Primary intracranial squamous cell carcinoma (SCC) arising from an epidermoid cyst is an exceptionally rare and aggressive malignancy with a dismal prognosis. Conventional management typically involves gross total resection followed by wide-field radiotherapy; however, this intensive approach is often unfeasible for elderly or frail patients. We present a case of primary intracranial SCC in a 75-year-old woman who presented with rapid cochleovestibular deterioration. Imaging revealed subtle enlargement of a long-standing cerebellopontine angle epidermoid cyst. Subtotal resection was performed to preserve critical neurovascular structures adherent to the infiltrative tumor. Given the patient's poor performance status and the risk of toxicity from broad-field radiation, adjuvant Gamma Knife radiosurgery (GKS) was selected as a focal salvage modality. Despite the limited surgical margin, the patient has maintained a progression-free status with no radiographic evidence of disease progression for 18 months without neurological decline. This case highlights the diagnostic challenge of malignant transformation disguised by radiologic mimicry and demonstrates that GKS can serve as an effective and tolerable adjuvant strategy. We propose that for high-risk patients precluded from intensive multimodal therapy, focused stereotactic irradiation offers a viable alternative to secure local control while preserving quality of life and systemic immune integrity.

Metastasis is the leading cause of cancer-related death, underscoring the need to elucidate the key mechanisms behind this process. Neutrophil extracellular traps (NETs) have emerged as critical regulators of tumor progression and metastasis. This review summarizes the primary stimuli and signaling pathways that govern NET formation and outlines the mechanistic roles of NET components in tumor growth and metastatic spread. We focus on environmental and tumor microenvironment-derived factors, including psychological stress, tumor-secreted cytokines, and treatment-related responses, that drive NET formation. The involvement of NETs in multiple stages of the metastatic cascade is discussed, including angiogenesis, tumor cell intravasation and extravasation, circulating tumor cell survival, metastatic colonization, and the reactivation of dormant tumor cells. Additionally, we examine how NETs contribute to the establishment of an immunosuppressive microenvironment. Finally, emerging therapeutic strategies targeting NETs are briefly reviewed, highlighting their potential relevance in metastatic cancer treatment.

KRAS-targeted therapy has opened new doors in the world of oncology, and many trials are underway for KRAS specific treatments for gastrointestinal (GI) malignancies. Outlining the current state of KRAS therapy and the remaining research gaps pertaining to these deadly cancers is crucial for the development of future therapeutics. In this review, we focus on the relationship between KRAS and GI malignancies. Current therapies are discussed with an in-depth exploration of the KRAS gene and how it connects to pancreatic, colorectal and other GI malignancies. Promising clinical trials and future therapies are highlighted while discussing the molecular biology behind them. Specifically, trials focusing on upcoming KRAS on and off inhibitors in development as well as variant focused inhibitors targeting the more common mutations G12D and G12V. We discuss exciting new pan/multi KRAS inhibitors that have been successful in pre-clinical trials. More unique therapeutic options include KRAS T cell therapies, vaccines, and combination strategies with immunotherapy. Furthermore, we address the difficulties with KRAS therapy, and the potential future directions needed to overcome them. An in-depth current literature review was done along with a review of the active clinical trials for KRAS-targeted therapeutics involving GI malignancies.

Juvenile nasopharyngeal angiofibroma (JNA), a rare vascular tumor in adolescent males, involves dysregulated angiogenesis and hormonal interplay. Key molecular drivers include HIF-1α, VEGF, bFGF, and β-catenin, promoting tumor growth via pathways like Wnt/β-catenin and Ras signaling. Androgens and estrogen modulate progression, though mechanisms remain debated. Targeted therapies reduce tumor proliferation and vascularity in preclinical studies, yet clinical translation is hindered by drug resistance and inconsistent biomarker expression. Hormonal and MMP-targeted approaches also show potential but require validation. This review consolidates JNA's molecular landscape, emphasizing the need for personalized strategies, biomarker refinement, and combination therapies to improve therapeutic outcomes for this challenging tumor.

Electrochemotherapy is a minimally invasive treatment based on the principle of reversible electroporation of target cells in pathologic tissues in order to increase the local effect of chemotherapeutic agents. The mechanism of action relies on temporarily increasing cell permeability to increase the uptake of cytotoxic drugs in the intracellular space. Originally developed for the treatment of cutaneous malignancies, electrochemotherapy has significantly evolved over the past few decades, thanks to advancements in electrode design and image guidance, finding fertile ground in musculoskeletal oncological pathologies, such as bone and soft tissue tumors and different kinds of vascular malformations. Moreover, initial experiences have reported on the treatment of other soft tissue tumors such as desmoid fibromatosis. The aim of this review is to summarize the literature on the role of electrochemotherapy across a variety of musculoskeletal conditions, starting from established oncologic indications, such as metastatic bone or soft tissue tumors, to emerging evidence on primary musculoskeletal pathology, with particular attention paid to the results of the leading studies relating to the efficacy, complications, and recurrence rate.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, and liver transplantation (LT) remains the only curative treatment addressing both tumor burden and underlying liver disease. Despite an adequate candidate selection, HCC recurrence after LT occurs in 8-20% of cases and is associated with a poor prognosis, particularly in patients who experience an early relapse. The management of HCC recurrence remains particularly challenging due to the lifelong immunosuppression required after LT, which may promote tumor progression and restrict therapeutic options. This review synthesizes the current evidence on systemic therapies for recurrent HCC after LT, focusing on tyrosine kinase inhibitors (TKIs), immunotherapy, and the current available immunosuppression strategies. Unfortunately, in this setting, robust prospective studies are lacking, and clinical decision-making remains based on retrospective data and expert consensus. Future research should prioritize the prospective evaluation of systemic regimens, integration of immunosuppression modulation, and careful exploration of immunotherapy or new target therapies in this special population.

