Dear Editor,

Leukoplakia is an oral, possibly malignant condition that manifests as a white lesion that does not peel away upon contact. It originates in the oral mucosa, especially the buccal mucosa and tongue [1]. Fungal infection, frictional keratosis, and lichen planus are all potential differential diagnoses for leukoplakia. Frictional keratosis can develop near ill-fitting dentures or shrill teeth and quickly vanish if the cause is identified. Oral cancer predictors include heterogeneous and extensive lesions on the adjacent boundary lesions or floor of the tongue and lesions with histological dysplasia [2]. Known risk factors for leukoplakia include smoking, alcohol intake, and human papillomavirus infections. PLD - Pegylated liposomal doxorubicin is an anticancer medication used to treat recurrent malignancies such as ovarian cancer. On the left side of the tongue, a white lesion was observed; on the oral mucosa, the white lesion was not removed. Hazard factors for tongue cancer and leukoplakia include smoking and drinking history, sharp teeth, syphilitic glossitis, ill-fitting dentures, candida infection and persistent cheek biting. As a result, leukoplakia was established, and it was assumed that the leukoplakia was caused by the injection of PLD. The histological identification was tongue pT1aNxM0-squamous cell carcinoma [3]. In various investigations, the altered pharmacokinetics and pharmacodynamics of PLD have been shown to reduce cardiac toxicity. The polyethylene glycol coating prevents the uptake of mononuclear phagocytes, extending their half-life. The liposomal formulation reduces the occurrence of acute and chronic cardiomyopathy by improving biodistribution. The medicine accumulates in the liver, spleen, and tumor rather than in the heart. PLD was initially licensed for treating refractory AIDS-related Kaposi’s sarcoma, as well as metastatic breast cancer, in phase III trials [4]. PLD is also routinely used to treat gynecologic cancers, and many patients receive substantial cumulative dosages.

A pharmacokinetic study revealed that PLD had greater plasma concentrations than nonliposomal doxorubicin did because of its narrow volume of distribution. Liposomes that discharge doxorubicin and accumulate metabolites, particularly in the mucous and skin membranes. On the left lingual edge, a whitish lesion was discovered; the lesion was histologically classified as atypical epithelium that does not regulate neoplastic transformation on the basis of the leading biopsy, which revealed invasive SCC with dyskeratosis. The experimental stage was thus defined as cT2N0M0 according to the TNM classification. Upon greater enlargement, the tumor cells revealed very large round-to-oval nuclei with hyperchromasia, an elevated nuclear‒cytoplasmic ratio, and conspicuous nucleoli; the unclear cell boundary had a syncytial appearance. Long-term doxorubicin exposure is thought to be the source of secondary oral cancers [5]. Malignant tongue cancer can progress uniformly after PLD treatment is accomplished.

The study concluded that oral cancer develops following PLD delivery during a dated period of leukoplakia and that its danger of malignant transition to mouth cancer persists immediately after PLD treatment is completed. Continuous oral observation is required in the extended period, and the level after PLD treatment is concluded, especially in cases where the total dose is dependent.