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PAR-1 AND MASPIN
Protease activated receptor-1 (PAR-1) inhibits the Maspin tumor-suppressor gene to determine the melanoma metastatic phenotype.
Source: Villares GJ, Proc Natl Acad Sci USA 2011, 108:626-31.
The histone variant macroH2A suppresses melanoma progression through regulation of CDK8.
Source: Kapoor A, Nature 2010, 468:1105-9.
CXCL9 induces chemotaxis, chemorepulsion and endothelial barrier disruption through CXCR3-mediated activation of melanoma cells.
Source: Amatschek S, Br J Cancer 2011, 104:469-79.
In this meta-analysis of randomized controlled trials, excision margins affect both disease-free and disease-specific survival, which questions the common belief that narrow excision margins are as safe as wide margins in the management of primary melanoma.
Source: Mocellin S, Ann Surg 2011, 253:238-43.
The dual PI3K/mTOR inhibitor NVP-BEZ235 is highly active in melanoma cells in vitro, suggesting that concurrent PI3K and mTOR targeting in melanoma warrants further investigation.
Source: Aziz SA, Clin Cancer Res 2010, 16:6029-39.
NODAL AND NOTCH4
Regulation of the embryonic morphogen Nodal by Notch4 facilitates manifestation of the aggressive melanoma phenotype.
Source: Hardy KM, Cancer Res 2010, 70:10340-50.
BRAF INHIBITOR RESISTANCE
Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K.
Source: Villanueva J, Cancer Cell 2010, 18:683-95.
CXCL10 reduces melanoma proliferation and invasiveness in vitro and in vivo.
Source: Antonicelli F, Br J Dermatol 2011, 164:720-8.
RASSF1A suppresses melanoma development by modulating apoptosis and cell cycle progression.
Source: Yi M, J Cell Physiol 2010, Epub ahead of print.
Rb-Raf-1 interaction disruptor RRD-251 induces apoptosis in metastatic melanoma cells and synergizes with dacarbazine.
Source: Singh S, Mol Cancer Ther 2010, 9:3330-41.
PROTEOMICS AND SYSTEMS BIOLOGY
A systems biology analysis of metastatic melanoma using in-depth three-dimensional protein profiling provides novel insights into cellular pathways implicated in melanoma metastasis.
Source: Han MJ, Proteomics 2010, 10:4450-62.
Molecular upstaging based on paraffin-embedded sentinel lymph nodes confirms prognostic utility in melanoma patients.
Source: Nicholl MB, Ann Surg 2011, 253:116-22
In a randomized trial, Australian people using daily sunscreen resulted at lower risk of invasive melanoma as compared to those using sunscreen discretionarily.
Source: Green AC, J Clin Oncol 2011, 29:257-63
High PTP4A3 phosphatase expression correlates with metastatic risk in uveal melanoma patients.
Source: Laurent C, Cancer Res 2011, 71:666-74
MENIN: NEW MELANOMA SUPPRESSOR
Menin represses malignant phenotypes of melanoma through regulating multiple pathways.
Source: Gao SB, J Cell Mol Med 2010, Epub ahead of print
C-KIT AND MELANOMA RISK
A variant in a microRNA complementary site in the 3' UTR of the KIT oncogene increases risk of acral melanoma.
Source: Godshalk SE, Oncogene 2011, 30:1542-50
LYMPH NODE RATIO
Lymph node ratio provides prognostic information in addition to american joint committee on cancer N stage in patients with melanoma, even if quality of surgery is standardized.
Source: Spillane AJ, Ann Surg 2011; 253:109-15
PHASE III TRIAL OF IPILIMUMAB + DTIC
Ipilimumab (anti-CTLA4 antibody) in combination with dacarbazine, as compared with dacarbazine plus placebo, improved overall survival in patients with previously untreated metastatic melanoma (n=502).
Source: Robert C, N Engl J Med 2011, Epub ahead of print.
PHASE III TRIAL OF VEMURAFENIB
Vemurafenib (PLX4032, BRAF inhibitor) produced improved rates of overall and progression-free survival in patients with previously untreated metastatic melanoma with the BRAF V600E mutation.
Source: Chapman PB, N Engl J Med 2011, Epub ahead of print.
PHASE III TRIAL OF VACCINE + IL2
In patients with advanced melanoma (n=185), the response rate was higher and progression-free survival longer with gp100 vaccine and interleukin-2 (IL2) than with IL2 alone.
Source: Schwartzentruber DJ, N Engl J Med 2011, 364:2119-27.
PHASE II TRIAL OF DASATINIB
Dasatinib (inhibitor of c-Kit, PDGFR, EPHA2, c-Src, c-Yes, Lck and Fyn) has minimal activity in unselected patients (n=36) with advanced melanoma, and is poorly tolerated.
Source: Kluger HM, Cancer 2011, Epub ahead of print.
Intronic miR-211 assumes the tumor suppressive function of its host gene (melastatin) in melanoma.
Source: Levy C, Mol Cell 2010, 40:841-9.
Melanoma cells express ICOS ligand to promote the activation and expansion of T-regulatory cells.
Source: Martin-Orozco N, Cancer Res 2010, 70:9581-90.
In a preclinical model, Melanoma-associated Chondroitin Sulfate Proteoglycan (MCSP)-targeted delivery of soluble TRAIL potently inhibits melanoma outgrowth in vitro and in vivo.
Source: de Bruyn M, Mol Cancer 2010, 9:301.
LONG TERM RESPONSE
Sensitivity to apoptosis may be a major determinant of long-term responses of B-RAF(V600E) melanomas to specific inhibitors (e.g. PLX4720) and rebound melanoma growth after initial treatment may not be responsive to MEK inhibitors, but may be susceptible to inhibition of PI3k/Akt pathway.
Source: Jiang CC, Clin Cancer Res 2011, 17:721-30.
TGF-beta-RI kinase inhibitor SD-208 reduces the development and progression of melanoma bone metastases.
Source: Mohammad KS, Cancer Res 2011, 71:175-84.
Out of 186 human uveal melanomas, 83% had somatic mutations in GNAQ or GNA11. In a mouse model, mutations in GNA11 induced spontaneously metastasizing tumors and activated the MAPK pathway.
Source: Van Raamsdonk CD, N Engl J Med 2010, 363:2191-9.
Gene expression profiles of human melanoma cells with different invasive potential reveal TSPAN8 as a novel mediator of invasion.
Source: Berthier-Vergnes O, Br J Cancer 2011, 104:155-65.
STAGING AND SURVEILLANCE
In a meta-analysis of the literature, ultrasonography was superior for detecting lymph node metastases, and PET-CT was superior for the detection of distant metastases in both the staging and surveillance of melanoma patients.
