Primary aortic wall myxoma is exceptionally rare and may mimic mural thrombus or acute aortic dissection.

A 38-year-old man presented after approximately 12 hours of acute left lower-limb ischemia with concomitant left upper-limb occlusion. Computed tomography angiography showed filling defects in the ascending and descending thoracic aorta. Recurrent embolization after peripheral thromboembolectomy prompted emergency ascending aortic exploration. A friable intramural myxoma was excised with ascending aortic graft replacement; the descending lesion was excluded by staged thoracic endovascular aortic repair while therapeutic anticoagulation was maintained.

Histopathology confirmed an aortic wall myxoma. The case illustrates the limitations of imaging and an individualized hybrid strategy for suspected multifocal aortic involvement.

Recurrent embolization after embolectomy should prompt urgent proximal-source control. Hybrid repair may be considered when anatomy and clinical urgency support it.

Solute carrier family 35 member F2 (SLC35F2) is a transporter located predominantly at the plasma membrane and Golgi apparatus and is predicted to contain ten transmembrane helices. Recent studies have identified SLC35F2 as the only currently known queuosine (Q)-specific transporter in human cells and as the principal high-affinity transporter of queuine (q), although it is not the absolutely exclusive route for q uptake. SLC35F2 is also aberrantly expressed in multiple cancers and has been associated with cell proliferation, migration, invasion, chemoresistance, and ferroptosis regulation. However, the available evidence derives mainly from database analyses, individual cell-based studies, and limited animal experiments and does not yet demonstrate that its tumor-promoting effects directly depend on q/Q uptake or tRNA queuosine modification. SLC35F2 is also an important uptake transporter for the anticancer agent YM155, and its expression can influence intracellular drug exposure and DNA-damage toxicity. YM155 was initially classified as a survivin transcriptional inhibitor, but subsequent studies indicate that its actions also involve DNA intercalation and oxidative DNA damage. Previous clinical trials did not prospectively stratify patients by SLC35F2 expression and showed limited overall efficacy; consequently, its clinical value remains translationally uncertain and biomarker-dependent. Using a structured narrative-review approach, this article critically evaluates the structure and localization of SLC35F2, q/Q transport, regulation of its expression and protein stability, tumor-associated functions, and YM155 delivery. It distinguishes replicated mechanisms from findings supported by single studies and from testable hypotheses, thereby providing a framework for future mechanistic research and precision drug delivery.

AIM: To present cases of spontaneous cerebrospinal fluid (CSF) rhinorrhea and otorrhea, and to conduct a systematic literature review examining the relationship between benign tumor location and the leak side. MATERIAL and METHODS: A PRISMA-based systematic review was conducted to evaluate studies on spontaneous CSF leaks caused by benign intracranial tumors, alongside three newly reported cases. RESULTS: All three cases exhibited CSF leaks ipsilateral to the tumor: Case 1 involved a pituitary ACTH-secreting macroadenoma with rhinorrhea; Case 2, a pineocytoma with hydrocephalus and nasal encephalocele; and Case 3, a petromastoid meningioma with otorrhea. In the systematic literature review, 28 of 125 studies met the inclusion criteria. The median patient age was 42 years, with a male-to-female ratio of 16:12. Macroprolactinoma was the most frequent tumor (25%), primarily located in the sella (46.4%). Tumors were located at the midline (39.3%), right side (35.7%), or left side (25%). The sphenoid sinus was the most common site of CSF leak (39.3%). The leak occurred through the right nostril (39.3%), left nostril (39.3%), both nostrils (10.7%), right ear (7.1%), and both the nostril and ear (3.5%). Hydrocephalus was present in 25% of cases. CONCLUSION: Although our cases demonstrated ipsilateral leaks, the literature review revealed equal rates of left-sided rhinorrhea, even with midline or right-sided tumors, suggesting skull base bone destruction alone does not explain CSF leaks, particularly in benign intracranial tumors outside mastoid involvement. Careful patient history regarding the side of rhinorrhea, comprehensive preoperative imaging, and hydrocephalus evaluation are essential for identifying the leak site and preventing complications, such as recurrent meningitis.

AIM: To examine the selective cytotoxic effects of Electro-Capacitive Cancer Therapy (ECCT) on human glioblastoma (GBM) cell lines (U87-MG and T98-G) and to evaluate its impact on normal epithelial cells. MATERIAL and METHODS: U87-MG and T98-G glioblastoma cells, along with Beas-2B normal epithelial cells, were exposed to ECCT at 100 kHz frequency and 20 V for 24 hours. Cell viability was determined using the MTT assay, while morphological changes were assessed through phase-contrast microscopy. Statistical analyses were conducted using one-way ANOVA and Student's t-test, with statistical significance defined as p < 0.05. RESULTS: ECCT exposure caused a time-dependent reduction in the viability of both GBM cell lines. U87-MG cells showed significant inhibition at all exposure durations, whereas T98-G cells exhibited a marked decrease only after 24 hours (p < 0.0001). In contrast, Beas-2B cells maintained their morphology and viability, suggesting that ECCT selectively targets malignant cells while sparing normal epithelial cells. CONCLUSION: ECCT significantly inhibits glioblastoma cell proliferation without adversely affecting normal cells, highlighting its promise as a non-invasive adjunctive treatment option for GBM. Further preclinical and clinical studies are warranted to clarify its underlying mechanisms, optimize exposure parameters, and determine its potential integration into multimodal glioblastoma therapy.

