# Effectiveness and Mechanism of Cryoablation in the Treatment of Oral Mucosal Melanoma

**Authors:** Zhu You, Tianqi Zhang, Li Dai, Jie Wen, Mingyang Liu, Tengda Zhao, Guozhu Yin, Yihua Wu, Shizhou Zhang

PMC · DOI: 10.1002/cam4.71577 · Cancer Medicine · 2026-02-06

## TL;DR

Cryoablation is a safe and effective treatment for oral mucosal melanoma, potentially working by changing the immune environment and cell death processes.

## Contribution

This study provides new insights into the mechanisms of cryoablation in treating oral mucosal melanoma.

## Key findings

- Cryoablation showed a postoperative survival rate of 72.22% in OMM patients.
- Cryoablation modulates the immune microenvironment by increasing CD4+, CD8+, and CD66+ cell infiltration.
- The antitumor effect of cryoablation is primarily due to apoptosis induction.

## Abstract

To assess the effectiveness and safety of cryoablation for oral mucosal melanoma (OMM) and explore its underlying mechanisms to provide insights for precision treatment of OMM.

Patients diagnosed with OMM were divided into a cryoablation group and a noncryoablation therapy group. We compared the therapeutic outcomes of these groups and investigated the effects of cryoablation on glycometabolism, the immune microenvironment, and cell death modalities in the OMM.

The study included 32 OMM patients, with 18 in the cryoablation group and 14 in the noncryoablation therapy group. Cryoablation demonstrated high safety and effectiveness, with a postoperative survival rate of 72.22% (13/18). The median overall survival was 85.5 months (95% CI: 57.3–113.6) in the cryoablation group and 72.4 months (95% CI: 51.36–93.4) in the non‐cryoablation group. Significant changes in the immune microenvironment, including increased infiltration of CD4+, CD8+, and CD66+ cells and elevated expression of PD‐1, PD‐L1+, and CTLA4+ immune checkpoints, were observed postcryoablation. Conversely, FOXP3+ and CD19+ cell densities significantly decreased. Additionally, the expression levels of GLUT‐1, HIF‐1α, and PK‐M2 were notably reduced. The primary antitumor effect of cryoablation is attributed to apoptosis.

Cryoablation is an effective treatment for OMM, and its antitumor effects are potentially linked to the modulation of the immune microenvironment, alteration of glucose metabolism, and induction of apoptosis.

## Linked entities

- **Proteins:** CD4 (CD4 molecule), CD8A (CD8 subunit alpha), PDCD1 (programmed cell death 1), CD274 (CD274 molecule), CTLA4 (cytotoxic T-lymphocyte associated protein 4), FOXP3 (forkhead box P3), CD19 (CD19 molecule), SLC2A1 (solute carrier family 2 member 1), HIF1A (hypoxia inducible factor 1 subunit alpha), PKM (pyruvate kinase M1/2)