Source: Xing Y, J Natl Cancer Inst 2011, 103:129-42.
MicroRNA miR-196a controls melanoma-associated genes by regulating HOX-C8 expression.
Source: Mueller DW, Int J Cancer 2011, Epub ahead of print.
TARGETED THERAPY ANALYZER
The Targeted Therapy Analyzer (TTA) - the first computational tool for exploring the personalized treatment of melanoma based on the literature data - is now freely available as a new feature of the Melanoma Molecular Map Project (MMMP) website.
Source: TTA_The MMMP Team
MELANOMA PHENOTYPIC HETEROGENEITY
Most melanoma cells appear to retain their tumorigenic potential irrespective of their phenotype: in particular, none of 22 heterogeneously expressed markers (including CD271 and ABCB5) enriched tumorigenic cells.
Source: Quintana E, Cancer Cell 2010, 18:510-23.
Experimental evidence suggests that microRNA 211 acts as a melanoma suppressor gene.
Source: Mazar J, PLoS One 2010, 5:e13779.
VINCRISTINE AND AMPK
Activation of AMP-activated protein kinase is involved in vincristine-induced cell apoptosis in B16 melanoma cell.
Source: Chen MB, J Cell Physiol 2010, Epub ahead of print.
Nitric oxide-modified saquinavir (HIV protease inhibitor) shows cytotoxic and immune-sensitizing properties of in inducible nitric oxide synthase (iNOS)-positive human melanoma cells.
Source: Mijatovic S, J Cell Physiol 2010, Epub ahead of print.
DENDRITIC CELL VACCINE
Wild-type and modified gp100 peptide-pulsed dendritic cell vaccination of advanced melanoma patients can lead to long-term clinical responses independent of the peptide used.
Source: Lesterhuis WJ, Cancer Immunol Immunother 2011, 60:249-60.
In a phase II trial of albumin-bound paclitaxel (ABI-007) plus carboplatin in patients with metastatic melanoma, investigators reported a response rate of 25.6% in chemo-naive (90%CI: 16.7%-42.3%) and 8.8% in previously treated patients (90%CI: 2.5%-21.3%).
Source: Kottschade LA, Cancer 2010, Epub ahead of print.
ING4 AND BRMS1
Cell cycle regulator ING4 is a suppressor of melanoma angiogenesis that is regulated by the metastasis suppressor BRMS1.
Source: Li J, Cancer Res 2010, 70:10445-53.
CXCR4 signaling regulates metastasis of chemoresistant melanoma cells by a lymphatic metastatic niche.
Source: Kim M, Cancer Res 2010, 70:10411-21.
mTOR/PI3K VERTICAL INHIBITION
Vertical inhibition of the mTORC1/mTORC2/PI3K pathway shows synergistic effects against melanoma in vitro and in vivo.
Source: Werzowa J, J Invest Dermatol 2011, 131:495-503.
Silencing HSF1 by short hairpin RNA decreases cell proliferation and enhances sensitivity to hyperthermia in human melanoma cell lines.
Source: Nakamura Y, J Dermatol Sci 2010, 60:187-92.
CTLA4 POLYMORPHISMS AND IFN
No correlation appears to exist between CTLA4 polymorphisms and therapeutic benefit of adjuvant interferon (IFN) alpha.
Source: Gogas H, J Transl Med 2010, 8:108.
TARGETED THERAPY ANALYZER
The MMMP Team is going to launch by the end of March the Targeted Therapy Analyzer (TTA), a free access tool for the personalized treatment of melanoma based on the automated analysis of the data collected in the Targeted Therapy Database.
BEVACIZUMAB + FOTEMUSTINE
In a phase II trial (n=20), a regimen based on bevacizumab plus fotemustine obtained one complete response, 2 partial responses and 10 patients with stable disease.
Source: Del Vecchio M, Clin Cancer Res 2010, 16:5862-72.
Recombinant human arginase inhibits the in vitro and in vivo proliferation of human melanoma by inducing cell cycle arrest and apoptosis.
Source: Lam TL, Pigment Cell Melanoma Res 2010, Epub ahead of print.
Plexin B1 inhibits integrin-dependent pp125FAK and Rho activity in melanoma.
Source: McClelland L, Pigment Cell Melanoma Res 2011, 24:165-74.
mTOR AND PROGNOSIS
mTOR pathway activation in cutaneous melanoma is associated with poorer prognosis characteristics.
Source: Populo H, Pigment Cell Melanoma Res 2011, 24:254-7.
In a preclinical melanoma model, tumorigenic circulating tumor cells (CTC) could be isolated from the peripheral blood using the ABCB5 marker.
Source: Ma J, Biochem Biophys Res Commun 2010, 402:711-7.
The antimicrobial peptide human cationic antimicrobial protein-18/cathelicidin LL-37 acts as a putative growth factor for malignant melanoma.
Source: Kim JE, Br J Dermatol 2010, 163:959-67.
TRAIL GENE THERAPY
Efficient melanoma cell killing and reduced melanoma growth was observed in mice using a selective replicating adenovirus armed with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
Source: Fecker LF, Hum Gene Ther 2011, Epub ahead of print.
IMATINIB + VATALANIB
Combination therapy using imatinib and vatalanib improves the therapeutic efficiency of paclitaxel towards a mouse melanoma model.
Source: Klosowska-Wardega A, Melanoma Res 2010, Epub ahead of print.
Berberine, an isoquinoline alkaloid, inhibits melanoma cancer cell migration by reducing the expressions of cyclooxygenase-2, prostaglandin E2 and prostaglandin E2 receptors.
Source: Singh T, Carcinogenesis 2011, 32:86-92.
TARGETED THERAPY FINDER
CollabRx introduces the Targeted Therapy Finder — Melanoma: This new, innovative web application uses an advanced molecular model of melanoma to identify laboratory tests and finds treatments targeted to the patient's unique tumor.
BRG1 AND PROGRESSION
Modulation of extracellular matrix/adhesion molecule expression by BRG1 is associated with increased melanoma invasiveness.
Source: Saladi SV, Mol Cancer 2010, 9:280.
In this phase II trial (n=33), although well tolerated, UCN-01 (7-hydroxystaurosporine, a cell cycle inhibitor) as a single agent did not have sufficient clinical activity to warrant further study in refractory metastatic melanoma.
Source: Li T, Invest New Drugs 2010, Epub ahead of print.
Elastin-derived peptides enhance melanoma growth in vivo by upregulating the activation of Mcol-A (MMP-1) collagenase.
Source: Devy J, Br J Cancer 2010, 103:1562-70.
