Background: Oral or laryngeal leukoplakia has an increased risk for malignant transformation but the risk of the two anatomical sites has not been compared to each other yet. Materials and Methods: Clinical data of 253 patients with leukoplakia (oral = 221 or laryngeal = 32) enrolled from January 1996 to January 2022 were analyzed. One hundred and seventy underwent biopsy and 83 did not. The mean follow-up time was 148.8 months. Risk factors for the malignant transformation of leukoplakia were identified using Cox proportional hazard models. Results: In the oral or laryngeal group, the rate of cancer was 21.7% and 50% (p = 0.002), respectively. The 10-year estimated malignant transformation was 15.1% and 42% (p < 0.0001), respectively. The laryngeal group had an increased risk of malignant transformation (p < 0.0001). The 5-year estimated survival with leukoplakia-associated cancer for the oral or laryngeal group was 40.9% and 61.1% (p = 0.337), respectively. Independent predictors of malignant transformation in the oral group were dysplasia and the grade of dysplasia of the leukoplakia, and in the laryngeal group, dysplasia had a significant impact. The malignant transformation rate was low for oral patients without biopsy or with no dysplasia, 3.9% and 5.1%, respectively. The malignant transformation occurred over 10 years. Conclusions: Patients with dysplastic leukoplakia have an increased risk of malignant transformation, but the risk is higher with laryngeal than with oral leukoplakia. There is no significant difference between the groups regarding survival with leukoplakia-associated cancer. Oral patients with no dysplastic lesions have a low risk of malignant transformation. A complete excision and long-term follow up are suggested for high-risk patients to diagnose cancer in an early stage and to control late (over 10 years) malignant events.

Purpose: To evaluate the mutagen sensitivity phenotype on the risk of second primary cancer (SPC) in patients with head and neck squamous cell carcinoma (HNSCC), and to estimate the long-term rate of SPC and the outcome with SPC.Methods: A survey was made regarding SPC among 124 younger (≤ 50 years) adults with HNSCC who were enrolled in a pretreatment mutagen sensitivity investigation during 1996–2006. Mutagen sensitivity was assessed by exposing lymphocytes to bleomycin in vitro and quantifying the bleomycin-induced chromatid breaks per cell (b/c). Patients were classified as hypersensitive (> 1 b/c) or not hypersensitive (≤ 1 b/c).Results: Mean follow-up time for all patients was 68 months (range: 5–288 months), and the 15-year cancer-specific survival was 15%. Twenty patients (16%) developed a SPC (15-year estimated rate: 41%), and half of them was hypersensitive. The crude rate of SPC for hypersensitive (n = 65) or not hypersensitive (n = 59) patients were 15 and 17%, respectively (p = 0.4272). The 15-year estimated rate of SPC for hypersensitive and not hypersensitive patients was 36 and 48%, respectively (p = 0.3743). Gender, UICC stages, anatomical sites of index cancer did not prove to be a significant risk factor for SPC. Forty-five percent of SPC developed after the 10-year follow-up. The 3‑year cancer-specific survival was 23% with SPC.Conclusion: According to our findings, mutagen hypersensitivity was not associated with an increased SPC risk in HNSCC patients. Patients are at a lifelong risk of developing a SPC. Survival with SPC is very poor.

Most of the neck node metastases from cancer of unknown primary (CUP) are squamous cell carcinomas (SCCs). The majority of which are human papillomavirus (HPV)-related, frequently show cystic morphology referring to Waldeyer’s ring origin. Here, we report four cases of neck node SCCs metastases from CUP. In our institute, 432 patients with head and neck (HN) SCC underwent pretreatment mutagen sensitivity (MS) assay between 1996 and 2006. Among them, 4 patients ≤50 years of age had metastatic cervical nodes from CUP. The primary treatment was cervical node dissection ± radiotherapy. All patients had elevated (>1.0 chromatid break/cell) MS. One male patient died of progressive neck metastasis within 3 years and the 3 female patients are still alive more than 15 years after initial treatment of HPV+ (two) or cystic (one) SCC. Two female patients developed second and third distant site metachronous primary cancers. HPV+ or cystic HNSCC from CUP with elevated MS indicates good outcome. Distant site metachronous cancers of different histologic origins cannot be explained by field cancerization. The clinical significance of elevated MS in neck node SCC metastasis from CUP requires further investigation.

Bevezetés: A szájüregi potenciálisan rosszindulatú elváltozások közül az egyik leggyakoribb lézió a leukoplakia. Fontostisztázni, hogy a klinikailag leukoplakiának diagnosztizált esetek mögött milyen hisztopatológiai diagnózis áll, amely döntőenmeghatározza a prognózist és a szükséges terápiát.Anyag és módszer: 2021. április és 2024. április között 75 szájüregi leukoplakiával diagnosztizált betegnél történt szövettanimintavétel a Semmelweis Egyetem Orális Diagnosztikai Tanszék Dento-alveolaris Sebészeti Osztályán. A szövettaniminták hisztopatológiai elemzése hematoxilin-eozin festett minták alapján történt a Semmelweis Egyetem Patológiaiés Kísérleti Rákkutató Intézetében, bizonyos esetekben immunhisztokémiai vizsgálattal kiegészítve.Eredmények és megbeszélés: A 75 betegnél a leukoplakiák előfordulási helye, gyakoriság szerinti csökkenő sorrendben:gingiva/fogatlan állcsontgerinc (n = 26), bucca (n = 16), szájfenék (n = 12), nyelv (n = 11), szájpad (n = 6), ajak (n = 2).Ritka esetben multifocalis megjelenés is előfordult (n = 2). A szövettani mintavétel általában próba excisio volt, nem történtmeg az elváltozás teljes kimetszése. A hisztopatológiai eredmény 51 esetben hyperkeratosis (dysplasia nélkül),19 esetben enyhe dysplasia, 5 esetben mérsékelt dysplasia volt. Súlyos dysplasiás eset nem volt. Klinikai homogenitásttekintve 61 esetben homogén és 14 esetben non-homogén volt a leukoplakia. A nem dysplasiás és dysplasiás betegcsoportokattekintve szignifikánsan gyakrabban állt dysplasia az elváltozás mögött, amennyiben klinikailag non-homogénmegjelenést mutatott a leukoplakia (p = 0,0088). A vizsgált beteganyagon 75 beteg közül 32 dohányzik, 43 nem dohányzik.Eredményeink alapján a dohányzás nem volt szignifikáns hatással a dysplasia jelenlétére és súlyosságára.A betegek követése folyamatos (félévenkénti kontrollvizsgálat). Átlagos követési idő: 17,4 hónap (tartomány: 1–38 hónap).Következtetés: A szájüregi leukoplakiával diagnosztizált betegek esetében szövettani mintavétel szükséges a hisztopatológiaidiagnózis felállításához, valamint hosszú távú követés javasolt a késői rosszindulatú átalakulás elkerülésére.