Aliases & Classifications for Melanoma

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Aliases & Descriptions for Melanoma:

Name: Melanoma 8 10 44 32 30 61
Malignant Melanoma 8
 
Naevocarcinoma 8


Classifications:



External Ids:

Disease Ontology8 DOID:1909
MeSH33 D008545
NCIt39 C3224
ICD1025 D03.9

Summaries for Melanoma

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MedlinePlus:32 Melanoma is the most serious type of skin cancer. often the first sign of melanoma is a change in the size, shape, color, or feel of a mole. most melanomas have a black or black-blue area. melanoma may also appear as a new mole. it may be black, abnormal, or "ugly looking." thinking of "abcde" can help you remember what to watch for: asymmetry - the shape of one half does not match the other border - the edges are ragged, blurred or irregular color - the color is uneven and may include shades of black, brown and tan diameter - there is a change in size, usually an increase evolving - the mole has changed over the past few weeks or months surgery is the first treatment of all stages of melanoma. other treatments include chemotherapy and radiation, biologic, and targeted therapies. biologic therapy boosts your body's own ability to fight cancer. targeted therapy uses substances that attack cancer cells without harming normal cells. nih: national cancer institute

MalaCards based summary: Melanoma, also known as malignant melanoma, is related to uveal melanoma and ocular melanoma. An important gene associated with Melanoma is PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha), and among its related pathways is Immune response IL 23 signaling pathway. The drugs carmustine and dacarbazine and the compounds rantes and hemocyanin have been mentioned in the context of this disorder. Affiliated tissues include skin, t cells and lymph node, and related mouse phenotypes are no phenotypic analysis and homeostasis/metabolism.

Disease Ontology:8 A cell type cancer that has material basis in abnormally proliferating cells derived from melanocytes which are found in skin, the bowel and the eye.

Novus Biologicals:45 Melanoma is a malignant tumor that results from uncontrolled growth of pigmented cells, called melanocytes. Several types of melanoma exist, including superficial spreading melanoma, nodular melanoma and lentigo melanoma. Melanoma diagnosis is traditionally supported by the presence of the S-100 protein marker and HMB-45, however research has determined the sensitivity and specificity of three novel antibodies as markers for melanoma: Mitf, Melan-A and tyrosinase.

Wikipedia:64 Melanoma (i/?m?l??no?m?/; from Greek ????? melas, \"dark\") is a type of skin cancer which forms from... more...

Related Diseases for Melanoma

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Diseases related to Melanoma via text searches within MalaCards or GeneCards Suite gene sharing:

(show top 50)    (show all 642)
idRelated DiseaseScoreTop Affiliating Genes
1uveal melanoma32.4MAGEA1, MAGEA3, PMEL
2ocular melanoma32.2MAGEA1, MAGEA3
3breast cancer31.2PIK3CA, CXCL1, IL24, MAGEA3, MAGEA1, CD63
4leukemia31.0CSPG4, MAGEA1, MAGEA3, CXCL1, PIK3CA, MRPL28
5influenza30.8MRPL28, PMEL, IL24, MAGEA3
6lung cancer30.6PIK3CA, IL24, MAGEA3, MAGEA1, CD63
7hepatocellular carcinoma30.6PIK3CA, MAGEA3, MAGEA1, CD63
8prostate cancer30.6PIK3CA, MCAM, CXCL1, IL24, CD63
9malignant glioma29.9CSPG4, IL24, MCAM, PMEL, PIK3CA
10amelanotic melanoma10.9
11skin melanoma10.8
12choroiditis10.8
13lentigo maligna melanoma10.8
14acral lentiginous melanoma10.8
15endotheliitis10.8
16melanoma metastasis10.8
17posterior uveal melanoma10.7
18sarcoma10.7
19intraocular melanoma10.7
20superficial spreading melanoma10.7
21clear cell sarcoma10.7
22mucosal melanoma10.7
23dysplastic nevus syndrome10.6
24microphthalmia10.6
25melanoma of soft parts10.6
26hypoxia10.6
27hepatitis10.6
28renal cell carcinoma10.6
29vulvar melanoma10.6
30testicular cancer10.5MAGEA1, MAGEA3, PMEL
31esophageal cancer10.5MAGEA3, MAGEA1, CTAG2
32basal cell carcinoma10.5
33keratosis10.5
34spitz nevus10.5
35orbital melanoma10.5
36nodular malignant melanoma10.5
37melanoma-associated retinopathy10.5
38pancreatitis10.4
39retinitis10.4
40malignant melanoma, somatic10.4
41burns10.4
42cystic teratoma10.4
43thyroiditis10.4
44teratoma10.4
45burn scar10.4
46nevus of ota10.4
47retinoblastoma10.4
48adenocarcinoma10.4
49pancreatic cancer10.4
50dermatomyositis10.3