AKT AND AZD6244
Basal and treatment-induced activation of AKT mediates resistance to cell death by AZD6244 (ARRY-142886) in Braf-mutant human cutaneous melanoma cells.
Source: Gopal YN, Cancer Res 2010, 70:8736-47.
In a phase I trial of subcutaneous interleukin-21, the cytokine was well tolerated and showed some antitumor activity in patients with advanced melanoma.
Source: Schmidt H, Clin Cancer Res 2010, 16:5312-9.
MicroRNA-200 family members differentially regulate morphological plasticity and mode of melanoma cell invasion.
Source: Elson-Schwab I, PLoS One 2010, 5(10) pii: e13176.
KLOTHO AND PROGRESSION
Loss of Klotho during melanoma progression leads to increased filamin cleavage, increased Wnt5A expression, and enhanced melanoma cell motility.
Source: Camilli TC, Pigment Cell Melanoma Res 2011, 24:175-86.
LONAFARNIB AND SORAFENIB
The farnesyl transferase inhibitor lonafarnib inhibits mTOR signaling and enforces sorafenib-induced apoptosis in melanoma cells.
Source: Niessner H, J Invest Dermatol 2011, 131:468-79.
siRNA knockdown of ribonucleotide reductase inhibits melanoma cell line proliferation alone or synergistically with temozolomide.
Source: Zuckerman JE, J Invest Dermatol 2011, 131:453-60.
TARGETED THERAPY ADVISOR
Over the next few months the MMMP website is going to provide users with a free access to an unprecedented tool for the personalized treatment of melanoma based on the automated analysis of the data collected in the Targeted Therapy Database.
Source: The MMMP Team.
A novel class of specific Hsp90 small molecule inhibitors (including PF-4470296 and PF-3823863) demonstrate in vitro and in vivo anti-tumor activity in human melanoma cells.
Source: Mehta PP, Cancer Lett 2011, 300:30-9.
In a phase II trial of sagopilone (a novel epothilone analog) in metastatic melanoma, tumor responses were observed even in previously treated patients.
Source: DeConti RC, Br J Cancer 2010, 103:1548-53.
The fibroblast growth factor-2 (FGF-2) derived peptide FREG inhibits melanoma growth by inhibiting FGF-2-dependent angiogenesis.
Source: Aguzzi MS, Mol Ther 2010, Epub ahead of print.
The expression of over 90 genes encoding proteins involved in drug resistance was correlated with melanoma sensitivity to different chemotherapeutics.
Source: Parker KA, J Clin Pathol 2010, 63:1012-20.
IFN-GAMMA AND VACCINE
In this preclinical model, peptide vaccines can eradicate large, established tumors in circumstances under which the inhibitory activities of interferon (IFN) gamma are curtailed.
Source: Cho HI, Blood 2011, 117:135-44.
NESTIN, CD133 AND CTC
In melanoma patients, circulating tumor cells (CTC) express stem cell-associated markers NESTIN and CD133; higher expression of NESTIN on CTC might represent an index of poor prognosis.
Source: Fusi A, J Invest Dermatol 2011, 131:487-94.
CDKN2A MUTATION CARRIERS
MC1R variants, hair color, and number of nevi are jointly associated with melanoma risk in CDKN2A mutation carriers.
Source: Demenais F, J Natl Cancer Inst 2010, 102:1568-83.
hTERTC27 VIRAL COCKTAIL
In C57BL/6 mice, melanoma growth can be inhibited by subcutaneous administration of hTERTC27 (a 27 kDa C-terminal polypeptide of human telomerase reverse transcriptase) viral cocktail that induces NK cell activation.
Source: Huo L, PLoS One 2010, 5:e12705.
CASPASE-3, XIAP AND TRAIL
Caspase-3 cleaves XIAP in a positive feedback loop to sensitize melanoma cells to TRAIL-induced apoptosis.
Source: Hörnle M, Oncogene 2010, Epub ahead of print.
DHA-PACLITAXEL vs DTIC
In a phase III trial of docosahexaenoic acid-paclitaxel versus dacarbazine in patients with metastatic malignant melanoma, no significant survival difference was found.
Source: Bedikian AY, Ann Oncol 2010, Epub ahead of print.
Metalloproteinase ADAM15 is downregulated in melanoma metastasis compared to primary melanoma.
Source: Ungerer C, Biochem Biophys Res Commun 2010, 401:363-9.
ALPHAVIRUS REPLICON PARTICLES
Alphavirus replicon particles expressing TRP-2 provide potent therapeutic effect on melanoma through activation of humoral and cellular immunity.
Source: Avogadri F, PLoS One 2010, 5: e12670.
MicroRNA miR-125b is downregulated in primary cutaneous melanomas that produced early metastases (T2, N1, M0) compared with the sentinel lymph node-negative (T2, N0, M0) melanomas.
Source: Glud M, Melanoma Res 2010, 20:479-84.
EMMPRIN promotes melanoma cells malignant properties through a HIF-2 alpha mediated upregulation of VEGF-receptor-2.
Source: Bougatef F, PLoS One 2010, 5:e12265.
PLX4032 STRIKING ANTI-MELANOMA ACTIVITY
In a phase I-II trial (n=82), treatment of metastatic melanoma carrying the V600E BRAF mutation with PLX4032 (also known as RG7204, an orally available inhibitor of mutated BRAF), resulted in complete or partial tumor regression in the majority of patients.
Source: Flaherty KT, N Engl J Med 2010, 363:809-19.
PLX4720 IN MUTANT N-RAS MELANOMA
In mutant N-RAS melanoma cells, PLX4720 (inhibitor of oncogenic B-RAF) can induce hyperactivation of MEK-ERK1/2 signaling and resistance to apoptosis.
Source: Kaplan FM, Oncogene 2010, Epub ahead of print.
Monoclonal antibody C11C1 targeting domain 5 of high molecular weight kininogen inhibits metastasis of syngeneic murine melanoma in vivo and vasculogenesis in vitro.
Source: Khan ST, Cancer Immunol Immunother 2010, 59:1885-93.
NUCLEOTIDE EXCISION REPAIR (NER)
Cisplatin-induced DNA damage is recognized and repaired by the NER pathway; NER genes are upregulated in melanoma, which might explain cisplatin resinstance.
Source: Bowden NA, Cancer Res 2010, 70:7918-26.
Anti-apoptotic factor survivin enhances motility of melanoma cells by supporting AKT/PKB activation and integrin-alpha-5 upregulation.
Source: McKenzie JA, Cancer Res 2010, 70:7927-37.
CREB AND AP-2 ALPHA
CREB inhibits AP-2alpha expression to promote the malignant phenotype of melanoma.
