Home / Deep Research / KIT Mutant Melanoma

KIT Mutant Melanoma

1. Disease Information

2026-04-05
Falcon MONDO:0003865 Model: Edison Scientific Literature 37 citations

1. Disease Information

Overview / definition

KIT-mutant melanoma refers to melanoma in which KIT (CD117) proto-oncogene receptor tyrosine kinase is altered in a way that functionally drives tumor behavior (typically activating point mutations/indels, sometimes with concurrent copy-number gain). Clinically, KIT-driven melanomas are most often described in mucosal, acral, and chronically sun-damaged primary sites, and are therapeutically relevant because they can be sensitive to KIT tyrosine kinase inhibitors (TKIs) when activating KIT mutations are present. In a key phase II trial, the investigators framed the actionable setting as “metastatic mucosal, acral, or chronically sun-damaged (CSD) melanoma with KIT amplifications and/or mutations,” and concluded that such melanomas “should be assessed for KIT mutations” because imatinib “can be effective when tumors harbor KIT mutations, but not if KIT is amplified only.” (hodi2013imatinibformelanomas pages 1-2)

Common synonyms / alternative names

  • KIT-altered melanoma
  • KIT-driven melanoma
  • c-KIT-mutated melanoma / CD117-mutant melanoma
  • KIT-mutant acral melanoma; KIT-mutant mucosal melanoma

Aggregation level of evidence

The characterization here is derived primarily from aggregated disease-level resources (genomic subtype reviews) and prospective clinical trials enrolling defined KIT-altered populations, rather than individual EHR-derived case series (yang2023thegenomiclandscape pages 2-4, larkin2024nilotinibinkitdriven pages 3-5, guo2011phaseiiopenlabel pages 1-2, hodi2013imatinibformelanomas pages 1-2, guo2017efficacyandsafety pages 1-7).

2. Etiology

Disease causal factors

Primary causal factor (molecular): somatic activating alterations in KIT, a receptor tyrosine kinase, producing constitutive or exaggerated pro-survival/proliferation signaling through canonical RTK pathways (PI3K/AKT, MAPK/ERK, JAK/STAT, SRC family pathways) (cilloni2024detectionofkit pages 3-5, abdellateif2023ckitreceptorsas pages 1-2).

Risk factors

Evidence in the retrieved corpus supports subtype and anatomic-site association rather than classic exposure-based risk factors: - KIT alterations are uncommon overall but enriched in mucosal and acral melanomas, and occur in a subset of melanomas on chronically sun-damaged skin (jung2022clinicalandgenomic pages 1-2).

Protective factors / gene–environment interactions

Not identified in the retrieved sources.

3. Phenotypes (clinical presentation)

Because KIT-mutant melanoma is a molecular subtype spanning multiple anatomic melanoma subtypes, phenotype is best summarized by the parent clinicopathologic subtype.

Acral melanoma phenotypes

Acral melanoma arises from palmar/plantar/nail unit melanocytes and has distinct biology and typically worse outcomes than non-acral cutaneous melanoma (yang2023thegenomiclandscape pages 2-4). Suggested phenotypes and ontology mappings: - Acral primary site involvement (UBERON: e.g., skin of palm, skin of sole, nail unit). - Advanced-stage presentation / metastatic disease at diagnosis (HPO: Neoplasm metastasis [HP:0003002]).

Mucosal melanoma phenotypes

Mucosal melanoma arises from mucosal melanocytes (anatomic sites vary: sinonasal, anorectal, vulvovaginal, etc.). In molecular surveys, KIT is commonly the most frequent driver in mucosal melanoma (yang2023thegenomiclandscape pages 2-4). Suggested mappings: - Mucosal primary site involvement (UBERON: mucosa plus site-specific terms). - Local invasion and metastasis (HPO: HP:0003002).