Graphical network of the top 20 diseases related to Melanoma:



Diseases related to melanoma

Symptoms for Melanoma

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Drugs & Therapeutics for Melanoma

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FDA approved drugs:

(show all 11)
id Drug Name Active Ingredient(s)13 Pharmaceutical Company Approval Date
1
Erivedge13 38 VISMODEGIB Genentech Approved January 2012
FDA Label: Erivedge
Malady that Drug Treats: basal cell carcinoma
Indications and Usage:13 ERIVEDGEèø (vismodegib) capsule is a hedgehog pathway inhibitor indicated; for the treatment of adults with metastatic basal cell carcinoma, or with locally; advanced basal cell carcinoma that has recurred following surgery or who are; not candidates for surgery, and who are not candidates for radiation. (1)
DrugBank Targets:11 1. Smoothened homolog
Mechanism of Action:13 
Target: hedgehog (Hh) signaling pathway
Action: innhibitor
FDA: Vismodegib is an inhibitor of the Hedgehog pathway. Vismodegib binds to and inhibits; Smoothened, a transmembrane protein involved in Hedgehog signal transduction.
2
Intron A13 38 INTERFERON ALFA-2B Schering-Plough Approved December 1997/ Approved December 1995/ Approved March 1997
FDA Label: Intron A
Malady that Drug Treats: non-Hodgkin's lymphoma/ malignant melanoma / Hepatitis C
Indications and Usage:13 Hairy Cell Leukemia INTRON® A is indicated for the treatment of patients 18 years of; age or older with hairy cell leukemia.; Malignant Melanoma INTRON A is indicated as adjuvant to surgical treatment in; patients 18 years of age or older with malignant melanoma who are free of disease but; at high risk for systemic recurrence, within 56 days of surgery.; Follicular Lymphoma INTRON A is indicated for the initial treatment of clinically; aggressive (see Clinical Pharmacology) follicular Non-Hodgkin s Lymphoma in; conjunction with anthracycline-containing combination chemotherapy in patients 18; years of age or older. Efficacy of INTRON A therapy in patients with low-grade, lowtumor; burden follicular Non-Hodgkin s Lymphoma has not been demonstrated.; Condylomata Acuminata INTRON A is indicated for intralesional treatment of selected; patients 18 years of age or older with condylomata acuminata involving external; surfaces of the genital and perianal areas (see DOSAGE AND ADMINISTRATION).; The use of this product in adolescents has not been studied.; AIDS-Related Kaposi's Sarcoma INTRON A is indicated for the treatment of selected; patients 18 years of age or older with AIDS-Related Kaposi's Sarcoma. The likelihood; of response to INTRON A therapy is greater in patients who are without systemic symptoms, who have limited lymphadenopathy and who have a relatively intact immune; system as indicated by total CD4 count.; Chronic Hepatitis C INTRON A is indicated for the treatment of chronic hepatitis C in; patients 18 years of age or older with compensated liver disease who have a history of; blood or blood-product exposure and/or are HCV antibody positive. Studies in these; patients demonstrated that INTRON A therapy can produce clinically meaningful effects; on this disease, manifested by normalization of serum alanine aminotransferase (ALT); and reduction in liver necrosis and degeneration.; A liver biopsy should be performed to establish the diagnosis of chronic hepatitis.; Patients should be tested for the presence of antibody to HCV. Patients with other; causes of chronic hepatitis, including autoimmune hepatitis, should be excluded. Prior; to initiation of INTRON A therapy, the physician should establish that the patient has; compensated liver disease. The following patient entrance criteria for compensated liver; disease were used in the clinical studies and should be considered before INTRON A; treatment of patients with chronic hepatitis C:; No history of hepatic encephalopathy, variceal bleeding, ascites, or other; clinical signs of decompensation; Bilirubin Less than or equal to 2 mg/dL; Albumin Stable and within normal limits; Prothrombin Time Less than 3 seconds prolonged; WBC Greater than or equal to 3000/mm3; Platelets Greater than or equal to 70,000/mm3; Serum creatinine should be normal or near normal.; Prior to initiation of INTRON A therapy, CBC and platelet counts should be; evaluated in order to establish baselines for monitoring potential toxicity. These tests; should be repeated at Weeks 1 and 2 following initiation of INTRON A therapy, and; monthly