Source: Melnikova VO, PLoS One 2010, 5:e12452.
FATTY ACID SYNTHASE
Inhibition of fatty acid synthase (FASN) in melanoma cells activates the intrinsic pathway of apoptosis.
Source: Zecchin KG, Lab Invest 2010, Epub ahead of print.
In a murine in vivo model, a novel melanoma-targeting peptide screened by phage display exhibits antitumor activity.
Source: Matsuo AL, J Mol Med 2010, 88:1255-64.
CHEST X-RAY AND FOLLOW-UP
In this study the routine use of surveillance CXR did not provide clinically useful information in the follow-up of patients with melanoma.
Source: Brown RE, Surgery 2010, 148:711-6.
VATALANIB CLINICAL TRIAL
In a phase 2 trial in metastatic melanoma patients, Vatalanib stabilized disease in a proportion of patients, although overall survival was disappointing.
Source: Cook N, Eur J Cancer 2010, 46:2671-3.
ALDH POSITIVE CELLS
Aldehyde dehydrogenase (ALDH) positive melanoma cells have enhanced tumorigenicity over ALDH negative cells and superior self-renewal ability.
Source: Boonyaratanakornkit JB, J Invest Dermatol 2010, 130:2799-808.
ULCERATION AND IFN-ALPHA
Adjuvant interferon (IFN) was a significant independent predictor of survival among patients with ulcerated primary melanoma, but not among patients without ulceration, which suggests that ulceration might be a marker of responsiveness to IFN.
Source: McMasters KM, Ann Surg 2010, 252:460-5.
SMAD7 restricts melanoma invasion by restoring N-cadherin expression and establishing heterotypic cell-cell interactions in vivo.
Source: DiVito KA, Pigment Cell Melanoma Res 2010, 23:795-808.
MGMT gene promoter methylation correlates with tolerance of temozolomide treatment in melanoma but not with clinical outcome.
Source: Hassel JC, Br J Cancer 2010, 103:820-6.
Tenascin-C promotes melanoma progression by maintaining the ABCB5-positive side population.
Source: Fukunaga-Kalabis M, Oncogene 2010, 29:6115-24.
PTEN AND RAS
PTEN inactivation can drive the genesis and promote the metastatic progression of RAS-activated Ink4a/Arf-deficient melanomas.
Source: Nogueira C, Oncogene 2010, 29:6222-32.
PIRIN AND MIGRATION
A small-molecule inhibitor (triphenyl compound) shows that pirin (nuclear protein of unknown function) regulates migration of melanoma cells.
Source: Miyazaki I, Nat Chem Biol 2010, 6:667-73.
PHX-3 PRECLINICAL ACTIVITY
2-aminophenoxazine-3-one (Phx-3) prevents pulmonary metastasis of mouse B16 melanoma cells in mice, likely by activating both intrinsic and extrinsic apoptotic pathways.
Source: Hongo T, J Pharmacol Sci 2010, 114:63-8.
CASEIN KINASE 1 ALPHA
Suppression of casein kinase 1 alpha in melanoma cells induces a switch in beta-catenin signaling to promote metastasis.
Source: Sinnberg T, Cancer Res 2010, 70:6999-7009.
Methyl sulfone induces loss of metastatic properties and reemergence of normal phenotypes in a metastatic cloudman S-91 (M3) murine melanoma cell line.
Source: Caron JM, PLoS One 2010, 5:e11788.
A Phase II trial of 17-AAG (tanespimycin, a HSP90 inhibitor) in patients with metastatic melanoma was prematurely interrupted due to drug inefficacy.
Source: Pacey S, Invest New Drugs 2010, Epub ahead of print.
TYROSINE PHOSPHATASE INHIBITOR
Tyrosine phosphatase inhibitor-3 sensitizes melanoma and colon cancer to biotherapeutics and chemotherapeutics.
Source: Kundu S, Mol Cancer Ther 2010, 9:2287-96.
Sunbed use during adolescence and early adulthood is associated with increased risk of early-onset melanoma.
Source: Cust AE, Int J Cancer 2010, Epub ahead of print.
MMP13 AND CELL CYCLE
In vitro studies of migration and proliferation show that matrix metallo-proteinase-13 (MMP13) mediates cell cycle progression in melanocytes and melanoma cells.
Source: Meierjohann S, Mol Cancer 2010, 9:201.
KLF6 MELANOMA SUPPRESSOR
In melanoma cells, the tumor suppressor gene at 10p15 appears to be KLF6. Signaling from the collagen I-rich extracellular matrix appears to be involved in the tumor suppressive activity of KLF6.
Source: Huh SJ, J Natl Cancer Inst 2010, 102:1131-47.
TGFB AND GLI2
GLI2, a mediator of the Hedgehog pathway, is as a transcriptional target of TGF-beta signaling and is directly involved in driving melanoma metastasis in this preclinical study.
Source: Alexaki VI, J Natl Cancer Inst 2010, 102:1148-59.
Polymorphisms of the matrix metallopeptidase 1 gene have been associated with the risk of developing melanoma.
Source: Wang LE, Eur J Cancer 2010, Epub ahead of print.
In human xenograft model, investigators could obtain the inhibition of melanoma angiogenesis by using telomere homolog oligonucleotides.
Source: Coleman C, J Oncol 2010; 2010:928628.
The EphB4 receptor promotes the growth of melanoma cells expressing the ephrin-B2 ligand.
Source: Yang NY, Pigment Cell Melanoma Res 2010, 23:684-7.
AKT AND MUTATED BRAF
Intrinsically resistant metastatic melanoma cells displayed elevated Akt phosphorylation and were rendered susceptible to PLX4720 by Akt3 knockdown.
Source: Shao Y, Cancer Res 2010, 70:6670-81.
miR-148 AND MITF
miR-148 regulates MITF expression in melanocytes and melanoma cells: loss of this regulation, either by mutations or by shortening of the 3'UTR sequence, might promote melanoma formation and/or progression.
Source: Haflidadottir BS, PLoS One 2010, 5:e11574.
Nitrogen-containing bisphosphonate, YM529/ONO-5920, inhibits tumor metastasis in mouse melanoma through suppression of the Rho/ROCK pathway.
Source: Tanimori Y, Clin Exp Metastasis 2010, 27:529-38.
In a European-Australian case-control study, interferon regulatory factor 4 (IRF4) variants have age-specific effects on nevus count and predispose to melanoma.
Source: Duffy DL, Am J Hum Genet 2010, 87:6-16.
Targeting glutamine metabolism sensitizes some melanoma cell lines to TRAIL-induced death in vitro.
Source: Qin JZ, Biochem Biophys Res Commun 2010, 398:146-52.