HPO term suggestions (general melanoma manifestations)

  • Neoplasm of the skin / melanoma: Cutaneous melanoma (disease concept; HPO terms may vary by knowledge base)
  • Metastatic disease: HP:0003002 (Neoplasm metastasis)
  • Lymph node metastasis: HP:0001416 (if present clinically)

Frequency/severity/progression: Specific symptom-level frequencies (pain, bleeding, etc.) are not quantified in the retrieved sources; the strongest quantitative phenotype-like data available are subtype distributions and treatment responses by subtype and genotype (jung2022clinicalandgenomic pages 4-5, larkin2024nilotinibinkitdriven pages 5-6).

4. Genetic / Molecular Information

Causal gene

  • KIT (KIT proto-oncogene, receptor tyrosine kinase)

Pathogenic variant spectrum (melanoma)

KIT alterations in melanoma are heterogeneous and can involve multiple exons. Across imatinib- and nilotinib-era data, responses are enriched in exon 11 and exon 13 alterations, particularly L576P (exon 11) and K642E (exon 13) (jung2022clinicalandgenomic pages 1-2, guo2011phaseiiopenlabel pages 1-2).

Subtype enrichment and mutation frequency: - In a 2023 genomic review summarizing multiple studies, KIT mutation frequency was 1.8% in “UV-related” melanomas, 10.9–24.4% in acral melanoma, and 19.1–23.1% in mucosal melanoma (yang2023thegenomiclandscape pages 4-5, yang2023thegenomiclandscape media 3d8ffda1). - Another 2022 pooled analysis summarizes that KIT alterations are ~1–7% overall, enriched to ~10–20% in mucosal and acral melanoma, and ~1–2% in melanomas arising from chronically sun-damaged skin (jung2022clinicalandgenomic pages 1-2).

Somatic vs germline

The clinical trials and genomic reviews accessed describe KIT alterations as tumor (somatic) alterations in advanced melanoma populations (guo2011phaseiiopenlabel pages 1-2, hodi2013imatinibformelanomas pages 1-2, guo2017efficacyandsafety pages 1-7, janku2022efficacyandsafety pages 3-4). Germline predisposition was not addressed in the retrieved sources.

Functional consequences / mechanism (molecular chain)

  1. Upstream trigger: activating KIT mutation (e.g., juxtamembrane/kinase-domain variants) → ligand-independent or dysregulated RTK signaling.
  2. Receptor activation and phosphorylation: SCF binding normally induces KIT dimerization and autophosphorylation; in cancer, gain-of-function KIT alterations can cause constitutive activation (cilloni2024detectionofkit pages 3-5, abdellateif2023ckitreceptorsas pages 1-2).
  3. Downstream signaling: activation of PI3K/AKT (survival/proliferation), MAPK/ERK (transcription/proliferation), SRC kinases (motility/angiogenesis), and JAK/STAT (transcription programs) (cilloni2024detectionofkit pages 3-5, abdellateif2023ckitreceptorsas pages 1-2).
  4. Cellular outcomes: sustained proliferation and apoptosis resistance → tumor growth and metastasis potential.

Suggested GO (biological process) terms

  • GO:0007169 transmembrane receptor protein tyrosine kinase signaling pathway
  • GO:0008284 positive regulation of cell population proliferation
  • GO:0043065 positive regulation of apoptotic process (context-specific; KIT signaling can inhibit apoptosis)
  • GO:0000165 MAPK cascade
  • GO:0014066 regulation of phosphatidylinositol 3-kinase signaling

Suggested Cell Ontology (CL) terms

  • CL:0000148 melanocyte (primary lineage cell)
  • CL:0000236 B cell / CL:0000624 CD8-positive, alpha-beta T cell (relevant to tumor microenvironment discussions, especially when considering immunotherapy combinations; mechanistic immunology was not deeply quantified in retrieved sources)

5. Environmental Information

No KIT-mutant-specific environmental triggers were identified in the retrieved sources. KIT-mutant melanoma is instead primarily associated with anatomic subtype and non-UV (acral/mucosal) biology (yang2023thegenomiclandscape pages 2-4, jung2022clinicalandgenomic pages 1-2).