thereafter. Serum ALT should be evaluated at approximately 3-month intervals; to assess response to treatment (see DOSAGE AND ADMINISTRATION).; Patients with preexisting thyroid abnormalities may be treated if thyroidstimulating; hormone (TSH) levels can be maintained in the normal range by medication.; TSH levels must be within normal limits upon initiation of INTRON A treatment and TSH; testing should be repeated at 3 and 6 months (see PRECAUTIONS, Laboratory; Tests).; INTRON A in combination with REBETOL® is indicated for the treatment of; chronic hepatitis C in patients 3 years of age and older with compensated liver disease; previously untreated with alpha interferon therapy and in patients 18 years of age and; older who have relapsed following alpha interferon therapy. See REBETOL prescribing; information for additional information. Chronic Hepatitis B INTRON A is indicated for the treatment of chronic hepatitis B in; patients 1 year of age or older with compensated liver disease. Patients who have been; serum HBsAg positive for at least 6 months and have evidence of HBV replication; (serum HBeAg positive) with elevated serum ALT are candidates for treatment. Studies; in these patients demonstrated that INTRON A therapy can produce virologic remission; of this disease (loss of serum HBeAg) and normalization of serum aminotransferases.; INTRON A therapy resulted in the loss of serum HBsAg in some responding patients.; Prior to initiation of INTRON A therapy, it is recommended that a liver biopsy be; performed to establish the presence of chronic hepatitis and the extent of liver damage.; The physician should establish that the patient has compensated liver disease. The; following patient entrance criteria for compensated liver disease were used in the; clinical studies and should be considered before INTRON A treatment of patients with; chronic hepatitis B:; No history of hepatic encephalopathy, variceal bleeding, ascites, or other; signs of clinical decompensation; Bilirubin Normal; Albumin Stable and within normal limits; Prothrombin Time Adults less than 3 seconds prolonged; Pediatrics less than or equal to 2 seconds prolonged; WBC Greater than or equal to 4000/mm3; Platelets Adults greater than or equal to 100,000/mm3; Pediatrics greater than or equal to 150,000/mm3; Patients with causes of chronic hepatitis other than chronic hepatitis B or chronic; hepatitis C should not be treated with INTRON A. CBC and platelet counts should be; evaluated prior to initiation of INTRON A therapy in order to establish baselines for; monitoring potential toxicity. These tests should be repeated at treatment Weeks 1, 2,; 4, 8, 12, and 16. Liver function tests, including serum ALT, albumin, and bilirubin,; should be evaluated at treatment Weeks 1, 2, 4, 8, 12, and 16. HBeAg, HBsAg, and; ALT should be evaluated at the end of therapy, as well as 3- and 6-months posttherapy,; since patients may become virologic responders during the 6-month period; following the end of treatment. In clinical studies in adults, 39% (15/38) of responding; patients lost HBeAg 1 to 6 months following the end of INTRON A therapy. Of; responding patients who lost HBsAg, 58% (7/12) did so 1 to 6 months post-treatment.; A transient increase in ALT greater than or equal to 2 times baseline value (flare); can occur during INTRON A therapy for chronic hepatitis B. In clinical trials in adults; and pediatrics, this flare generally occurred 8 to 12 weeks after initiation of therapy and; was more frequent in responders (adults 63%, 24/38; pediatrics 59%, 10/17) than in; nonresponders (adults 27%, 13/48; pediatrics 35%, 19/55). However, in adults and; pediatrics, elevations in bilirubin greater than or equal to 3 mg/dL (greater than or equal; to 2 times ULN) occurred infrequently (adults 2%, 2/86; pediatrics 3%, 2/72) during; therapy. When ALT flare occurs, in general, INTRON A therapy should be continued unless signs and symptoms of liver failure are observed. During ALT flare, clinical; symptomatology and liver function tests including ALT, prothrombin time, alkaline; phosphatase, albumin, and bilirubin, should be monitored at approximately 2-week; intervals (see WARNINGS).
DrugBank Targets:11 1. Interferon alpha/beta receptor 2; 2. Interferon alpha/beta receptor 1
Mechanism of Action:13 
Target: intracellular oncogene expression, natural killer and cytotoxic T-cells, microphage, cytokine production