## Full-text entities

- **Genes:** PKM (pyruvate kinase M1/2) [NCBI Gene 5315] {aka CTHBP, HEL-S-30, OIP3, PK3, PKM2, TCB}, Cd19 (CD19 antigen) [NCBI Gene 12478], BRAF (B-Raf proto-oncogene, serine/threonine kinase) [NCBI Gene 673] {aka B-RAF1, B-raf, BRAF-1, BRAF1, NS7, RAFB1}, SLC2A1 (solute carrier family 2 member 1) [NCBI Gene 6513] {aka CSE, DYT17, DYT18, DYT9, EIG12, GLUT}, TERT (telomerase reverse transcriptase) [NCBI Gene 7015] {aka CMM9, DKCA2, DKCB4, EST2, PFBMFT1, TCS1}, PTEN (phosphatase and tensin homolog) [NCBI Gene 5728] {aka 10q23del, BZS, CWS1, DEC, GLM2, MHAM}, Cd274 (CD274 antigen) [NCBI Gene 60533] {aka A530045L16Rik, B7h1, Pdcd1l1, Pdcd1lg1, Pdl1}, KIT (KIT proto-oncogene, receptor tyrosine kinase) [NCBI Gene 3815] {aka C-Kit, CD117, MASTC, PBT, SCFR}, HIF1A (hypoxia inducible factor 1 subunit alpha) [NCBI Gene 3091] {aka HIF-1-alpha, HIF-1A, HIF-1alpha, HIF1, HIF1-ALPHA, MOP1}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}, CD274 (CD274 molecule) [NCBI Gene 29126] {aka ADMIO5, B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1}, CTLA4 (cytotoxic T-lymphocyte associated protein 4) [NCBI Gene 1493] {aka ALPS5, CD, CD152, CELIAC3, CTLA-4, GRD4}, CD19 (CD19 molecule) [NCBI Gene 930] {aka B4, CVID3}, ARID1B (AT-rich interaction domain 1B) [NCBI Gene 57492] {aka 6A3-5, BAF250B, BRIGHT, CSS1, DAN15, ELD/OSA1}, NF1 (neurofibromin 1) [NCBI Gene 4763] {aka NFNS, VRNF, WSS}, CCND1 (cyclin D1) [NCBI Gene 595] {aka BCL1, D11S287E, PRAD1, U21B31}, MDM2 (MDM2 proto-oncogene) [NCBI Gene 4193] {aka ACTFS, HDMX, LSKB, hdm2}, MITF (melanocyte inducing transcription factor) [NCBI Gene 4286] {aka CMM8, COMMAD, MI, MITF-A, WS2, WS2A}, CDKN2A (cyclin dependent kinase inhibitor 2A) [NCBI Gene 1029] {aka ARF, CAI2, CDK4I, CDKN2, CMM2, INK4}, Ctla4 (cytotoxic T-lymphocyte-associated protein 4) [NCBI Gene 12477] {aka Cd152, Ctla-4, Ly-56}, Casp3 (caspase 3) [NCBI Gene 12367] {aka A830040C14Rik, AC-3, CASP-3, CC3, CPP-32, CPP32}, CD80 (CD80 molecule) [NCBI Gene 941] {aka B7, B7-1, B7.1, BB1, CD28LG, CD28LG1}, ATM (ATM serine/threonine kinase) [NCBI Gene 472] {aka AT1, ATA, ATC, ATD, ATDC, ATE}, Cd68 (CD68 antigen) [NCBI Gene 12514] {aka Lamp4, Scard1, gp110}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, CDK4 (cyclin dependent kinase 4) [NCBI Gene 1019] {aka CMM3, MCPH31, PSK-J3}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, CD68 (CD68 molecule) [NCBI Gene 968] {aka GP110, LAMP4, SCARD1}, NOTCH2 (notch receptor 2) [NCBI Gene 4853] {aka AGS2, HJCYS, hN2}, Foxp3 (forkhead box P3) [NCBI Gene 20371] {aka JM2, scurfin, sf}, Fcgr3 (Fc receptor, IgG, low affinity III) [NCBI Gene 14131] {aka CD16}, FOXP3 (forkhead box P3) [NCBI Gene 50943] {aka AIID, DIETER, IPEX, JM2, PIDX, XPID}, FCGR3A (Fc gamma receptor IIIa) [NCBI Gene 2214] {aka CD16-II, CD16A, FCG3, FCGR3, FCRIIIA, FcGRIIIA}, Cd4 (CD4 antigen) [NCBI Gene 12504] {aka L3T4, Ly-4}, MLANA (melan-A) [NCBI Gene 2315] {aka MART-1, MART1}, CST12P (cystatin 12, pseudogene) [NCBI Gene 106478911] {aka Cst, Ctes4, E2}, PDCD1 (programmed cell death 1) [NCBI Gene 5133] {aka ADMIO4, AIMTBS, CD279, PD-1, PD1, SLEB2}, CD86 (CD86 molecule) [NCBI Gene 942] {aka B7-2, B7.2, B70, BU63, CD28LG2, CD86 v6}
- **Diseases:** CM (MESH:C562393), cervical lymphatic metastasis (MESH:D008207), skin tumors (MESH:D012878), Mucosal melanoma (MESH:D008545), malignancies (MESH:D009369), cytotoxic (MESH:D064420), bleeding (MESH:D006470), head and neck mucosal melanomas (MESH:D006258), oral cancers (MESH:D009062), metastases (MESH:D009362), deaths (MESH:D003643), trauma (MESH:D014947), necrosis (MESH:D009336), pain (MESH:D010146), inflammation (MESH:D007249)
- **Chemicals:** nitrogen (MESH:D009584), nivolumab (MESH:D000077594), DAPI (MESH:C007293), Glucose (MESH:D005947), TSA (MESH:C481298), ARD1001EA (-), EDTA (MESH:D004492), carbon (MESH:D002244), argon (MESH:D001128), H&amp;E (MESH:D006371), nitrous oxide (MESH:D009609), eosin (MESH:D004801), ipilimumab (MESH:D000074324), hematoxylin (MESH:D006416), carbon dioxide (MESH:D002245), paraffin (MESH:D010232)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

28 references — full list in the complete paper: https://tomesphere.com/paper/PMC12881701/full.md

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Source: https://tomesphere.com/paper/PMC12881701