6. Mechanism / Pathophysiology

Key pathways

Resistance mechanisms (clinical inference)

7. Anatomical Structures Affected

Primary sites (by subtype)

Metastatic sites

Common metastatic patterns are not enumerated in retrieved sources; advanced/metastatic disease is the predominant study population across trials (guo2011phaseiiopenlabel pages 1-2, hodi2013imatinibformelanomas pages 1-2, guo2017efficacyandsafety pages 1-7, janku2022efficacyandsafety pages 3-4).

8. Temporal Development

Onset

Typically adult-onset melanoma; age distribution not comprehensively extracted in the present evidence set.

Progression

KIT-mutant melanomas in trials are often advanced/metastatic. In multiple TKI trials, median PFS is generally on the order of months (see Treatment section), consistent with the common clinical observation that responses—when present—may be clinically meaningful but not uniformly durable (guo2011phaseiiopenlabel pages 1-2, hodi2013imatinibformelanomas pages 5-6, guo2017efficacyandsafety pages 1-7).

9. Inheritance and Population

Epidemiology (mutation frequency by subtype)

A 2023 genomic synthesis reported KIT mutation frequencies by subtype (compiled from multiple cohorts): - UV-related melanoma: 1.8% - Acral melanoma: 10.9–24.4% - Mucosal melanoma: 19.1–23.1% (Visual evidence: Table 2 in the review) (yang2023thegenomiclandscape pages 4-5, yang2023thegenomiclandscape media 3d8ffda1)

Another pooled clinical genomics analysis summarizes KIT alterations at: - ~1–7% overall melanoma - ~10–20% in mucosal melanoma - ~10–20% in acral melanoma - ~1–2% in chronically sun-damaged skin melanomas (jung2022clinicalandgenomic pages 1-2)

Population demographics

Not robustly extractable from the retrieved sources beyond subtype enrichment.

10. Diagnostics

Molecular testing approach (tumor)

Key trials used targeted KIT exon sequencing to identify actionable mutations. - NICAM eligibility required tumors with KIT mutations screened by “Sanger sequencing of exons 9, 11, 13 and 17” (larkin2024nilotinibinkitdriven pages 14-15). - Hodi et al. enrolled patients with KIT “amplifications and/or mutations” but the strongest benefit was in mutation-positive disease (hodi2013imatinibformelanomas pages 1-2).

KIT amplification assessment

Liquid biopsy / ctDNA (recent implementation)

NICAM provides notable contemporary evidence for ctDNA-based KIT testing: - “concordance between ctDNA and matched FFPE tumor mutation calls was 100%” (larkin2024nilotinibinkitdriven pages 6-8). - Authors state that “ddPCR-based KIT analysis appears feasible and accu-rate for KIT testing in patients with metastatic MM and AM and could be proposed for liquid biopsies testing” (larkin2024nilotinibinkitdriven pages 9-10).

Differential diagnosis

Not detailed in retrieved sources; in practice, differential diagnosis is dominated by distinguishing melanoma subtype and excluding alternative primary sites and other oncogene drivers (BRAF/NRAS/NF1), but detailed diagnostic criteria and pathology differentials were not accessed here.

11. Outcome / Prognosis

Prognostic notes (treatment-linked)

Prognosis in KIT-mutant melanoma is heterogeneous and strongly influenced by stage and treatment responsiveness. Across KIT TKI trials, median OS values ranged from ~7–18 months depending on study era, population, and treatment line (e.g., NICAM 7.7 months; TEAM 18.0 months; Hodi imatinib 12.5 months) (larkin2024nilotinibinkitdriven pages 5-6, hodi2013imatinibformelanomas pages 5-6, guo2017efficacyandsafety pages 1-7).

12. Treatment

Current applications (real-world implementation)

The principal real-world application is genotype-guided use of KIT TKIs in advanced KIT-mutant melanoma (especially acral/mucosal/CSD primary sites). A central practical point supported by a prospective trial is that KIT amplification without activating mutation is not a reliable predictor of imatinib response (hodi2013imatinibformelanomas pages 1-2).