Action: stimulation, induction (unspecified effects on oncogene expression)
FDA: -
3
Keytruda13 38 PEMBROLIZUMAB Merck Approved September 2014
FDA Label: Keytruda
Malady that Drug Treats: unresectable or metastatic melanoma
Indications and Usage:13 KEYTRUDA is a human programmed death receptor-1 (PD-1)-blocking; antibody indicated for the treatment of patients with unresectable or; metastatic melanoma and disease progression following ipilimumab; and, if BRAF V600 mutation positive, a BRAF inhibitor.; This indication is approved under accelerated approval based on tumor; response rate and durability of response. An improvement in survival; or disease-related symptoms has not yet been established. Continued; approval for this indication may be contingent upon verification and; description of clinical benefit in the confirmatory trials. (1)
DrugBank Targets:11 1. Programmed cell death protein 1
Mechanism of Action:13 
Target: PD-1 receptor
Action: blocks interaction with; PD-L1 and PD-L2
FDA: Binding of the PD-1 ligands, PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibits T cell; proliferation and cytokine production. Upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors.; Pembrolizumab is a monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with; PD-L1 and PD-L2, releasing PD-1 pathway-mediated inhibition of the immune response, including the; anti-tumor immune response. In syngeneic mouse tumor models, blocking PD-1 activity resulted in; decreased tumor growth.
4
Mekinist13 38 TRAMETINIB DIMETHYL SULFOXIDE GlaxoSmithKline Approved May of 2013
FDA Label: Mekinist
Malady that Drug Treats: unresectable or metastatic melanoma with BRAF V600E or V600K mutations
Indications and Usage:13 MEKINIST is a kinase inhibitor indicated as a single agent and in; combination with dabrafenib for the treatment of patients with unresectable or; metastatic melanoma with BRAF V600E or V600K mutations as detected by; an FDA-approved test. The use in combination is based on the demonstration; of durable response rate. Improvement in disease-related symptoms or overall; survival has not been demonstrated for MEKINIST in combination with; dabrafenib. (1, 14.1); Limitation of use: MEKINIST as a single agent is not indicated for treatment; of patients who have received prior BRAF-inhibitor therapy. (1)
DrugBank Targets:11 1. Dual specificity mitogen-activated protein kinase kinase 1; 2. Dual specificity mitogen-activated protein kinase kinase 2
Mechanism of Action:13 
Target: mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of MEK1 and MEK2 kinase
Action: inhibitor
FDA: Trametinib is a reversible inhibitor of mitogen-activated extracellular signal-regulated kinase 1; (MEK1) and MEK2 activation and of MEK1 and MEK2 kinase activity. MEK proteins are; upstream regulators of the extracellular signal-related kinase (ERK) pathway, which promotes; cellular proliferation. BRAF V600E mutations result in constitutive activation of the BRAF; pathway which includes MEK1 and MEK2. Trametinib inhibits BRAF V600 mutation-positive; melanoma cell growth in vitro and in vivo.; Trametinib and dabrafenib target two different tyrosine kinases in the RAS/RAF/MEK/ERK; pathway. Use of trametinib and dabrafenib in combination resulted in greater growth inhibition; of BRAF V600 mutation-positive melanoma cell lines in vitro and prolonged inhibition of tumor; growth in BRAF V600 mutation positive melanoma xenografts compared with either drug alone.
5
Odomzo13 38 SONIDEGIB PHOSPHATE Novartis Jul-15
FDA Label: Odomzo
Malady that Drug Treats: locally advanced basal cell carcinoma
Indications and Usage:13 ODOMZO is a hedgehog pathway inhibitor indicated for the treatment of; adult patients with locally advanced basal cell carcinoma (BCC) that has; recurred following surgery or radiation therapy, or those who are not; candidates for surgery or radiation therapy. (1)
DrugBank Targets: -
Mechanism of Action:13 
Target: Smoothened
Action: inhibitor
FDA: Sonidegib is an inhibitor of the Hedgehog pathway. Sonidegib binds to and inhibits Smoothened, a transmembrane protein; involved in Hedgehog signal transduction.
6
Opdivo13 38 NIVOLUMAB Bristol-Myers Squibb Approved March 2015/ Approved December 2014
FDA Label: Opdivo
Malady that Drug Treats: metastatic squamous non-small cell lung cancer/ unresectable or metastatic melanoma
