Heterogeneity of FDG-PET response to GSK2118436, an inhibitor of oncogenic mutant BRAF-kinase in BRAF-mutant metastatic melanoma.

2011 ◽  
Vol 29 (15_suppl) ◽  
pp. 8539-8539 ◽  
Author(s):  
M. S. Carlino ◽  
C. A. Saunders ◽  
V. Gebski ◽  
A. M. Menzies ◽  
B. Ma ◽  
...  
Keyword(s):  
Metastatic Melanoma ◽  
Fdg Pet ◽  
Braf Mutant ◽  
Mutant Braf

scholarly journals Correlation between early 18F-FDG PET/CT response to BRAF and MEK inhibition and survival in patients with BRAF-mutant metastatic melanoma

2016 ◽  
Vol 37 (2) ◽  
pp. 122-128 ◽  
Author(s):  
Ronald J. Schmitt ◽  
Sarah M. Kreidler ◽  
Deborah H. Glueck ◽  
Rodabe N. Amaria ◽  
Rene Gonzalez ◽  
...  
Keyword(s):  
Metastatic Melanoma ◽  
Fdg Pet ◽  
Mek Inhibition ◽  
Pet Ct ◽  
18F Fdg ◽  
Fdg Pet Ct ◽  
Braf Mutant

Circulating Tumor DNA Analysis and Functional Imaging Provide Complementary Approaches for Comprehensive Disease Monitoring in Metastatic Melanoma

2017 ◽  
pp. 1-14 ◽  
Author(s):  
Stephen Q. Wong ◽  
Jeanette M. Raleigh ◽  
Jason Callahan ◽  
Ismael A. Vergara ◽  
Sarah Ftouni ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Metastatic Melanoma ◽  
Fdg Pet ◽  
Disease Burden ◽  
Circulating Tumor Dna ◽  
Tumor Burden ◽  
Disease Monitoring ◽  
Ctdna Analysis ◽  
Mutant Braf

Purpose Circulating tumor DNA (ctDNA) allows noninvasive disease monitoring across a range of malignancies. In metastatic melanoma, the extent to which ctDNA reflects changes in metabolic disease burden assessed by 18F-labeled fluorodeoxyglucose positron emission tomography (FDG-PET) is unknown. We assessed the role of ctDNA analysis in combination with FDG-PET to monitor tumor burden and genomic heterogeneity throughout treatment. Patients and Methods We performed a comprehensive analysis of serial ctDNA and FDG-PET in 52 patients who received systemic therapy for metastatic melanoma. Next-generation sequencing and digital polymerase chain reaction were used to analyze plasma samples from the cohort. Results ctDNA levels were monitored across patients with mutant BRAF, NRAS, and BRAF/NRAS wild type disease. Mutant BRAF and NRAS ctDNA levels correlated closely with changes in metabolic disease burden throughout treatment. TERT promoter mutant ctDNA levels also paralleled changes in tumor burden, which provide an alternative marker for disease monitoring. Of note, subcutaneous and cerebral disease sites were not well represented in plasma. Early changes in ctDNA and metabolic disease burden were important indicators of treatment response. Patients with an early decrease in ctDNA post-treatment had improved progression-free survival compared with patients in whom ctDNA levels remained unchanged or increased over time (hazard ratio, 2.6; P = .05). ctDNA analysis contributed key molecular information through the identification of putative resistance mechanisms to targeted therapy. A detailed comparison of the genomic architecture of plasma and multiregional tumor biopsy specimens at autopsy revealed the ability of ctDNA to comprehensively capture genomic heterogeneity across multiple disease sites. Conclusion The findings highlight the powerful role of ctDNA in metastatic melanoma as a complementary modality to functional imaging that allows real-time monitoring of both tumor burden and genomic changes throughout therapy.

scholarly journals No Impact of NRAS Mutation on Features of Primary and Metastatic Melanoma or on Outcomes of Checkpoint Inhibitor Immunotherapy: An Italian Melanoma Intergroup (IMI) Study

