Newbie

You raise a good point about vocabulary.  We have a lot of these definitions in various places on the website, but I suspect a good melanoma dictionary where everything is in one place would be helpful.

You ask about IL-2, and here are a few thoughts:

Clark's level and Breslow thickness are both measures of how deep the lesion is.  Generally the deeper the more advanced and the higher the concern.

Mitotic Rate is a count of how many cells in a specific area are actively dividing.  Generally the lower the number the better.

Lymph Node: this is part of a drainage system that runs throughout the body.  Melanoma can spread by having tumor cells break off the tumor and migrate through the lymph system.

Sentinel Lymph Node is the specific lymph node that drains the area where the tumor is located.  Radioactive dye is injected into the lesion site, then surgery is done to find the node.  The node is removed and tested for tumor cells.  if present, the doctors often suggest more surgery.

Interferon is sometimes given after lymph node dissection.  It stimulates the immune system.  In big studies people who take interferon stay cancer free about 5% longer, but don't live longer.

Dacarbazine or DTIC is a chemotherapy used for advanced melanoma.  It is an old medicine is is not very effective.  These days it is mostly used to buy time for other therapies to come online.

IL2 or interleukin 2 is a drug approved about 15 years ago for treating advanced melanoma.  It stimulates the immune system in an attempt to get the immune system to attack tumor cells.  It is a hard drug to take, and you have to have good cardiovascular health.  About 15% of people who take it get some benefit; about 5% are cured.

Ipilimumab, ipi, or Yervoy is a drug approved in 2011.  It blocks a normal braking mechainism that keeps the immune system T-cells in check, this reactivating the immune system in the fight against the tumor.  About 20% of people who take it benefit from this drug, and a portion of those (we don't know what portion yet) have long-term response.

Zelboraf or Z or vemurafenib was also approved in 2011.  Rather than impact the immune system, this drug goes into the tumor cells to shut them down.  About half of people with melanoma have a mutation in their tumor in a gene called BRAF.  This codes for the BRAF protein, which is part of a series of signals that tell the cell when to grow and divide.  Normally BRAF is only activated in response to a signal that starts at the cell wall.  When mutated the BRAF protein is stuck on the "on" position and constantly tells the cell to divide.  Zelboraf shuts BRAF down.  After 6 months, about half of people on this drug will stop responding.

In addition to the above, several drugs are being tested and are still in clinical trials.

Anti-PD1 works a lot like ipi / Yervoy in that it reactivates T-cells.  It works on a different "checkpoint" and seems to be more tolerable and more effective that ipi.  It is likely to be approved next year.

Dabrafenib is, like vemurafenib, a BRAF inhibitor but is from a different company.  That company also has a drug, tremilumimab, that blocks MEK, the next step beyond BRAF.  When these two drugs are used together they seem to work much better than either along.  Both drugs will likely be approved by the FDA in early June.

Maybe that's a start, but please don't hesitate to ask questions.

Tim–MRF

Hi Tim,

FYI – think you might have meant Trametinib as the MEK inhibitor used with Dabrafenib. I believe tremilumimab was Pfizer's anti-CTLA-4 inhibitor that was in clinical trial several years ago.   

Mary

Hi Tim,

FYI – think you might have meant Trametinib as the MEK inhibitor used with Dabrafenib. I believe tremilumimab was Pfizer's anti-CTLA-4 inhibitor that was in clinical trial several years ago.   

Mary

Hi Tim,

FYI – think you might have meant Trametinib as the MEK inhibitor used with Dabrafenib. I believe tremilumimab was Pfizer's anti-CTLA-4 inhibitor that was in clinical trial several years ago.   

Mary

You raise a good point about vocabulary.  We have a lot of these definitions in various places on the website, but I suspect a good melanoma dictionary where everything is in one place would be helpful.

You ask about IL-2, and here are a few thoughts:

Clark's level and Breslow thickness are both measures of how deep the lesion is.  Generally the deeper the more advanced and the higher the concern.

Mitotic Rate is a count of how many cells in a specific area are actively dividing.  Generally the lower the number the better.

Lymph Node: this is part of a drainage system that runs throughout the body.  Melanoma can spread by having tumor cells break off the tumor and migrate through the lymph system.

Sentinel Lymph Node is the specific lymph node that drains the area where the tumor is located.  Radioactive dye is injected into the lesion site, then surgery is done to find the node.  The node is removed and tested for tumor cells.  if present, the doctors often suggest more surgery.

Interferon is sometimes given after lymph node dissection.  It stimulates the immune system.  In big studies people who take interferon stay cancer free about 5% longer, but don't live longer.

Dacarbazine or DTIC is a chemotherapy used for advanced melanoma.  It is an old medicine is is not very effective.  These days it is mostly used to buy time for other therapies to come online.