Indications and Usage:13 OPDIVO is a programmed death receptor-1 (PD-1) blocking antibody; indicated for the treatment of patients with:; unresectable or metastatic melanoma and disease progression following; ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. (1.1); This indication is approved under accelerated approval based on tumor; response rate and durability of response. Continued approval for this; indication may be contingent upon verification and description of clinical; benefit in the confirmatory trials. (1.1, 14.1); metastatic squamous non-small cell lung cancer with progression on or; after platinum-based chemotherapy. (1.2)
DrugBank Targets:11 1. Programmed cell death protein 1
Mechanism of Action:13 
Target: PD-1 receptor
Action: blocker of interaction with PD-L1 and PD-L2
FDA: Binding of the PD-1 ligands, PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibits; T-cell proliferation and cytokine production. Upregulation of PD-1 ligands occurs in some; tumors and signaling through this pathway can contribute to inhibition of active T-cell immune; surveillance of tumors. Nivolumab is a human immunoglobulin G4 (IgG4) monoclonal antibody; that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2, releasing PD-1; pathway-mediated inhibition of the immune response, including the anti-tumor immune; response. In syngeneic mouse tumor models, blocking PD-1 activity resulted in decreased tumor; growth.
7
Proleukin13 38 ALDESLEUKIN Chiron Approved January 1998
FDA Label: Proleukin
Malady that Drug Treats: Metastatic melanoma
Indications and Usage:13 Proleukin® (aldesleukin) is indicated for the treatment of adults with metastatic renal cell; carcinoma (metastatic RCC).; Proleukin is indicated for the treatment of adults with metastatic melanoma.; Careful patient selection is mandatory prior to the administration of Proleukin. See;  CONTRAINDICATIONS ,  WARNINGS and  PRECAUTIONS sections regarding patient; screening, including recommended cardiac and pulmonary function tests and laboratory; tests.; Evaluation of clinical studies to date reveals that patients with more favorable ECOG; performance status (ECOG PS 0) at treatment initiation respond better to Proleukin, with a; higher response rate and lower toxicity (See  CLINICAL PHARMACOLOGY section,;  CLINICAL STUDIES section and  ADVERSE REACTIONS section). Therefore, selection; of patients for treatment should include assessment of performance status.; Experience in patients with ECOG PS >1 is extremely limited.
DrugBank Targets:11 1. Interleukin-2 receptor subunit beta; 2. Interleukin-2 receptor subunit alpha; 3. Cytokine receptor common subunit gamma
Mechanism of Action:13 
Target: human cells
Action: enhancer of immune response and strnaght ( lymphocyte; mitogenesis, growth of human interleukin-2 dependent cell lines, lymphocyte cytotoxicity, induction of killer cell activity and interferon-gamma production)
FDA: Proleukin® (aldesleukin) has been shown to possess the biological activities of human native; interleukin-2.1,2 In vitro studies performed on human cell lines demonstrate the; immunoregulatory properties of Proleukin, including: a) enhancement of lymphocyte; mitogenesis and stimulation of long-term growth of human interleukin-2 dependent cell lines;; b) enhancement of lymphocyte cytotoxicity; c) induction of killer cell (lymphokine-activated; (LAK) and natural (NK)) activity; and d) induction of interferon-gamma production.; The in vivo administration of Proleukin in animals and humans produces multiple; immunological effects in a dose dependent manner. These effects include activation of; cellular immunity with profound lymphocytosis, eosinophilia, and thrombocytopenia, and the; production of cytokines including tumor necrosis factor, IL-1 and gamma interferon. 3 In vivo; experiments in murine tumor models have shown inhibition of tumor growth.4; The exact; mechanism by which Proleukin mediates its antitumor activity in animals and humans is; unknown.
8
Sylatron13 38 PEGINTERFERON ALFA-2B Merck Approved April 2011
FDA Label: Sylatron
Malady that Drug Treats: melanoma
Indications and Usage:13 PegIntron is an antiviral indicated for treatment of Chronic Hepatitis C; (CHC) in patients with compensated liver disease. (1.1)
DrugBank Targets:11 1. Interferon alpha/beta receptor 1; 2. Interferon alpha/beta receptor 2
Mechanism of Action:13 
Target: innate antiviral immune response
Action: inducer
FDA: Pegylated recombinant human interferon alfa-2b is an inducer of the innate antiviral immune response [see Microbiology (12.4)].
9
Tafinlar13 38 DABRAFENIB MESYLATE GlaxoSmithKline Approved May 2013