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 475
Author(s):  
Michele Guida ◽  
Nicola Bartolomeo ◽  
Pietro Quaglino ◽  
Gabriele Madonna ◽  
Jacopo Pigozzo ◽  
...  
Keyword(s):  
Metastatic Melanoma ◽  
Checkpoint Inhibitor ◽  
Progression Free Survival ◽  
Nras Mutation ◽  
Disease Free Interval ◽  
Free Survival ◽  
Mutational Status ◽  
Metastatic Sites ◽  
Disease Free ◽  
Mutant Braf

Aims: It is debated whether the NRAS-mutant melanoma is more aggressive than NRAS wildtype. It is equally controversial whether NRAS-mutant metastatic melanoma (MM) is more responsive to checkpoint inhibitor immunotherapy (CII). 331 patients treated with CII as first-line were retrospectively recruited: 162 NRAS-mutant/BRAF wild-type (mut/wt) and 169 wt/wt. We compared the two cohorts regarding the characteristics of primary and metastatic disease, disease-free interval (DFI) and outcome to CII. No substantial differences were observed between the two groups at melanoma onset, except for a more frequent ulceration in the wt/wt group (p = 0.03). Also, the DFI was very similar in the two cohorts. In advanced disease, we only found lung and brain progression more frequent in the wt/wt group. Regarding the outcomes to CII, no significant differences were reported in overall response rate (ORR), disease control rate (DCR), progression free survival (PFS) or overall survival (OS) (42% versus 37%, 60% versus 59%, 12 (95% CI, 7–18) versus 9 months (95% CI, 6–16) and 32 (95% CI, 23–49) versus 27 months (95% CI, 16–35), respectively). Irrespectively of mutational status, a longer OS was significantly associated with normal LDH, <3 metastatic sites, lower white blood cell and platelet count, lower neutrophil-to-lymphocyte (N/L) ratio. Our data do not show increased aggressiveness and higher responsiveness to CII in NRAS-mutant MM.

Can benign lymphoid tissue changes in 18F-FDG PET/CT predict response to immunotherapy in metastatic melanoma?

2018 ◽  
Vol 68 (2) ◽  
pp. 297-303 ◽  
Author(s):  
Christos Sachpekidis ◽  
Lionel Larribère ◽  
Annette Kopp-Schneider ◽  
Jessica C. Hassel ◽  
Antonia Dimitrakopoulou-Strauss
Keyword(s):  
Metastatic Melanoma ◽  
Fdg Pet ◽  
Lymphoid Tissue ◽  
Pet Ct ◽  
Tissue Changes ◽  
18F Fdg ◽  
Fdg Pet Ct

scholarly journals Detection of Mutant BRAF Alleles in the Plasma of Patients with Metastatic Melanoma

2007 ◽  
Vol 9 (2) ◽  
pp. 178-183 ◽  
Author(s):  
Molly Yancovitz ◽  
Joanne Yoon ◽  
Maryann Mikhail ◽  
Weiming Gai ◽  
Richard L. Shapiro ◽  
...  
Keyword(s):  
Metastatic Melanoma ◽  
Mutant Braf

scholarly journals BRAF in Melanoma: Pathogenesis, Diagnosis, Inhibition, and Resistance

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Ryan J. Sullivan ◽  
Keith T. Flaherty
Keyword(s):  
Standard Of Care ◽  
Diagnostic Techniques ◽  
Therapeutic Interventions ◽  
Molecular Testing ◽  
Braf Inhibitors ◽  
Testing Methods ◽  
Braf Mutations ◽  
Initial Discovery ◽  
Braf Mutant ◽  
Mutant Braf

Since the initial discovery that a subset of patients with cutaneous melanoma harbor BRAF mutations, substantial research has been focused on determining the pathologic consequences of BRAF mutations, optimizing diagnostic techniques to identify these mutations, and developing therapeutic interventions to inhibit the function of this target in mutation-bearing tumors. Recently, advances have been made which are revolutionizing the standard of care for patients with BRAF mutant melanoma. This paper provides an overview on the pathogenic ramifications of mutant BRAF signaling, the latest molecular testing methods to detect BRAF mutations, and the most recent clinical data of BRAF pathway inhibitors in patients with melanoma and BRAF mutations. Finally, emerging mechanisms of resistance to BRAF inhibitors and ways of overcoming this resistance are discussed.

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