Monoclonal antibodies targeting basic fibroblast growth factor (bFGF) inhibit the growth of B16 melanoma in vivo and in vitro.
Source: Li D, Oncol Rep 2010, 24:457-63.
CIGLITAZONE AND CXCL1
Ciglitazone (a well known PPARgamma agonist) negatively regulates CXCL1 signaling through MITF to suppress melanoma growth.
Source: Botton T, Cell Death Differ 2010, Epub ahead of print.
MELANOMA INITIATING CELLS
Human melanoma-initiating cells express neural crest nerve growth factor receptor CD271; they rarely express TYR, MART1 and MAGE, which might explain the failure of immunotherapies directed against these antigens.
Source: Boiko AD, Nature 2010, 466:133-7.
S100B, LDH AND SENTINEL NODE STATUS
Serum S100B and LDH are not useful in predicting the sentinel node status in melanoma patients (n=259).
Source: Egberts F, Anticancer Res 2010, 30:1799-805.
JNK AND DOXYCYCLINE
Activation of c-Jun N-terminal kinase is essential for mitochondrial membrane potential change and apoptosis induced by doxycycline in melanoma cells.
Source: Shieh JM, Br J Pharmacol 2010, 160:1171-84.
S100B AND P53
The calcium-binding protein S100B down-regulates p53 and apoptosis in malignant melanoma.
Source: Lin J, J Biol Chem 2010, 285:27487-98.
R-RAS AND MIGRATION
R-Ras regulates migration through an interaction with filamin A in melanoma cells.
Source: Gawecka JE, PLoS One 2010, 5:e11269.
Ganglioside GD3 enhances adhesion signals and augments malignant properties of melanoma cells by recruiting integrins to glycolipid-enriched microdomains.
Source: Miyazaki S, J Biol Chem 2010, 285:27213-23.
CURCUMIN ANALOG FLLL32
The small molecule curcumin analog FLLL32 induces apoptosis in melanoma cells via STAT3 inhibition and retains the cellular response to cytokines with anti-tumor activity.
Source: Bill MA, Mol Cancer 2010, 9:165.
SORAFENIB AND REGIONAL CHEMO
In an animal model of regional chemotherapy, sorafenib in combination with melphalan or temozolomide was more effective than either treatment alone in slowing tumor growth.
Source: Augustine CK, Mol Cancer Ther 2010, 9:2090-101.
NMB AND IMMUNITY
DC-HIL/glycoprotein Nmb promotes growth of melanoma in mice by inhibiting the activation of tumor-reactive T cells.
Source: Tomihari M, Cancer Res 2010, 70:5778-87.
RESVERATROL AND CHEMORESISTANCE
In a murine model, resveratrol induces cell cycle disruption and apoptosis in chemoresistant B16 melanoma.
Source: Gatouillat G, J Cell Biochem 2010, 110:893-902.
BEVACIZUMAB PLUS EVEROLIMUS
In a phase II trial, bevacizumab (anti-VEGF antibody) plus everolimus (anti-mTOR drug) was found to have moderate activity and was well tolerated in the treatment of patients with metastatic melanoma.
Source: Hainsworth JD, Cancer 2010, 116:4122-9.
BORTEZOMIB PLUS CHEMO
In a phase II trial, proteasome inhibitor bortezomib combined with paclitaxel and carboplatin showed no clinical activity against metastatic melanoma.
Source: Croghan GA, Cancer 2010, 116:3463-8.
In the so far largest study (n=252), desmoplastic melanoma was associated with lower sentinel node positivity rate, but the combined type was associated with worse prognosis.
Source: Murali R, Cancer 2010, 116:4130-8.
IMEXON PLUS DTIC
In a phase I-II trial, imexon (a reactive oxygen species - ROS - generator) plus dacarbazine was associated with 30% disease stabilization rate; encouraging survival data suggest further evaluation.
Source: Weber JS, Cancer 2010, 116:3683-91.
RG7204, a selective BRAFV600E inhibitor, displays potent antitumor activity in preclinical melanoma models (including melanoma xenograft).
Source: Yang H, Cancer Res 2010, 70:5518-27.
EPAC AND MIGRATION
Exchange protein directly activated by cyclic AMP increases melanoma cell migration by a Ca2+-dependent mechanism and is a potential target to suppress melanoma metastasis.
Source: Baljinnyam E, Cancer Res 2010, 70:5607-17.
BRAF-V600E AND IMMUNITY
Selective BRAFV600E inhibition enhances T-cell recognition of melanoma without affecting lymphocyte function.
Source: Boni A, Cancer Res 2010, 70:5213-9.
HLA AND PROGNOSIS
Among high-risk melanoma patients receiving adjuvant interferon alpha (IFN), HLA-Cw 06-positive patients have better relapse-free and overall survival.
Source: Gogas H, Cancer 2010, 116:4326-33.
VITAMIN A CHEMOSENSITIZATION
Vitamin A enhances antitumor effect of a green tea polyphenol on melanoma by upregulating the polyphenol sensing molecule 67-kDa laminin receptor.
Source: Lee JH, PLoS One 2010, 5:e11051.
PNPase AND miRNA221
Targeted overexpression of human polynucleotide phosphorylase (hPNPase) might provide an effective therapeutic strategy for miR-221-overexpressing and interferon(IFN)-resistant melanoma.
Source: Das SK, Proc Natl Acad Sci USA 2010, 107:11948-53.
In an in vitro model, downregulation of GRP78 by small-interfering RNA increased fenretinide- or bortezomib-induced apoptosis.
Source: Martin S, Pigment Cell Melanoma Res 2010, 23:675-82
TRAIL GENE THERAPY
Radiation-inducible human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) gene therapy is a potential treatment for radioresistant uveal melanoma.
Source: Zhou Y, Pigment Cell Melanoma Res 2010, 23:661-74
QUERCETIN AND CHEMORESISTANCE
In an in vitro model, quercetin abrogates chemoresistance in melanoma cells by modulating deltaNp73.
Source: Thangasamy T, BMC Cancer 2010, 10:282
LONG-TERM SURVIVAL (LTS)
LTS can occur in select patients who achieve a complete response to chemotherapy: however, this occurs in only a minority of patients and is likely the result of indolent disease biology.
Source: Kim C, Oncologist 2010, 15:765-71
CTC ISOLATION BY SIZE
Isolation of circulating tumor cells based on cell size is feasible not only in patients with epithelial cancers but also in those with melanoma.
Source: De Giorgi V, J Invest Dermatol 2010, 130:2440-7
The MDM2 SNP309 is not associated with the risk and age of onset of melanoma, but might be a risk genotype for increased tumor Breslow thickness.