FDA Label: Tafinlar
Malady that Drug Treats: unresectable or metastatic melanoma with BRAF V600E mutation
Indications and Usage:13  TAFINLAR is a kinase inhibitor indicated as a single agent for the; treatment of patients with unresectable or metastatic melanoma with; BRAF V600E mutation as detected by an FDA-approved test. (1.1, 2.1); TAFINLAR in combination with trametinib is indicated for the treatment; of patients with unresectable or metastatic melanoma with BRAF V600E; or V600K mutations as detected by an FDA-approved test. The use in; combination is based on the demonstration of durable response rate.; Improvement in disease-related symptoms or overall survival has not; been demonstrated for TAFINLAR in combination with trametinib. (1.2,; 2.1, 14.2); Limitation of Use: TAFINLAR is not indicated for treatment of patients with; wild-type BRAF melanoma. (1.3, 5.2)
DrugBank Targets:11 1. Serine/threonine-protein kinase B-raf; 2. RAF proto-oncogene serine/threonine-protein kinase; 3. Serine/threonine-protein kinase SIK1; 4. Serine/threonine-protein kinase Nek11; 5. LIM domain kinase 1
Mechanism of Action:13 
Target: some mutated forms of BRAF kinases, wild-type BRAF and CRAF kinases
Action: inhibitor
FDA: Dabrafenib is an inhibitor of some mutated forms of BRAF kinases with in vitro IC50 values of; 0.65, 0.5, and 1.84 nM for BRAF V600E, BRAF V600K, and BRAF V600D enzymes,; respectively. Dabrafenib also inhibits wild-type BRAF and CRAF kinases with IC50 values of 3.2; and 5.0 nM, respectively, and other kinases such as SIK1, NEK11, and LIMK1 at higher; concentrations. Some mutations in the BRAF gene, including those that result in BRAF V600E,; can result in constitutively activated BRAF kinases that may stimulate tumor cell growth [see; Indications and Usage (1)]. Dabrafenib inhibits BRAF V600 mutation-positive melanoma cell; growth in vitro and in vivo.; Dabrafenib and trametinib target two different tyrosine kinases in the RAS/RAF/MEK/ERK; pathway. Use of dabrafenib and trametinib in combination resulted in greater growth inhibition; of BRAF V600 mutation-positive melanoma cell lines in vitro and prolonged inhibition of tumor; growth in BRAF V600 mutation positive melanoma xenografts compared with either drug alone.
10
Yervoy13 38 IPILIMUMAB Bristol-Myers Squibb Approved March 2011
FDA Label: Yervoy
Malady that Drug Treats: metastatic melanoma
Indications and Usage:13 YERVOY is a human cytotoxic T-lymphocyte antigen 4 (CTLA-4)-blocking; antibody indicated for the treatment of unresectable or metastatic; melanoma. (1)
DrugBank Targets:11 1. Cytotoxic T-lymphocyte protein 4
Mechanism of Action:13 
Target: CTLA-4
Action: blocker of interation with CD80/CD86
FDA: CTLA-4 is a negative regulator of T-cell activity. Ipilimumab is a monoclonal antibody that; binds to CTLA-4 and blocks the interaction of CTLA-4 with its ligands, CD80/CD86. Blockade; of CTLA-4 has been shown to augment T-cell activation and proliferation, including the; activation and proliferation of tumor infiltrating T-effector cells. Inhibition of CTLA-4 signaling; can also reduce T-regulatory cell function, which may contribute to a general increase in T cell; responsiveness, including the anti-tumor immune response.
11
Zelboraf13 38 VEMURAFENIB Roche Approved August of 2011
FDA Label: Zelboraf
Malady that Drug Treats: BRAF + melanoma
Indications and Usage:13 ZELBORAF® is a kinase inhibitor indicated for the treatment of patients with; unresectable or metastatic melanoma with BRAF V600E mutation as detected; by an FDA-approved test. (1, 2.1); Limitation of Use: ZELBORAF is not indicated for treatment of patients with; wild-type BRAF melanoma. (2.1, 5.2)
DrugBank Targets:11 1. Serine/threonine-protein kinase B-raf
Mechanism of Action:13 
Target: some mutated forms of BRAF serinethreonine; kinase
Action: inhibitor
FDA: Vemurafenib is a low molecular weight, orally available inhibitor of some mutated forms of BRAF serinethreonine; kinase, including BRAF V600E. Vemurafenib also inhibits other kinases in vitro such as CRAF,; ARAF, wild-type BRAF, SRMS, ACK1, MAP4K5, and FGR at similar concentrations. Some mutations in the; BRAF gene including V600E result in constitutively activated BRAF proteins, which can cause cell; proliferation in the absence of growth factors that would normally be required for proliferation. Vemurafenib; has anti-tumor effects in cellular and animal models of melanomas with mutated BRAF V600E.

