In the past decade, photothermal therapy (PTT) of tumors based on gold nanomaterials has been widely studied because of their strong extinction ability and high photothermal conversion ability in the near-infrared (NIR) region. However, related research still faces two problems: First, the biosafety of the surface ligands on gold nanomaterials is not ideal and even has strong toxicity, so the surface modification or shell coating is very necessary; second, gold nanomaterials only have a single PTT function, which requires high temperature to achieve better treatment effect. Therefore, it is necessary to enrich the antitumor function of gold nanomaterials and realize synergistic therapy. Natural polyphenols can combine with each other or other substances through various supramolecular forces, forming shells on the surface of nanomaterials and reducing biotoxicity. In addition, natural polyphenols represented by resveratrol have antitumor activity and can induce apoptosis of tumor cells. Therefore, the surface coating method of gold nanomaterials with natural polyphenols with antitumor activity can effectively solve the above problems. In this work, we prepared resveratrol-coated gold nanoflowers (Au@Res NFs) and applied them to the treatment of malignant melanoma. Resveratrol in Au@Res NFs can induce the apoptosis of tumor cells, and Au@Res NFs can play a role in PTT under an NIR laser. In cell experiments, the synergistic effect of apoptosis/PTT on the A375 cells was extremely strong. In animal experiments, Au@Res NFs enriched in tumor sites identified the location and boundary of tumors by computed tomography (CT). The apoptosis induced by resveratrol had a certain inhibitory effect on tumor growth. Further applying the NIR laser, under the synergistic effect of apoptosis and PTT, the tumors were completely eliminated without recurrence during the experimental period.

Rationale: Thyroglossal duct carcinoma, a rare clinical condition characterized by ectopic thyroid adenocarcinoma within thyroglossal duct cysts (TGDCs), typically confirmed through intraoperative rapid pathology, this condition generally has a favorable prognosis. Nevertheless, comprehensive treatment guidelines across all disease stages are lacking, the purpose of this study is to report 1 case of the disease and propose the treatment plan for each stage of the disease. Patient concerns: A patient presented with thyroid swelling, classified as C-TIRADS 4A following a physical examination. Preoperative thyroid puncture identified papillary thyroid carcinoma, and genetic testing revealed a BRAF gene exon 15-point mutation. Ancillary tests showed a slightly decreased thyroid stimulating hormone (TSH) level (0.172) with no other significant abnormalities. Diagnoses: Preoperative fine-needle aspiration cytology (FNAC) confirmed right-side thyroid cancer. Intraoperative exploration uncovered a TGDC and intraoperative rapid pathology confirmed thyroglossal duct carcinoma. Interventions: A Sistrunk operation and ipsilateral thyroidectomy were performed. Outcomes: Postoperative recovery was satisfactory. Lessons: Thyroglossal duct carcinoma is a rare disease affecting the neck. Due to limited clinical cases and the favorable prognosis associated with this condition, there is currently no established set of diagnostic and treatment guidelines. According to tumor size, lymph node metastasis, thyroid status and other factors, the corresponding treatment methods were established for each stage of thyroglossal duct cancer, which laid the foundation for the subsequent treatment development of this disease.

Exposure to dexamethasone (DEX) causes cleft palate at high rates. Our previous studies proved that GATA binding protein 6 (GATA-6)/bone morphogenetic protein-2 (BMP-2) mediated apoptosis is related to DEX-induced cleft palate, but the specific mechanism is still unclear. The goal of this research was to understand the mechanism of apoptosis in cleft palate formation induced by DEX. Palatal mesenchymal cells from mouse embryos on embryonic day 13 were isolated as the experimental group, GATA-6 was silenced by GATA-6 small interfering Ribonucleic Acid (RNA). Cell Counting Kit-8, flow cytometry and Western Blot were applied to detect cell proliferation ability, cell cycle, the proportion of apoptotic cells, and the expression of apoptosis- related proteins of GATA-6 knockdown palatal mesenchymal cells. Further proteins on the BMP-2/Mitogen-activated protein kinase (MAPK) pathways were detected using Western Blot. T results showed that knockdown of GATA-6 by siRNA significantly decreased cell proliferation and increased the expression of apoptosis-related proteins. Bone morphogenetic protein-2/P38 mitogen Activated protein kinase (P38 MARK) pathway proteins decreased significantly among the GATA-6 knockdown group, DEX-cleft palate group and control +DEX groups. The results indicated that the GATA-6/BMP-2/P38 MAPK athway was involved in the apoptosis caused by GATA-6 silencing, which may be the possible mechanism of DEX inducing cleft palate.