Source: Capasso M, J Hum Genet 2010, 55:518-24
CHEMICAL EXPOSURE AND MELANOMA RISK
In a case-control study, exposure to polychlorinated biphenyls is associated with high risk of melanoma (OR: 7.02; 95% CI: 2.30-21.43 for highest quartile) even after controlling for sun exposure.
Source: Gallagher RP, Int J Cancer 2010, Epub ahead of print
In an in vitro study, combined BRAF/MEK inhibition results an effective strategy to prevent the emergence of drug resistance in BRAF-V600E-mutated melanomas.
Source: Paraiso KH, Br J Cancer 2010, 102:1724-30.
Screening a large cohort of patients showed that, although rare, recurrent rearrangements in the RAF pathway tend to occur in prostate cancer, gastric cancer and melanoma, suggesting that RAF and MEK inhibitors may be useful in a subset of gene fusion-harboring solid tumors.
Source: Palanisamy N, Nat Med 2010, 16:793-8.
High-throughput miRNA profiling showed that blood samples of melanoma patients and healthy individuals can be well differentiated from each other based on miRNA expression analysis.
Source: Leidinger P, BMC Cancer 2010, 10:262.
In mice, mutant HRas initiation of tumorigenesis requires IKKbeta-mediated NFKB activity (ablation of IKKB inhibits melanoma development).
Source: Yang J, J Clin Invest 2010, 120:2563-74.
The new alpha,beta-unsaturated ketone D6 is more effective in inhibiting melanoma cells growth when compared to curcumin.
Source: Pisano M, Mol Cancer 2010, 9:137.
A case-control study shows that, in a highly exposed population, frequent indoor tanning increases melanoma risk, regardless of age when indoor tanning begins.
Source: Lazovich D, Cancer Epidemiol Biomarkers Prev 2010, 19:1557-68.
Aldehyde dehydrogenase (ALDH) activity does not distinguish tumor-initiating and/or therapy-resistant melanoma cells.
Source: Prasmickaite L, PLoS One 2010, 5:e10731.
The glutamate release inhibitor Riluzole decreases migration, invasion, and proliferation of melanoma cells.
Source: Le MN, J Invest Dermatol 2010, 130:2240-9.
JARID1B POSITIVE MELANOMA CELLS
Using the H3K4 demethylase JARID1B as biomarker, investigators have characterized a small subpopulation of slow-cycling melanoma cells required for continuous tumor growth.
Source: Roesch A, Cell 2010, 141:583-94.
NUCLEOTIDE EXCISION REPAIR
Melanoma cells retain capacity for nucleotide excision repair (NER), the loss of which probably does not commonly contribute to melanoma progression.
Source: Gaddameedhi S, Cancer Res 2010, 70:4922-30.
In a mouse melanoma model, Tumor cells disseminate early, but immunosurveillance limits metastatic outgrowth, reinforcing the theory that immune responses favor dormancy of disseminated tumor cells.
Source: Eyles J, J Clin Invest 2010, 120:2030-9.
MTAP AND INTERFERON
Expression of methylthioadenosine phosphorylase (MTAP) might represent a predictive marker for response to adjuvant interferon therapy in patients with skin melanoma.
Source: Meyer S, Exp Dermatol 2010, 19:e251-7.
TARGETING RAP1 GTPase
Preventing the activation or cycling of the Rap1 GTPase alters adhesion and cytoskeletal dynamics and blocks metastatic melanoma cell extravasation into the lungs.
Source: Freeman SA, Cancer Res 2010, 70:4590-601.
FOLLOW-UP FOR STAGE III MELANOMA
Based on the analysis of retrospective data, investigators suggest new guidelines for the follow up of patients with stage III melanoma.
Source: Romano E, J Clin Oncol 2010, 28:3042-7.
Serum levels of anti-BPAG1 auto-antibodies are higher in melanoma patients than in healthy volunteers and thus are proposed as novel melanoma diagnostic marker.
Source: Shimbo T, PLoS One 2010, 5:e10566.
SHIELDS PROGNOSTIC INDEX
The Shields index, a non-invasive analysis based on immunohistochemistry of lymphatics surrounding primary lesions, is proposed to predict outcome of melanoma patients.
Source: Emmett MS, BMC Cancer 2010, 10:208.
PLK1 INHIBITOR BI-2536
In a phase II trial of polo-like kinase 1 inhibitor BI 2536, no objective tumor response was observed in patients with different types of metastatic cancer, including melanoma.
Source: Schoffski P, Eur J Cancer 2010, 46:2206-15.
TOPOISOMERASE I AMPLIFICATION
Topoisomerase I amplification in melanoma is associated with more advanced tumours and poor prognosis.
Source: Ryan D, Pigment Cell Melanoma Res 2010, 23:542-53.
NOVEL SMAC MIMETICS
Novel SMAC-mimetics synergistically stimulate melanoma cell death in combination with TRAIL and Bortezomib.
Source: Lecis D, Br J Cancer 2010, 102:1707-16.
CHIMERIC ANTIGEN RECEPTORS (CAR)
Designer T cells with second generation GD3-specific CAR plus systemic interleukin-2 (IL2) can eradicate subcutaneous established GD3+ melanoma in nude mice.
Source: Lo AS, Clin Cancer Res 2010, 16:2769-80.
The NK-1 receptor is expressed by human melanoma and is involved in the antitumor action of the NK-1 receptor antagonist aprepitant on human melanoma cell lines.
Source: Munoz M, Lab Invest 2010, 90:1259-69.
BEVACIZUMAB + IFNalpha
In a pilot trial, patients with metastatic ocular melanoma were treated with bevacizumab and IFN-alpha, which were well tolerated and showed some clinical activity.
Source: Guenterberg KD, Am J Clin Oncol 2010, Epub ahead of print.
Agonist anti-GITR monoclonal antibody induces melanoma tumor immunity in mice by altering regulatory T cell (Treg) stability and intra-tumor accumulation.
Source: Cohen AD, PLoS One 2010, 5:e10436.
The findings of a pharmacodynamic (phase 0) study using etaracizumab (a monoclonal antibody targeting integrin alpha V beta3) in advanced melanoma have been reported.
Source: Moschos S, J Immunother 2010, 33:316-25.
Depletion of CD147 (a cell surface receptor for cyclophilin A) sensitizes human malignant melanoma cells to hydrogen peroxide-induced oxidative stress.
Source: Li J, J Dermatol Sci 2010, 58:204-10.
9.2.27PE (Pseudomonas Exotoxin A) immunotoxin can efficiently cause cell death in malignant melanoma cells independent of their level of resistance to apoptosis and DTIC.