Drug clinical trials:

Search ClinicalTrials for Melanoma

Search NIH Clinical Center for Melanoma

Inferred drug relations via UMLS61/NDF-RT40:

Genetic Tests for Melanoma

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Anatomical Context for Melanoma

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MalaCards organs/tissues related to Melanoma:

31
Skin, T cells, Lymph node, Endothelial, Lung, Breast, Eye, Liver, Brain, Testes, Bone, Colon, Monocytes, Thyroid, Testis, Neutrophil, Kidney, Prostate, Nk cells, Bone marrow, Pancreas, Myeloid, B cells, Ovary, Cervix, Spinal cord, Small intestine, Pituitary, Heart, Placenta, Whole blood, Retina, Tongue, Pineal, Spleen, Smooth muscle, Adipocyte, Adrenal gland, Uterus

Animal Models for Melanoma or affiliated genes

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MGI Mouse Phenotypes related to Melanoma:

35
idDescriptionMGI Source AccessionScoreTop Affiliating Genes
1MP:000301210.4OTOF, CSPG4, MCAM, PMEL, PIK3CA
2MP:000537610.0RYR1, PIK3CA, MFI2, PMEL, MCAM, IL24

Publications for Melanoma

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Articles related to Melanoma:

(show top 50)    (show all 10308)
idTitleAuthorsYear
1
Pharmacological targeting of guanosine monophosphate synthase suppresses melanoma cell invasion and tumorigenicity. (25909885)
2015
2
Relationship between rate of posterior uveal melanoma flattening following plaque radiotherapy and GEP class of tumor cells. (24408979)
2014
3
Thermal sensitisation by lonidamine of human melanoma cells grown at low extracellular pH. (24295212)
2013
4
Melanoma of the sellar region mimicking pituitary adenoma. (22624497)
2013
5
Ocular immune privilege and ocular melanoma: parallel universes or immunological plagiarism? (22707951)
2012
6
RIN1 exhibits oncogenic property to suppress apoptosis and its aberrant accumulation associates with poor prognosis in melanoma. (22627834)
2012
7
PTEN loss confers BRAF inhibitor resistance to melanoma cells through the suppression of BIM expression. (21317224)
2011
8
Increases in serum TARC/CCL17 levels are associated with progression-free survival in advanced melanoma patients in response to dendritic cell-based immunotherapy. (19421847)
2009
9
MicroRNA-137 targets microphthalmia-associated transcription factor in melanoma cell lines. (18316599)
2008
10
PP2A activity is controlled by methylation and regulates oncoprotein expression in melanoma cells: a mechanism which participates in growth inhibition induced by chloroethylnitrosourea treatment. (18097542)
2008
11
Human high molecular weight-melanoma-associated antigen: utility for detection of metastatic melanoma in sentinel lymph nodes. (18519770)
2008
12
Polymorphisms of TP53 Arg72Pro, but not p73 G4C14>A4TA4 and p21 Ser31Arg, contribute to risk of cutaneous melanoma. (18049450)
2008
13
Involvement of E-cadherin, beta-catenin, Cdc42 and CXCR4 in the progression and prognosis of cutaneous melanoma. (17970806)
2007
14
Phase I trial of BAY 50-4798, an interleukin-2-specific agonist in advanced melanoma and renal cancer. (17545537)
2007
15
Genetic testing for melanoma predisposition: current challenges. (18025917)
2007
16
Phenotypic and functional changes of human melanoma xenografts induced by DNA hypomethylation: immunotherapeutic implications. (16252259)
2006
17
A collision tumor involving Basal cell carcinoma and lentigo maligna melanoma. (16121053)
2005
18
Effect of exogenous wild-type p53 on melanoma cell death pathways induced by irradiation at different linear energy transfer. (16409115)
2005
19
Transforming growth factor-beta and malignant melanoma: molecular mechanisms. (15953371)
2005
20
Unilateral conjunctival-corneal argyrosis simulating conjunctival melanoma. (14557191)
2003
21
Hypoxia-inducible factors 1alpha and 2alpha are related to vascular endothelial growth factor expression and a poorer prognosis in nodular malignant melanomas of the skin. (14512791)
2003
22
Ultrasound biomicroscopy in management of malignant iris melanoma. (12742854)
2003
23
A beneficial effect of a short-term formal training course in epiluminescence microscopy on the diagnostic performance of dermatologists about cutaneous malignant melanoma. (12877690)
2003
24
Fibroblast growth factor-2 but not Mel-CAM and/or beta3 integrin promotes progression of melanocytes to melanoma. (12823444)
2003
25
Regulation of CD36 expression in human melanoma cells. (12664607)
2002
26
Ribozyme-mediated attenuation of survivin expression sensitizes human melanoma cells to cisplatin-induced apoptosis. (11805141)
2002
27
Tumor necrosis factor-alpha-promoted expression of Bcl-2 and inhibition of mitochondrial cytochrome c release mediate resistance of mature dendritic cells to melanoma-induced apoptosis. (11300499)
2001
28
Cyclin-dependent kinase inhibitory protein expression in human choroidal melanoma tumors. (10967035)
2000
29
T cell immune responses against melanoma and melanocytes in cancer and autoimmunity. (11041376)
2000
30
ML-IAP, a novel inhibitor of apoptosis that is preferentially expressed in human melanomas. (11084335)
2000
31
Expression of epidermal growth factor receptor: risk factor in uveal melanoma. (10892838)
2000
32
Somatic mutations in the Peutz-Jeghers (LKB1/STKII) gene in sporadic malignant melanomas. (10201537)
1999
33
Expression and targeting of the apoptosis inhibitor, survivin, in human melanoma. (10594755)
1999
34
Relation of TNF-related apoptosis-inducing ligand (TRAIL) receptor and FLICE-inhibitory protein expression to TRAIL-induced apoptosis of melanoma. (10364001)
1999
35
Molecular genetics of familial cutaneous melanoma. (9469357)
1998
36
Development of targeted chemoradiotherapy for malignant melanoma by exploitation of metabolic pathway]. (9612704)
1998
37
Contrasting effects of T cell growth factors on T cell responses to melanoma in vitro. (9067406)
1997
38
Dose efficacy study of two schedules of high-dose bolus administration of interleukin 2 and interferon alpha in metastatic melanoma. (8826864)
1996
39
Familial uveal melanoma: absence of germline mutations involving the cyclin-dependent kinase-4 inhibitor gene (p16). (8740697)
1996
40
Interferon system defects in human malignant melanoma. (7664286)
1995
41
Stimulation of glycosphingolipid biosynthesis by L-threo-1-phenyl-2-decanoylamino-1-propanol and its homologs in B16 melanoma cells. (7592537)
1995
42
Transfection of human melanoma cells with type I interleukin-1 (IL-1) receptor cDNA rendered them IL-1-responsive and revealed the importance of ODC activity down-regulation in IL-1-induced growth inhibition. (8576096)
1995
43
Estramustine binding protein in primary tumours and metastases of malignant melanoma. (7703721)
1994
44
Two mechanisms of iron uptake from transferrin by melanoma cells. The effect of desferrioxamine and ferric ammonium citrate. (1629195)
1992
45
Neuron specific enolase (NSE) in serum of patients with malignant melanoma. (2354416)
1990
46
Effects of tumor promoters on adenylate cyclase activity in melanoma cells in culture. (2244938)
1990
47
Paraneoplastic syndromes, tumor markers, and other unusual features of malignant melanoma. (2869074)
1986
48
Malignant melanomas causing Horner's syndrome in a horse. (3948837)
1986
49
Acral lentiginous melanoma in situ. (7122752)
1982
50
Osseous choristoma of the choroid simulating a choroidal melanoma. Association with a positive 32P test. (697626)
1978