Key clinical evidence (prospective trials)

Table (click to expand)
Study (year, journal) Population/subtype and KIT alteration eligibility N Key outcomes (ORR/BORR, DCR, median PFS/TTP, median OS) Key genotype associations (exon/variant) Notes
Imatinib — Guo 2011, J Clin Oncol Metastatic melanoma with c-KIT mutation or amplification; open-label single-arm phase II (guo2011phaseiiopenlabel pages 1-2) 43 ORR 23.3% (10/43); DCR 53.5% (10 PR + 13 SD); median PFS 3.5 mo; 6-mo PFS 36.6%; 1-y OS 51.0% (guo2011phaseiiopenlabel pages 1-2) 9/10 PRs occurred in exon 11 or 13 mutations (guo2011phaseiiopenlabel pages 1-2) Dose escalation to 800 mg/d rarely restored disease control (guo2011phaseiiopenlabel pages 1-2)
Imatinib — Hodi 2013, J Clin Oncol Metastatic mucosal, acral, or chronically sun-damaged melanoma with KIT amplification and/or mutation; multicenter phase II (hodi2013imatinibformelanomas pages 1-2) 25 enrolled; 24 evaluable BORR 29% (21% excluding nonconfirmed responses); DCR 50%; overall TTP 3.7 mo; OS 12.5 mo (hodi2013imatinibformelanomas pages 1-2, hodi2013imatinibformelanomas pages 5-6) KIT-mutated tumors: BORR 7/13 (54%), DCR 77%; KIT amplified-only tumors: BORR 0%, DCR 18% (hodi2013imatinibformelanomas pages 1-2, hodi2013imatinibformelanomas pages 3-4) Amplification-only lacked objective responses; pretreatment NRAS mutations and KIT copy-number gain implicated in resistance (hodi2013imatinibformelanomas pages 1-2, hodi2013imatinibformelanomas pages 5-6)
Nilotinib — Carvajal 2015, Clin Cancer Res Melanoma with KIT mutations or amplification after prior KIT inhibitor; cohort A refractory/intolerant to prior KIT inhibitor, cohort B brain metastases (carvajal2015phaseiistudy pages 1-3) 20 enrolled; 19 treated Cohort A primary endpoint achieved in 27%; cohort B 12.5%; ORR 18.2% in cohort A, 0 in cohort B; median TTP 3.3 mo; median OS 9.1 mo (carvajal2015phaseiistudy pages 1-3) Maintains activity against a range of exon 9, 11, and 13 KIT mutations (carvajal2015phaseiistudy pages 1-3) Limited efficacy in brain metastases (carvajal2015phaseiistudy pages 1-3)
Nilotinib — TEAM 2017, Ann Oncol Advanced/inoperable KIT-mutated melanoma without prior KIT inhibitor; global single-arm phase II (guo2017efficacyandsafety pages 1-7) 42 ORR 26.2% (11/42); all responses PRs; median response duration 7.1 mo; median PFS 4.2 mo; 6-mo PFS 34.6%; median OS 18.0 mo (guo2017efficacyandsafety pages 7-12, guo2017efficacyandsafety pages 1-7) 10/11 responders had exon 11 mutations; exon 11 PR rate 10/26 (38.5%), exon 13 PR rate 1/13 (7.7%), exon 9/17 no responses; 4 responders had L576P (guo2017efficacyandsafety pages 7-12, guo2017efficacyandsafety pages 1-7) Activity similar to historical imatinib, strongest in exon 11/L576P (guo2017efficacyandsafety pages 1-7)