Bioactivation and clearance of anticancer agents are crucial factors in the efficacy and toxicity of anticancer drugs. Exosomes are membrane-bound vesicles secreted by tumor cells and the tumor microenvironment. These vesicles contain drug-metabolizing enzymes, transporters, and RNA. Exosomes can be non-invasively collected from the blood. This article has been prepared by combining the evidence of the role of exosomal cytochrome P450 isoforms, such as cytochrome P450 family 2 subfamily C member 19, cytochrome P450 family 2 subfamily D member 6, and cytochrome P450 family 3 subfamily A member 5, in the oxidation of anticancer drugs in the first phase of drug metabolism. Exosomal UDP-glucuronosyltransferase 1A1 has been found to help in the conjugation of anticancer drugs in the second phase of drug metabolism. Exosomal ATP-binding cassette transporters, P-glycoprotein, multidrug resistance-associated protein 1, and breast cancer resistance protein have been found to act as intercellular conveyors of drug efflux capacity. These transporters can modulate the efficacy of chemotherapy. Exosomal microRNAs, such as microRNA-21, microRNA-155, and microRNA-1246, have been found to modulate apoptosis, DNA repair, metabolic adaptation, and chemotherapy resistance through the PI3K/AKT pathway, EZH2/STAT3 pathway, and PDCD4 pathway. Long non-coding RNAs, such as UCA1 and HOXA antisense RNA, can reprogram the chromatin structure. These long non-coding RNAs can suppress tumor suppressor genes, thus leading to chemotherapy resistance. Bioinformatics pipelines have been designed to bridge the gap between exosomal RNA and protein levels in the profile of dynamic metabolic states. The challenges in the field of exosomal therapy drug monitoring have been discussed in the article. The article has recommended the use of artificial intelligence in the integration of omics with microfluidic technology for the improvement of exosomal therapy drug monitoring.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder, and its treatment remains a significant challenge. This study investigated the mechanism of Jujuboside A (JuA) in the treatment of PCOS through mitophagy. Granulosa cells (GCs) were collected from follicular fluid derived from PCOS women. The effects of JuA on PCOS were determined by measuring body weight, ovarian weight, estrous cycle, glucose level, insulin tolerance, and ovarian morphology in dehydroepiandrosterone-induced mice. SIRT3 expression levels were quantified in GCs, KGN cells, and mouse ovaries. The effects of JuA on SIRT3-related oxidative stress and mitochondrial damage were investigated in KGN cells and mice. Transmission electron microscopy was used to observe mitochondrial damage and mitophagy in GCs. The expression of mitophagy-related proteins (PINK1 and Parkin) was analyzed. JuA significantly improved body weight, estrous cycle, ovarian morphology, glucose tolerance, and insulin resistance, partially restoring ovarian function in PCOS mice. Moreover, JuA significantly activated SIRT3 expression and alleviated SIRT3-related oxidative stress and mitochondrial damage in mouse ovaries, GCs, and KGN cells. Mechanistically, JuA upregulated SIRT3 and inhibited excessive activation of the PINK1/Parkin pathway to reduce mitophagy. These findings demonstrated JuA protected GCs from mitochondrial damage by activating SIRT3 and inhibiting PINK1/Parkin-mediated mitophagy.

Thermoradiotherapy at 40-43 °C is an effective treatment for locoregional recurrent (LRR) breast cancer patients. During hyperthermia temperature monitoring is often limited to skin temperatures, but their predictive value for achieving locoregional tumor control (LRC) remains unclear for tumor depths ≥1cm. This study compared predictive value of skin versus invasive intratarget temperatures.

We reported earlier the thermal dose-effect relationship in 112 patients with LRR breast cancer treated in 2010-2017 with postoperative re-irradiation (8 × 4 Gy/23 × 2 Gy) and 4-5 weekly hyperthermia sessions with 434 MHz microwave applicators. Bolus cooling enabled semi-superficial target depths (1-4 cm), thermocouple thermometry monitored both skin and intratarget temperatures. The present study analyzes relationships between LRC and average skin and intratarget median temperature T₅₀ and best session with highest median thermal dose CEM43T50 (cumulative equivalent minutes at 43 °C). Pearson correlation coefficient analysis evaluated correlation between intratarget and skin temperature parameters.

