and down days leading up to tests etc. Some days I think I'm doomed and other days I feel positive. I'm thinking about seeing a shrink just because alot of people don't want to hear about it. So anyhow has anyone heard of the inflamation and secondly has anyone gone to counseling over this?   

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Dual Inhibition of VEGF and c-MET in Cancer Promises to Decrease Metastasis

A combined dual inhibition of vascular endothelial growth factor (VEGF) and c-MET is showing promise in preventing tumor invasion and metastasis. The data thus far are in a laboratory model of pancreatic neuroendocrine tumors (PNET). The results are published in the journal Cancer Discovery.

Neuroendocrine Pancreatic Tumor—main pancreatic duct (MPD), tumor (T), portal vein (PV), splenic vein (SV), superior mesenteric artery (SMA)

According to the lead author of the study, Donald M. McDonald, MD, PhD, Comprehensive Cancer Center, University of California, San Francisco, this study was designed to demonstrate a proof of principle. The concept is likely to extend to other tumor types.

McDonald explained that the inhibition of both VEGF and c-MET signaling has a synergistic effect on tumors that leads to slowing down of the tumor growth and decreased metastasis.

"The translational significance of the work is not necessarily to demonstrate a promising approach in PNET, but rather to show in general that targeting MET simultaneously with VEGFR is a better general approach than targeting the VEGF pathway alone without inhibiting MET," says Dana T. Aftab, PhD, part of the translational research team at Exelixis, and coauthor of the Cancer Discovery paper.

Many cancers show increased c-MET activity and mutations, including breast, liver, lung, kidney, thyroid, and ovarian cancers. Deregulated c-MET signaling has been shown to be associated with a more aggressive tumor phenotype.

McDonald and his team assessed the role of c-MET signaling when VEGF signaling is inhibited using a pancreatic neuroendocrine tumor mouse model and a second model that exhibited late-onset aggressive and metastatic tumors when the mice are in old age. The range of timing of tumor onset, including the very late-timing in the one model uniquely allows the assessment of whether the aggressive tumor characteristic can be advanced or reversed.

"Because tumors in [one of our mouse models] naturally become more invasive and metastatic with age, but generally do so near the time the mice succumb, this model provided the opportunity to determine whether aggressiveness could be advanced, delayed, or reversed by treatment with a c-MET inhibitor," explained McDonald.

Previous laboratory research showed that while inhibition of VEGF decreased tumor size, there is also a downside. According to Dana T. Aftab, "increased invasiveness after anti-VEGF therapy has been studied in the clinic most extensively in glioblastoma, where frequent imaging with high resolution techniques is standard."

The researchers now show that c-MET expression and activity increase upon VEGF inhibition and tumor hypoxia is elevated. When both the VEGF and c-MET pathways were inhibited, invasion and metastasis went down. This effect was also observed in mouse models of two more types of pancreatic cancers.

The team used a murine anti-VEGF antibody. The c-MET inhibitors used were crizotinib (Xalkori) and PF-04217903. Crizotinib was approved last year for metastatic non–small-cell lung cancer that harbors the EML4-ALK fusion gene. Crizotinib works by inhibiting both the anaplastic lymphoma kinase (ALK), as well as the tyrosine kinase c-MET. PF-04217903 is currently in phase I trials as a monotherapy for a range of advanced solid tumor types.

Cabozantinib, an oral, small-molecule inhibitor, blocks both c-MET and VEGF signaling. "A trial for cabozantinib in patients with pancreatic neuroendocrine tumors will open for patient recruitment soon," said Aftab. "However, the translational significance of the [currently published] work is not necessarily to demonstrate a promising approach in PNET," he added.

The drug is showing promising results in early-stage clinical trials. There was promising activity in metastatic medullary thyroid cancer (MTC) in a phase I trial published last year in the Journal of Clinical Oncology. Of 35 patients, 10 showed a partial response, a notable achievement for a disease that has no standard treatment options. A phase III medullary thyroid clinical trial of cabozantinib further showed an almost three-fold improvement in progression-free survival (PFS) compared to placebo in results announced last October. The median PFS in the cabozantinib arm was 11.2 months compared to 4 months in the placebo arm (P < .0001). The full results will be presented at a clinical meeting.

"We have evaluated cabozantinib in many preclinical models with generally good results, but to my knowledge the only careful examination of VEGF plus MET inhibition, using combinations of selective inhibitors, is [this Cancer Discovery paper]," said Dana T. Aftab.

Activity with cabozantinib was also seen for many solid tumors. In a phase II trial presented at the 2011 American Society of Clinical Oncology annual meeting, cabozantinib showed an ability to shrink bone metastases in prostate cancer, breast, and melanoma patients. It also showed activity in ovarian, and prostate cancers, and preliminary data from a phase II liver cancer trial shows an increased progression-free survival for both treatment-naïve and previously treated patients.

McDonald and his team are already working further along these lines of research. "We are continuing to study the effects of c-MET inhibitors on tumor invasiveness and metastasis," he says.

I'm me, not a statistic. Praying to not be one for years yet.