IL2 or interleukin 2 is a drug approved about 15 years ago for treating advanced melanoma.  It stimulates the immune system in an attempt to get the immune system to attack tumor cells.  It is a hard drug to take, and you have to have good cardiovascular health.  About 15% of people who take it get some benefit; about 5% are cured.

Ipilimumab, ipi, or Yervoy is a drug approved in 2011.  It blocks a normal braking mechainism that keeps the immune system T-cells in check, this reactivating the immune system in the fight against the tumor.  About 20% of people who take it benefit from this drug, and a portion of those (we don't know what portion yet) have long-term response.

Zelboraf or Z or vemurafenib was also approved in 2011.  Rather than impact the immune system, this drug goes into the tumor cells to shut them down.  About half of people with melanoma have a mutation in their tumor in a gene called BRAF.  This codes for the BRAF protein, which is part of a series of signals that tell the cell when to grow and divide.  Normally BRAF is only activated in response to a signal that starts at the cell wall.  When mutated the BRAF protein is stuck on the "on" position and constantly tells the cell to divide.  Zelboraf shuts BRAF down.  After 6 months, about half of people on this drug will stop responding.

In addition to the above, several drugs are being tested and are still in clinical trials.

Anti-PD1 works a lot like ipi / Yervoy in that it reactivates T-cells.  It works on a different "checkpoint" and seems to be more tolerable and more effective that ipi.  It is likely to be approved next year.

Dabrafenib is, like vemurafenib, a BRAF inhibitor but is from a different company.  That company also has a drug, tremilumimab, that blocks MEK, the next step beyond BRAF.  When these two drugs are used together they seem to work much better than either along.  Both drugs will likely be approved by the FDA in early June.

Maybe that's a start, but please don't hesitate to ask questions.

Tim–MRF

You raise a good point about vocabulary.  We have a lot of these definitions in various places on the website, but I suspect a good melanoma dictionary where everything is in one place would be helpful.

You ask about IL-2, and here are a few thoughts:

Clark's level and Breslow thickness are both measures of how deep the lesion is.  Generally the deeper the more advanced and the higher the concern.

Mitotic Rate is a count of how many cells in a specific area are actively dividing.  Generally the lower the number the better.

Lymph Node: this is part of a drainage system that runs throughout the body.  Melanoma can spread by having tumor cells break off the tumor and migrate through the lymph system.

Sentinel Lymph Node is the specific lymph node that drains the area where the tumor is located.  Radioactive dye is injected into the lesion site, then surgery is done to find the node.  The node is removed and tested for tumor cells.  if present, the doctors often suggest more surgery.

Interferon is sometimes given after lymph node dissection.  It stimulates the immune system.  In big studies people who take interferon stay cancer free about 5% longer, but don't live longer.

Dacarbazine or DTIC is a chemotherapy used for advanced melanoma.  It is an old medicine is is not very effective.  These days it is mostly used to buy time for other therapies to come online.

IL2 or interleukin 2 is a drug approved about 15 years ago for treating advanced melanoma.  It stimulates the immune system in an attempt to get the immune system to attack tumor cells.  It is a hard drug to take, and you have to have good cardiovascular health.  About 15% of people who take it get some benefit; about 5% are cured.

Ipilimumab, ipi, or Yervoy is a drug approved in 2011.  It blocks a normal braking mechainism that keeps the immune system T-cells in check, this reactivating the immune system in the fight against the tumor.  About 20% of people who take it benefit from this drug, and a portion of those (we don't know what portion yet) have long-term response.

Zelboraf or Z or vemurafenib was also approved in 2011.  Rather than impact the immune system, this drug goes into the tumor cells to shut them down.  About half of people with melanoma have a mutation in their tumor in a gene called BRAF.  This codes for the BRAF protein, which is part of a series of signals that tell the cell when to grow and divide.  Normally BRAF is only activated in response to a signal that starts at the cell wall.  When mutated the BRAF protein is stuck on the "on" position and constantly tells the cell to divide.  Zelboraf shuts BRAF down.  After 6 months, about half of people on this drug will stop responding.

In addition to the above, several drugs are being tested and are still in clinical trials.

Anti-PD1 works a lot like ipi / Yervoy in that it reactivates T-cells.  It works on a different "checkpoint" and seems to be more tolerable and more effective that ipi.  It is likely to be approved next year.

Dabrafenib is, like vemurafenib, a BRAF inhibitor but is from a different company.  That company also has a drug, tremilumimab, that blocks MEK, the next step beyond BRAF.  When these two drugs are used together they seem to work much better than either along.  Both drugs will likely be approved by the FDA in early June.

Maybe that's a start, but please don't hesitate to ask questions.