Background: Although infantile hemangiomas (IHs) are usually self-limiting, residual elevated appearance may remain. Topical beta-blockers are effective in superficial IHs management, while intralesionally injected diprospan is effective at treating deep, localized IHs. A single application of topical timolol or injected diprospan has obvious limitations. Therefore, for elevated, localized mixed IHs, we applied topical timolol combined with intralesionally injected diprospan, using their respective advantages to maximize benefits. Purpose: To evaluate the clinical efficacy and safety of topical timolol combined with intralesionally injected diprospan for the treatment of elevated, localized mixed IHs and identify the optimal injection time. Methods: Infants with elevated, localized mixed IHs in the proliferative phase were treated with injected diprospan combined with topical timolol between March 2018 and March 2020. The injection was administered only when the tumor surface was higher than that of the surrounding tissue. The patients were asked to return every 4 weeks for a treatment response evaluation, and complications were recorded. Results: Thirty-six patients with elevated, localized mixed IHs (thickness >3 mm on Doppler ultrasound) were recruited. The mean age at treatment initiation was 3.58 ± 1.50 months (range: 1.00–6.00 months). The follow-up period ranged from 9 to 24 months. Considering the size of the IH at the end of treatment, regression was observed in 31 (86.1%) cases, stabilization was observed in 5 (13.9%) cases, and no treatment failure was observed. All the IHs improved in color and height after treatment. Conclusion: Topical timolol combined with intralesionally injected diprospan is an effective and safe treatment for elevated, localized mixed IH. The injection is needed only when we forecast the elevated tissue may remain after regression.

Malignant skin tumors mainly include basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. There is currently observational research suggesting that changes in cathepsin (CTS) may be a factor in the development of malignant skin tumors, but no studies have yet demonstrated a causal relationship between tissue protease changes and the occurrence of malignant skin tumors. Current studies have shown that cathepsin is involved in tumor cell invasion and metastasis by regulating growth factors and cellular immune function in tumor microenvironment, decomposing extracellular matrix and basement membrane, and promoting angiogenesis. In this study, we conducted a bidirectional Mendelian-randomization study using publicly available genome-wide association study (GWAS; GWAS Catalog) data. This study applies a bidirectional multivariate Mendelian randomization (MR) approach to investigate the causal relationship between cathepsin, basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. In cases where multiple cathepsins are implicated as etiological factors in certain diseases, a multivariable analysis is conducted to assess the direct and indirect causal effects of the exposure factors. In this study, we present a comprehensive MR analysis to investigate the relationship between 9 cathepsin and basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Based on our MR analysis using the largest GWAS Catalog dataset available, we are able to draw relatively reliable conclusions. In the MR study, we found that tissue protease L2 can promote skin cancer, Cathepsin O, and Cathepsin F are associated with an increased risk of basal cell carcinoma. Cathepsin H can inhibit basal cell carcinoma and malignant melanoma. In the reverse MR study, it was found that squamous cell carcinoma may cause an increase in Cathepsin O expression. In the multivariate analysis, it was found that Cathepsin H is a direct factor in reducing the occurrence of skin cancer and melanoma, with no apparent causal relationship to non-melanoma skin cancer. Cathepsin has a dual impact on skin cancer cells, and the expression of different cathepsins at the edge of skin tumors may indicate different developmental tendencies of skin cancer. Cathepsin may serve as effective biomarkers for predicting tumors.