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http://www.eyesite.ca/CJO/4201/i06-109.pdf

metastatic uveal melanoma
Ana C.A. Frota,* MD; Alexandre N. Odashiro,*† MD, PhD; Patricia R. Pereira,*† MD;
Bruno F. Fernandes,* MD; Katyanne Dantas Godeiro,* MD;
Joao Pessoa Souza Filho,*† MD, PhD; Miguel N. Burnier, Jr.,*† MD, PhD
ABSTRACT • RÉSUMÉ
Case report: We report a case of choroidal melanoma metastatic to the liver diagnosed by fine-needle
aspiration.The biopsy sample was immunostained for COX-2 and c-kit.
Comments: Accurate diagnosis and identification of potential therapeutic targets are important for
subsequent therapy and can be achieved by radiologically guided fine-needle aspiration biopsy.
Observation : Nous signalons un cas de mélanome choroïdien métastatique au foie, diagnostiqué par
ponction-biopsie à fine aiguille. L’échantillon obtenu a été immunocoloré pour la COX-2 et le gène c-kit.
Commentaires : Il importe d’établir un diagnostic précis et d’identifier les cibles thérapeutiques possibles pour
la thérapie subséquente; la ponction-biopsie à fine aiguille (PBFA) guidée par la radiologie permet d’y parvenir.

Malignant uveal melanoma (UM) is the most common primary intraocular tumour in adults, and the liver is the most common site for metastases. The use of fine-needle aspiration biopsy (FNAB) for diagnosis of metastatic UM to the liver has been described by Liu et al1 exhibiting successful rates.2,3 Sensitivity reported in the literature ranges from 67% to 100% and specificity from 80% to 100%.4 To our knowledge, the study of immunohistochemical expression of the COX-2 enzyme and c-kit protein and their role in metastatic UM cells obtained by FNAB has never been described.
CASE REPORT
A 78-year-old man was referred to the oncology clinic of the Montreal General Hospital, McGill University for
evaluation of a choroidal mass in his left eye. Fundoscopy revealed a pigmented, well-circumscribed tumour in the
choroid, displaying low reflectivity on A-scan ultrasound. The tumour measured 9 mm × 6 mm on its basal diameter and 5 mm in height. The diagnosis of choroidal melanoma was established and the patient was treated
with iodine-125 episcleral brachytherapy. After 3 years, abdominal computerized axial tomography scans
revealed hepatic, mesentery, and spleen lesions. Liver FNAB under ultrasound guidance confirmed metastatic
melanoma, epithelioid cell type predominant. Immunohistochemistry for COX-2 and the c-kit protein
CD117 was performed in the sample, revealing positivity for COX-2 (Fig. 1) and negativity for c-kit.
COMMENTS
COX-2 is a prostaglandin synthase involved in human carcinogenic processes such as angiogenesis, invasion,
and metastasis.5 The increased expression of COX-2 has been identified in several malignant diseases including
From *the Department of Ophthalmology, Federal University of São Paulo, São Paulo, Brazil, and †the Henry C. Witelson Ocular Pathology Laboratory and Registry, McGill University Health Center, Montreal, Que.
Originally received Dec. 2, 2005. Revised May 29, 2006 Accepted for publication July 13, 2006 Correspondence to: Ana Carolina de Arantes Frota, MD, 3775 University St., Lyman Duff Building, Rm. 216, Montreal, Que.; fax 514-398-5728; carolafrota@click21.com.br
This article has been peer-reviewed. Cet article a été évalué par les pairs.
Can J Ophthalmol 2007;42:145–6
doi:10.3129/can j ophthalmol.06-109
COX-2 and c-kit—Frota et al 145
Fig. 1—Positive staining for COX-2 in fine-needle aspiration sample of liver metastasis from uveal melanoma (original magnification ×100).
colorectal cancer,6 cutaneous melanoma,7 and recently, uveal melanoma.8 The presence of COX-2 in mixedcell-
type UM is correlated to worse prognostic factors.7 The U.S. Food and Drug Administration (FDA)
approved COX-2 inhibitors for the treatment of patients with familial adenomatous polyposis coli9 and
epidemiologic studies have shown that these drugs reduce the mortality from colorectal, breast, and lung
cancer.10 In fact, the use of COX-2 inhibitors warrants investigation as an adjuvant treatment for UM.
The c-kit protein CD11711,12 is a membrane-bound tyrosinase kinase receptor and its overexpression has been
observed in several malignancies.13–18 Imatinib mesylate (STI571, Gleevec, Novartis Pharma AG, Basel,
Switzerland) is a compound that inhibits kinase receptors19 and is FDA-approved for the treatment of c-kit–positive gastrointestinal stromal tumours (GIST) and Philadelphia chromosome-positive chronic myelogenous
leukemia.20More than 75% of UM cells were shown to be positive for c-kit, and imatinib mesylate decreased the proliferation and invasiveness of different cell lines of human UM.21 These results suggest that the drug may also
decrease the ability of cells to implant at the metastatic site.
We conclude that FNAB is not only a diagnostic tool but is also useful in tumour classification with regard to
COX-2 and c-kit expression. Patients with UM who present with positive staining for COX-2 and c-kit may
be candidates for tumour therapy with anti–c-kit and COX-2 inhibitors. Currently, the most important goals
are to increase the quality of life and the survival rates of these patients. These new therapeutic interventions
could lead to a decrease in cell invasiveness in patients free from metastasis, as well as delaying the on-going
process in those who already have metastasis, thus reducing the aggressiveness of the disease.
The authors have no financial conflict of interested regarding this manuscript.

I'm me, not a statistic. Praying to not be one for years yet.

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