Nilotinib — NICAM 2024, Cell Reports Medicine KIT-mutated metastatic mucosal and acral melanoma; single-arm phase II; prior TKI excluded; exploratory KIT amplification/FISH and ctDNA ddPCR analyses (larkin2024nilotinibinkitdriven pages 14-15, larkin2024nilotinibinkitdriven pages 1-3) 29 treated; 26 evaluable 6-mo PFS by local review 25%; by central review 29%; OR at 12 wk 19% (5/26); median PFS 3.7 mo; median OS 7.7 mo; 12-mo OS 44% (larkin2024nilotinibinkitdriven pages 3-5, larkin2024nilotinibinkitdriven pages 5-6) Mutations concentrated in exon 11 (69%), exon 13 (14%), exon 17 (14%), exon 9 (3%); OR at 12 wk: exon 11 16%, exon 13 25%, exon 17 67%; median PFS: exon 11 2.9 mo, exon 13 2.3 mo, exon 17 5.4 mo; L576 in 31% (larkin2024nilotinibinkitdriven pages 3-5, larkin2024nilotinibinkitdriven pages 5-6, larkin2024nilotinibinkitdriven pages 8-9) Acral tumors had worse median PFS/OS than mucosal; ctDNA/FFPE concordance 100%; KIT copy number not clearly associated with outcome (larkin2024nilotinibinkitdriven pages 5-6, larkin2024nilotinibinkitdriven pages 6-8, larkin2024nilotinibinkitdriven pages 8-9)
Dasatinib — E2607 2017, Cancer Locally advanced or stage IV mucosal, acral, vulvovaginal melanoma; stage I included KIT-mutant and KIT−; stage II restricted to KIT+ (kalinsky2017aphase2 pages 1-2) 51 analyzable stage I; 22 analyzable stage II; 73 evaluable overall Stage I PR 3/51 (5.9%); stage II PR 4/22 (18.2%); median response duration 4.2 mo; median PFS 2.1 mo; median OS 7.5 mo (kalinsky2017aphase2 pages 1-2, kalinsky2017aphase2 pages 4-5) Among exon 11 and/or 13 KIT mutations, PR rate 20%; median PFS 4.7 mo; no responses with common L576P and K642E in one analysis, but responses seen with P577-D579 deletion and dual exon 11/13 mutations (kalinsky2017aphase2 pages 4-5, kalinsky2017aphase2 pages 7-8) Exploratory analyses found no significant PFS/OS difference by overall KIT status; authors concluded response rate lower than expected and imatinib should remain KIT TKI of choice (kalinsky2017aphase2 pages 7-8, kalinsky2017aphase2 pages 1-2)
Ripretinib — Janku 2022, ESMO Open KIT-altered metastatic melanoma phase I expansion; KIT mutation and/or amplification; heavily pretreated; starting dose 150 mg QD, BID escalation after progression allowed (janku2022efficacyandsafety pages 1-2, janku2022efficacyandsafety pages 2-3) 26 Confirmed ORR 23% (95% CI 9–44); among patients with follow-up imaging ORR 32% (8/25; CR 1, PR 7); median duration of confirmed response 9.1 mo; median PFS 7.3 mo (janku2022efficacyandsafety pages 5-6, janku2022efficacyandsafety pages 1-2, janku2022efficacyandsafety pages 3-4) Confirmed ORR 44% in exon 11 and 18% in exon 17; median PFS 10.2 mo (exon 11) and 13.6 mo (exon 17); examples of responses include exon 11 L576P, exon 17 D820Y, exon 17 Y823D; D816V associated with PD in one case (janku2022efficacyandsafety pages 5-6, janku2022efficacyandsafety pages 4-5, janku2022efficacyandsafety pages 3-4) KIT-inhibitor–naive patients had ORR 29% and mPFS 10.2 mo vs prior KIT inhibitor ORR 11% and mPFS 2.9 mo (janku2022efficacyandsafety pages 1-2, janku2022efficacyandsafety pages 4-5)