Variations for Melanoma

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Clinvar genetic disease variations for Melanoma:

5
id Gene Variation Type Significance SNP ID Assembly Location
1RYR1NM_000540.2(RYR1): c.487C> T (p.Arg163Cys)single nucleotide variantPathogenic, risk factorrs118192161GRCh37Chr 19, 38934851: 38934851
2PIK3CANM_006218.2(PIK3CA): c.1633G> A (p.Glu545Lys)single nucleotide variantPathogenicrs104886003GRCh37Chr 3, 178936091: 178936091
3OTOFNM_194248.2(OTOF): c.2887C> T (p.Arg963Ter)single nucleotide variantPathogenicrs80356595GRCh37Chr 2, 26698886: 26698886

Expression for genes affiliated with Melanoma

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Search GEO for disease gene expression data for Melanoma.

Pathways for genes affiliated with Melanoma

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Pathways related to Melanoma according to GeneCards Suite gene sharing:

idSuper pathways (with members indented)ScoreTop Affiliating Genes
1
Show member pathways
IL23-mediated signaling events36
Immune response IL 10 signaling pathway59
Angiopoietin receptor Tie2-mediated signaling36
Development PDGF signaling via STATs and NF kB59
Development Angiopoietin Tie2 signaling59
10.4IL24, CXCL1, PIK3CA

Compounds for genes affiliated with Melanoma

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Sources:
44Novoseek
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Compounds related to Melanoma according to GeneCards Suite gene sharing:

idCompoundScoreTop Affiliating Genes
1rantes4410.4CD63, CXCL1, MRPL28
2hemocyanin4410.3MAGEA3, PMEL
3ethidium bromide4410.1MAGEA1, MAGEA3

GO Terms for genes affiliated with Melanoma

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Biological processes related to Melanoma according to GeneCards Suite gene sharing:

idNameGO IDScoreTop Affiliating Genes
1melanin biosynthetic processGO:004243810.4SLC45A2, PMEL

Sources for Melanoma

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2CDC
12ExPASy
13FDA
14FMA
22GTR
23HGMD
24HMDB
25ICD10
26ICD10 via Orphanet
27ICD9CM
28IUPHAR
29KEGG
33MeSH
34MESH via Orphanet
35MGI
38NCI
39NCIt
40NDF-RT
43NINDS
44Novoseek
46OMIM
47OMIM via Orphanet
51PubMed
52QIAGEN
57SNOMED-CT via Orphanet
61UMLS
62UMLS via Orphanet