Source: Risberg K, J Immunother 2010, 33:272-8.
TARGETED INTERNAL RADIONUCLIDE THERAPY
Melanin targeting radionuclide therapy with a quinoxaline-derived molecule (ICF01012) has strong anti-tumoral efficacy in pigmented versus unpigmented melanomas.
Source: Bonnet M, Pigment Cell Melanoma Res 2010, Epub ahead of print
NRASQ61R and CRE-RECOMBINASE
Targeted delivery of mutationally activated NRAS (NRASQ61R) and Cre-recombinase to post-natal melanocytes induces melanoma in Ink4a/Arflox/lox mice.
Source: VanBrocklin MW, Pigment Cell Melanoma Res 2010, 23:531-41
microRNA DEREGULATED IN MELANOMA
miRNA-200c is consistently downregulated in melanocytes, melanoma cell lines and patient samples, whereas miRNA-205 and miRNA-23b are markedly reduced only in patient samples. miR-146a and miR-155 are upregulated in all analyzed patients but none of the cell lines.
Source: Philippidou D, Cancer Res 2010, 70:4163-73
In a xenograft model, 131-I-labeled benzamide proved to be effective for targeted radiotherapy of human melanoma.
Source: Joyal JL, Cancer Res 2010, 70:4045-53
MIC-1 AND ANGIOGENESIS
Inhibition of macrophage inhibitory cytokine 1 (MIC-1) retards melanoma tumor vascular development, subsequently affecting tumor cell proliferation and apoptosis.
Source: Huh SJ, Am J Pathol 2010, 176:2948-57
3-bromopyruvate (BrPA) - an inhibitor of glucose metabolism - selectively kills melanoma cells with low levels of glutathione.
Source: Qin JZ, Biochem Biophys Res Commun 2010, 396:495-500
c-RET AND GDNF
Constitutively activated RET-carrying transgenic mice (RET-mice) spontaneously develop malignant melanoma and glial cell line-derived neurotrophic factor (GDNF)-mediated c-RET kinase activation is associated with melanoma pathogenesis.
Source: Ohshima Y, PLoS One 2010, 5:e10279
Disruption of insulin-like growth factor 1 receptot (IGF1R) signaling increases TRAIL-induced apoptosis in human melanoma cell lines.
Source: Karasic TB, Exp Cell Res 2010, 316:1994-2007
IL-24 AND ERLOTINIB
Interleukin-24 (IL-24) gene transfer sensitizes melanoma cells to erlotinib through modulation of the Apaf-1 and Akt signaling pathways.
Source: Deng WG, Melanoma Res 2010, Epub ahead of print
PROTEIN KINASE C ALPHA
RNA interference (RNAi)-mediated knockdown of protein kinase C-alpha (PKC-alpha) inhibits cell migration in MM-RU human metastatic melanoma cell line.
Source: Byers HR, Melanoma Res 2010, 20:171-8
NITRIC OXIDE SYNTHASE INHIBITION
Targeted inhibition of inducible nitric oxide synthase (iNOS)inhibits growth of human melanoma in vivo and synergizes with chemotherapy.
Source: Sikora AG, Clin Cancer Res 2010, 16:1834-44
The COOH-terminal peptide of platelet factor-4 variant (CXCL4L1/PF-4var47-70) strongly inhibits angiogenesis and suppresses B16 melanoma growth in vivo.
Source: Vandercappellen J, Mol Cancer Res 2010, 8:322-34
Intratumoral forkhead box P3-positive regulatory T (Treg) cells predict poor survival in cyclooxygenase-2 (COX2) positive uveal melanoma.
Source: Mougiakakos D, Cancer 2010, 116:2224-33
Human TRIB2 is a repressor of FOXO that contributes to the malignant phenotype of melanoma cells.
Source: Zanella F, Oncogene 2010, 29:2973-82
IPILIMUMAB IMPROVES SURVIVAL
In a phase III RCT, anti-CTLA4 antibody ipilimumab (combined or not with gp100 vacination) significantly improves the survival of patients with advanced melanoma resistant to conventional chemotherapy (as compared to gp100 vaccination).
Source: Hodi FS, N Engl J Med 2010, 363:711-23
MELANOMA INITIATING CELLS AND CD271
Human melanoma-initiating cells express neural crest nerve growth factor receptor CD271.
Source: Boiko AD, Nature 2010, 466:133-7
RCT OF THYMOSIN ALPHA 1
In a phase III RCT, thymosin increases tumor response rates but not overall survival as compared to DTIC + interferon (IFN) alpha.
Source: Maio M, J Clin Oncol 2010, 28:1780-7
LEPTIN AND MELANOMA GROWTH
The metabolic hormone leptin is a melanoma growth factor: a leptin-based autocrine loop may contribute to the proliferation of melanoma cells.
Source: Ellerhorst JA, Oncol Rep 2010, 23:901-7
IGFBP7 GENE THERAPY
Intratumoral injection of pEGFC1-IGFBP7 inhibits malignant melanoma growth in C57BL/6J mice by inducing apoptosis and downregulating VEGF expression.
Source: Chen RY, Oncol Rep 2010, 23:981-8
B-CELLS AND ANTI-MELANOMA IMMUNITY
B cells are required for optimal CD4+ and CD8+ T cell tumor immunity: therapeutic B cell depletion enhances B16 melanoma growth in mice.
Source: DiLillo DJ, J Immunol 2010, 184:4006-16
PD-1 BLOCKADE + COMBINED IMMUNOTHERAPY
Blockade of programmed death ligand 1 (PD-1) enhances the therapeutic efficacy of combination immunotherapy against murine melanoma in vivo.
Source: Pilon-Thomas S, J Immunol 2010, 184:3442-9
BIOMARKERS FOR ANTI-ANGIOGENIC THERAPY
Using both a murine model and patient biopsies, investigators suggest that resistance to antiangiogenic therapy is directed by vascular phenotype, vessel stabilization, and maturation in melanoma.
Source: Helfrich I, J Exp Med 2010, 207:491-503
MC1R VARIANTS AND CDKN2A MUTATIONS
In a meta-analysis of the literature, MC1R variants significantly increase the penetrance of CDKN2A mutations in melanoma-prone families.
Source: Fargnoli MC, Eur J Cancer 2010, 46:1413-20
IL-24 PLUS DTIC
In a human in vitro model, the combination of interleukin-24 gene therapy and dacarbazine showed anti-melanoma synergism.
Source: Jiang G, Cancer Lett 2010, Epub ahead of print
CONDITIONAL SURVIVAL ANALYSIS (CSA)
Using the SEER database (n=8,647), investigators found that - 8 years after primary surgery - survival differences between low (T2-3N0M0) and high (T4N0M0 or T2-4N1-3M0) risk melanoma patients are no longer significant.