Average median skin and invasive temperatures were T₅₀ = 40.6 °C (Interquartile Range IQR 40.3-40.8) and T₅₀ = 40.7 °C (IQR 40.0-41.3), respectively, without association between skin and intratarget temperatures. Median CEM43T50 for skin and intratarget were 2.8 (IQR 2.0-4.3) and 7.2 min (IQR 3.4-15.9) in the best hyperthermia session, respectively. Twenty-four patients developed infield recurrences; median time-to-recurrence was 3.4 years (IQR 2.7-4.6 years). Univariate and multivariate analysis showed significant association of intratarget temperature parameters with LRC (p = 0.015; p = 0.021, respectively), but not for skin temperature parameters and LRC (p = 0.131; p = 0.215, respectively).

Temperature monitoring using both skin and invasive intratarget measurements is key for ensuring good quality superficial hyperthermia delivery for tumor depths ≥1cm.

Fishermen are among the occupational groups with substantial sun exposure and are prone to dehydration, sunburn, photoaging, actinic cheilitis, and oral cancer. The objective of this study was to evaluate the dermatological condition of the lips of fishermen in the Guarujá/Santos port region, investigate whether they use preventive measures to avoid such lesions, and develop a suitable product for lip protection.

Thirty participants underwent an initial clinical examination and photo-graphic documentation. All 30 participants received the developed lip protector, which contained UV filters and moisturizing agents. At re-evaluation one month later, 17 participants returned, corresponding to a loss to follow-up of 43.40%.

All fishermen were male, with a minimum age of 23 and a maximum age of 74. When asked about lip balm use, only 1 of the 30 participants reported using it. At follow-up, among the 17 participants, only 1 reported using the provided lip balm and reapplying it during the day; this use was described as "sporadic."

The findings highlight the need for educational strategies to promote lip protection and prevent potentially malignant lesions among outdoor workers exposed to ultraviolet radiation.

Epidemiological and survival data on osteosarcoma of the jaws (OSJ) in Latin America remain scarce. We characterized the clinicopathological, radiographic, treatment-related, and survival features of OSJ in Latin America.

This multicenter case series involved 22 institutions from Brazil, Chile, Argentina, Colombia, Venezuela, Uruguay, and Mexico. Demographic, clinical, radiographic, histopathological, treatment, and survival data were analyzed using descriptive and inferential statistical methods. Survival outcomes were assessed using Kaplan-Meier analysis and Cox regression models.

A total of 119 OSJ cases were included. The median age was 33 years, with a female predominance (58%), and the mandible was the most commonly affected site (68.9%). A mixed radiographic appearance predominated and was frequently accompanied by cortical perforation and a sunburst periosteal reaction. Histologically, the osteoblastic subtype accounted for 63.5% of cases. Surgical resection was the main treatment modality (71.2%). Increasing age (p = 0.034) and multimodal or nonsurgical management (p = 0.023) were independently associated with poorer survival. The estimated overall survival rates were 67.5% at 12 months and 37.5% at 60 months.

Data corroborate previous literature and demonstrate that OSJ in Latin America predominantly affects adults and exhibits aggressive patterns. Surgical management remains central to improving survival whenever it is technically feasible.

Talazoparib is a potent poly(ADP-ribose) polymerase (PARP) inhibitor approved for use in patients with germline BRCA1/2-mutated human epidermal growth factor receptor 2-negative locally advanced or metastatic breast cancer. Although PARP inhibitor sensitivity has traditionally been attributed to synthetic lethality in tumors with BRCA1/2 mutations or homologous recombination repair deficiency, emerging evidence indicates that clinical and preclinical activity may extend to selected tumors beyond those harboring germline BRCA1/2 mutations. This study investigated the mechanism underlying talazoparib efficacy in both BRCA1/2-mutant and BRCA1/2 wild-type breast cancer cells.

Twenty-one breast cancer cell lines, including both BRCA-1/2-mutant and wild-type cells, were treated with talazoparib, and the effects of the treatment on cell proliferation, cell cycle progression, DNA damage accumulation, and apoptosis were evaluated.

Talazoparib demonstrated antiproliferative effects in BRCA1/2-mutant and wild-type cells in a long-term culture system, as assessed by colony formation assays. Accumulation of single-stranded and double-stranded DNA damage was observed in talazoparib-sensitive cell lines, as indicated by phosphorylated RPA and γ-H2AX, respectively. This was accompanied by G2/M arrest and subsequent apoptosis, as evidenced by cleaved caspase-3 expression and Annexin V staining. Abnormal mitotic nuclei were observed in talazoparib-sensitive cell lines, which also exhibited potent and sustained PARP1 trapping on chromatin.

Talazoparib exerts anti-tumor effects in BRCA1/2-mutant and wild-type breast cancer cells by promoting the formation of abnormal mitotic nuclei and inducing apoptosis in sensitive cells. Our findings support the potential therapeutic application of talazoparib beyond its current indications for BRCA1/2-mutant tumors.