Tim–MRF

Also, if you haven't gone there already, try clicking on the "Learn More >>" menu button on the top left of this page. It linkes to a cascade of pages underneath that go into, for example, "melanoma treatment" which describes various treatment options. There are a lot more subjects on that menu that would probably be of interest to look at, too.

Also, if you haven't gone there already, try clicking on the "Learn More >>" menu button on the top left of this page. It linkes to a cascade of pages underneath that go into, for example, "melanoma treatment" which describes various treatment options. There are a lot more subjects on that menu that would probably be of interest to look at, too.

Also, if you haven't gone there already, try clicking on the "Learn More >>" menu button on the top left of this page. It linkes to a cascade of pages underneath that go into, for example, "melanoma treatment" which describes various treatment options. There are a lot more subjects on that menu that would probably be of interest to look at, too.

Here are a few:

Abbreviations

AEs = adverse effects
BRAFi = BRAF inhibitor/inhibition
BRIM-3 = BRAF Inhibitor in Melanoma-3
CR = complete response
CTLA-4 = cytotoxic T lymphocyte antigen-4
DTIC = dacarbazine
ECOG = Eastern Cooperative Oncology Group
EGFR = epidermal growth factor receptor
ERKi = ERK inhibitor
FDA = Food and Drug Administration
IL-2 = interleukin-2

Here are a few:

Abbreviations

AEs = adverse effects
BRAFi = BRAF inhibitor/inhibition
BRIM-3 = BRAF Inhibitor in Melanoma-3
CR = complete response
CTLA-4 = cytotoxic T lymphocyte antigen-4
DTIC = dacarbazine
ECOG = Eastern Cooperative Oncology Group
EGFR = epidermal growth factor receptor
ERKi = ERK inhibitor
FDA = Food and Drug Administration
IL-2 = interleukin-2

IRAE = immune-related adverse effects
IRRC = immune-related response criteria
MAPK = mitogen-activated protein kinase
MEKi = MEK inhibitor
MRA = Melanoma Research Alliance
mWHO = modified World Health Organization

mTOR = mammalian target of rapamycin
PDGFB = platelet-derived growth factor, B chain
PDGFRβ = platelet derived growth factor receptor-beta
PI3K = phosphatidylinositol 3'-kinase
PR = partial response
NSCLC = non-small cell lung cancer
SCC = squamous-cell carcinoma
SD = stable disease
TKI = tyrosine kinase inhibitor
ULN = upper limit of normal
VBD = vinblastine, bleomycin, cisplatin

IRAE = immune-related adverse effects
IRRC = immune-related response criteria
MAPK = mitogen-activated protein kinase
MEKi = MEK inhibitor
MRA = Melanoma Research Alliance
mWHO = modified World Health Organization

mTOR = mammalian target of rapamycin
PDGFB = platelet-derived growth factor, B chain
PDGFRβ = platelet derived growth factor receptor-beta
PI3K = phosphatidylinositol 3'-kinase
PR = partial response
NSCLC = non-small cell lung cancer
SCC = squamous-cell carcinoma
SD = stable disease
TKI = tyrosine kinase inhibitor
ULN = upper limit of normal
VBD = vinblastine, bleomycin, cisplatin

I also had LDH = l.a.c.t.a.t.e dehydrogenase in the list, but apparently the word "l.a.c.t.a.t.e" is profanity and is rejected by the profanity filter.

I also had LDH = l.a.c.t.a.t.e dehydrogenase in the list, but apparently the word "l.a.c.t.a.t.e" is profanity and is rejected by the profanity filter.

I also had LDH = l.a.c.t.a.t.e dehydrogenase in the list, but apparently the word "l.a.c.t.a.t.e" is profanity and is rejected by the profanity filter.

IRAE = immune-related adverse effects
IRRC = immune-related response criteria
MAPK = mitogen-activated protein kinase
MEKi = MEK inhibitor
MRA = Melanoma Research Alliance
mWHO = modified World Health Organization

mTOR = mammalian target of rapamycin
PDGFB = platelet-derived growth factor, B chain
PDGFRβ = platelet derived growth factor receptor-beta
PI3K = phosphatidylinositol 3'-kinase
PR = partial response
NSCLC = non-small cell lung cancer
SCC = squamous-cell carcinoma
SD = stable disease
TKI = tyrosine kinase inhibitor
ULN = upper limit of normal
VBD = vinblastine, bleomycin, cisplatin

Here are a few:

Abbreviations

AEs = adverse effects
BRAFi = BRAF inhibitor/inhibition
BRIM-3 = BRAF Inhibitor in Melanoma-3
CR = complete response
CTLA-4 = cytotoxic T lymphocyte antigen-4
DTIC = dacarbazine
ECOG = Eastern Cooperative Oncology Group
EGFR = epidermal growth factor receptor
ERKi = ERK inhibitor
FDA = Food and Drug Administration
IL-2 = interleukin-2