Source: Rueth NM, Ann Surg Oncol 2010, Epub ahead of print
PLEXIN-B1: MELANOMA SUPPRESSOR GENE ?
Plexin B1 can act as a tumor-suppressor protein in melanoma, in part through suppression of c-MET signaling: however, since it also activates AKT, plexin B1 may function as a tumor promoter in melanomas not driven by c-MET activation.
Source: Stevens L, J Invest Dermatol 2010, Epub ahead of print
PESTICIDES AND MELANOMA RISK
In the Agricultural Health Study cohort of licensed pesticide applicators, some pesticides were significantly associated with increased melanoma risk.
Source: Dennis LK, Environ Health Perspect 2010, Epub ahead of print
MITF-MDEL: NEW MELANOMA BIOMARKER
MITF-Mdel, a novel melanocyte/melanoma-specific isoform (splice variant) of microphthalmia-associated transcription factor-M, is proposed as a candidate biomarker for melanoma.
Source: Wang Y, BMC Med 2010, 8:14
4-MU inhibits tumour cell growth and the activation of stromal hyaluronan synthesis by melanoma cell-derived factors.
Source: Edward M, Br J Dermatol 2010, Epub ahead of print
PD1 AND CTLA4 BLOCKADE
PD-1 and CTLA-4 combination blockade expands infiltrating T-cells and reduces regulatory T-cells (Treg) and myeloid suppressor cells within B16 melanoma tumors.
Source: Curran MA, Proc Natl Acad Sci USA 2010, 107:4275-80
ETV1: NEW MELANOMA ONCOGENE
ETV1 in combination with oncogenic NRAS(G12D) transformed primary melanocytes (which was dependent on MITF overexpression) and promoted tumor formation in mice.
Source: Jané-Valbuena J, Cancer Res 2010, 70:2075-84
IGFBP7 GENE THERAPY
In vivo transfection of pcDNA3.1-IGFBP7 inhibits melanoma growth in mice through apoptosis induction and VEGF downregulation.
Source: Chen RY, J Exp Clin Cancer Res 2010, 29:13
SELENIUM ANTI-MELANOMA ACTIVITY
In a mouse model, selenium inhibits melanoma metastasis through the induction of cell cycle arrest and cell death.
Source: Song H, Immune Netw 2009, 9:236-42
OCCULT NODAL METASTASIS
In a large series of patients with thin melanoma (n=1732), a scoring system and nomogram for the risk of nodal involvement was created using 3 variables: sex, age and Breslow tumor thickness.
Source: Faries MB, Arch Surg 2010, 145:137-42
CD4+ CYTOTOXIC T-CELLS
Tumor-reactive CD4(+) T-cells - especially in association with anti-CTLA4 antibody - develop cytotoxic activity and eradicate large established syngeneic melanoma after transfer into lymphopenic hosts.
Source: Quezada SA, J Exp Med 2010, 207:637-50
TRICHOSTATIN PLUS 5-AZA
Histone deacetylase inhibitor (HDACI) trichostatin A (TSA) and the DNA methyltransferase inhibitor (DNMTI) 5-azacytidine (5-AZA) show synergistic anti-melanoma activity in vitro.
Source: Essa S, J Steroid Biochem Mol Biol 2010, Epub ahead of print
S100B SERUM LEVELS
Elevated serum levels of protein S100B during the follow-up of patients with melanoma (n=46) showed a low positive predictive value (50%) for disease recurrence.
Source: Aukema TS, Ann Surg Oncol 2010, Epub ahead of print
NEW PROBE FOR PET
In a preclinical in vivo model, (18)F-MEL050 - a melanin selective compound - showed to perform better than standard (18)F-FDG as a PET probe.
Source: Denoyer D, J Nucl Med 2010, 51:441-7
IMIDAZOLE DERIVATIVE 7A
In a human in vitro model, pyrimidin-4-yl-1H-imidazole derivative 7a showed greater anti-melanoma activity than sorafenib and turned out to be a strong CRAF inhibitor.
Source: Lee J, Bioorg Med Chem Lett 2010, 20:1573-7
PLX4032: BRAF V600E SELECTIVE INHIBITOR
PLX4032, a selective BRAF(V600E) kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAF melanoma cells.
Source: Halaban R, Pigment Cell Melanoma Res 2010, 23:190-200
NOW AVAILABLE: TARGETED THERAPY DATABASE
The MMMP website now hosts a new database coupled with an original model to match the patient's molecular profile with the available evidence on melanoma targeted therapy (drug ranking system).
Source: MMMP_Targeted Therapy Database
FIRST HUMAN EXPERIENCE OF siRNA + TARGETED NANOPARTICLES
The first phase I clinical trial involving the systemic administration of small interfering RNA (siRNA) to patients with solid cancers using targeted nanoparticles is ongoing. Evidence of inducing RNA intereference in a patient with melanoma has been provided.
Source: Davis ME, Nature 2010, Epub ahead of print
RESPONSE TO IPILIMUMAB
In a multicenter single-arm phase II trial of ipilimumab (monotherapy) for pretreated advanced melanoma (n=155), the best overall response rate was 5.8% and the disease control rate was 27%.
Source: O'Day SJ, Ann Oncol 2010, Epub ahead of print
GENOME-WIDE METHYLATION PROFILING
Genome-wide methylation and expression profiling identifies promoter characteristics affecting demethylation-induced gene upregulation in melanoma.
Source: Rubinstein JC, BMC Med Genomics 2010, 3:4
PD1 LIGAND AND PROGNOSIS
Tumor cell expression of programmed cell death-1 (PD1) ligand is an independent prognostic factor for patients with melanoma (n=59).
Source: Hino R, Cancer 2010, 116:1757-66
IPILIMUMAB AND LYMPHOCYTE COUNT
Absolute lymphocyte count determined in the peripheral blood after 2 cycles of ipilimumab correlates with improved survival of patients with advanced melanoma (n=53).
Source: Ku GY, Cancer 2010, 116:1767-75
POPULATION ATTRIBUTABLE FRACTION (PAF)
In a meta-analysis of 66 studies, the PAF for people with skin phototypes I/II, presence of freckling and blond hair color were 27%, 23% and 23%, respectively.
Source: Olsen CM, Int J Cancer 2010, Epub ahead of print
IFN-GAMMA + GGTI298
Human melanoma cells treated with IFN-gamma and geranylgeranyl transferase inhibitor GGTI-298 enhance generation and activity of melanoma-specific cytotoxic T cells.
Source: Sarrabayrouse G, PLoS One 2010, 5:e9043