Table: This table summarizes key prospective clinical evidence for KIT-altered melanoma therapies across major studies of imatinib, nilotinib, dasatinib, and ripretinib. It highlights outcomes, genotype-response patterns, and practical caveats such as amplification-only disease and prior KIT inhibitor exposure.

Imatinib (KIT TKI)

Nilotinib (KIT TKI)

Dasatinib (multi-kinase/SRC and KIT activity)

  • E2607 (Cancer 2017, published Jul 2017): modest activity; median PFS 2.1 months, median OS 7.5 months; authors conclude low response rate and recommend imatinib remain KIT TKI of choice in unresectable KIT+ melanoma (kalinsky2017aphase2 pages 1-2).

Ripretinib (switch-control TKI; KIT/PDGFRA)

  • Janku et al., ESMO Open 2022 (published Aug 2022): confirmed ORR 23% (95% CI 9–44) with median PFS 7.3 months and median response duration 9.1 months; activity differed by exon and prior KIT inhibitor exposure (KIT-inhibitor–naïve ORR 29% and mPFS 10.2 months vs prior KIT inhibitor ORR 11% and mPFS 2.9 months) (janku2022efficacyandsafety pages 1-2, janku2022efficacyandsafety pages 4-5).

MAXO term suggestions (treatments/actions)

  • Tyrosine kinase inhibitor therapy (MAXO: TKI treatment)
  • Molecular targeted therapy (MAXO: targeted therapy)
  • Tumor mutation profiling / genomic sequencing (MAXO: genetic test / tumor genomic profiling)
  • Liquid biopsy (MAXO: liquid biopsy testing)

13. Prevention

No KIT-mutant-specific prevention strategies were identified in the retrieved sources. General melanoma prevention and early detection principles apply, but are not addressed in the accessed KIT-focused literature.

14. Other Species / Natural Disease

Not supported by the retrieved evidence set.

15. Model Organisms

The retrieved evidence set does not provide detailed descriptions of KIT-mutant melanoma animal models or engineered systems. (This is a gap for the current report.)

Recent Developments (2023–2024 emphasis)

  1. 2024 NICAM trial (nilotinib; metastatic mucosal/acral KIT-mutant melanoma) provides updated prospective efficacy estimates (median PFS 3.7 months; OR at 12 weeks 19%) and highlights a clinically actionable diagnostic development: plasma ddPCR ctDNA testing with 100% concordance to tumor calls in available matched samples (larkin2024nilotinibinkitdriven pages 3-5, larkin2024nilotinibinkitdriven pages 5-6, larkin2024nilotinibinkitdriven pages 6-8).
  2. 2023 genomic synthesis consolidates KIT mutation frequency ranges across melanoma subtypes, providing a practical expectation for testing yield by subtype (yang2023thegenomiclandscape pages 4-5, yang2023thegenomiclandscape media 3d8ffda1).

Visual evidence (mutation frequency by subtype)

The figure below (Table 2 from a 2023 review) provides the subtype-specific KIT mutation frequencies used in the epidemiology section (yang2023thegenomiclandscape media 3d8ffda1).

Key Statistics (quick reference)

Limitations of this report

  • Formal ontology identifiers (MONDO/MeSH/ICD-10/11) and comprehensive phenotype/quality-of-life metrics were not available in the retrieved corpus and would require dedicated searches in OMIM/Orphanet/MeSH/MONDO resources.
  • Model-organism and non-human disease information for KIT-mutant melanoma was not captured in the currently retrieved sources.

References

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  2. (yang2023thegenomiclandscape pages 2-4): Ting-Ting Yang, Sebastian Yu, Chiao-Li Khale Ke, and Shih-Tsung Cheng. The genomic landscape of melanoma and its therapeutic implications. Genes, 14:1021, Apr 2023. URL: https://doi.org/10.3390/genes14051021, doi:10.3390/genes14051021. This article has 29 citations.

  3. (larkin2024nilotinibinkitdriven pages 3-5): James Larkin, Richard Marais, Nuria Porta, David Gonzalez de Castro, Lisa Parsons, Christina Messiou, Gordon Stamp, Lisa Thompson, Kim Edmonds, Sarah Sarker, Jane Banerji, Paul Lorigan, Thomas R Jeffry Evans, Pippa Corrie, Ernest Marshall, Mark R Middleton, Paul Nathan, Steve Nicholson, Christian Ottensmeier, Ruth Plummer, Judith Bliss, Sara Valpione, and Samra Turajlic. Nilotinib in kit-driven advanced melanoma: results from the phase ii single-arm nicam trial. Cell Reports Medicine, Feb 2024. URL: https://doi.org/10.1016/j.xcrm.2024.101435, doi:10.1016/j.xcrm.2024.101435. This article has 21 citations and is from a peer-reviewed journal.

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