Background: Esophageal squamous cell carcinoma (ESCC) is the predominant subtype of esophageal cancer, with poor outcomes following neoadjuvant chemoradiotherapy (NCRT). Neoadjuvant chemoimmunotherapy (NCIT) has emerged as a promising strategy, but reliable predictive biomarkers remain lacking. This study aimed to develop an AI-driven pathomic model for NCIT response prediction and explore its biological mechanisms. Methods: We analyzed 269 H&E-stained whole-slide images (WSIs) from 198 ESCC patients (104 from Tongji Hospital, 94 from TCGA). Using ResNet152, we segmented WSIs into four tissue categories (tumor cells, stroma, lymphocytes, and necrosis), extracted spatially weighted pathomic features, and constructed the ECiT score via logistic regression. An integrated model combining the ECiT score with clinical variables (T stage, P53 status) was developed. Mechanistic analyses were performed using TCGA-ESCA and GSE160269 datasets. Results: The integrated model achieved AUCs of 0.897 (training) and 0.809 (temporal validation), outperforming clinical (AUC = 0.624) and pathomic-only (AUC = 0.751) models. Mechanistically, a high ECiT score correlated with enhanced immune activation (elevated CD4⁺ memory T cell infiltration), while low scores were linked to endoplasmic reticulum (ER) stress-unfolded protein response (UPR) activation. EIF2S3 was identified as a key molecular mediator, correlating with three pathomic features, UPR activation, and poor prognosis. Conclusions: This study may offer a preliminary indicator that could assist in personalized clinical decision-making. Correlative evidence suggests that the EIF2S3-mediated ER stress-UPR axis represents a potential candidate therapeutic target to overcome NCIT resistance, generating testable hypotheses to advance precision oncology for resectable locally advanced ESCC.

Fear of cancer recurrence (FCR) is a significant but understudied concern among parents of childhood cancer survivors. This study quantitatively characterized parental FCR and explored potential demographic and clinical correlates among parents of children treated for cancer. Parents (N = 192) completed the Fear of Cancer Recurrence Inventory-Parent Short Form (FCRI-Parent) and provided demographic information. Clinical variables were obtained from medical chart review. Associations between FCR and demographic or clinical variables were analyzed using t-tests, ANOVAs, and Pearson's correlations. Parents reported a mean FCR score of 18.64 (SD = 8.73), with 42.2% of parents endorsing FCR above a score of 22. Parental FCR significantly varied by parent race, education, and spirituality. Higher FCR was also significantly negatively correlated with child age, time since diagnosis, and time since treatment completion. Parents of children with central nervous system tumors or hematological malignancies endorsed significantly higher FCR compared to parents of children with solid tumors. Findings build on previously identified psychosocial needs for parents of children treated for cancer by quantitatively describing parental FCR and exploring subgroups that may be at increased risk for FCR. Tailored interventions, including strategies that support spiritual coping, may help mitigate FCR among at-risk parents.

Granular cell tumors are uncommon neoplasms of neural origin that may involve the skin and often present with nonspecific clinical features, making diagnosis challenging. Cutaneous granular cell tumors rarely exhibit overlying hypertrichosis, a finding that may obscure their clinical recognition. In this report, we describe a rare case of a primary cutaneous granular cell tumor with prominent overlying terminal hair growth in an adult patient. A 27-year-old woman presented with a slowly enlarging, firm, pigmented plaque on the upper back associated with pruritus and increased hair growth. Histopathologic examination revealed sheets of large polygonal cells with abundant granular eosinophilic cytoplasm, and immunohistochemical staining was positive for S100, SOX10, CD68, and calretinin, confirming the diagnosis. The lesion was completely excised with no evidence of malignancy. To our knowledge, this represents the second reported instance of a cutaneous granular cell tumor associated with hypertrichosis and the first described in an adult. It underscores the importance of clinicopathologic correlation in evaluating unusual cutaneous lesions and expands the spectrum of recognized presentations of cutaneous granular cell tumors.

Background/Objectives: Phyllodes tumors are rare fibroepithelial neoplasms of the breast, accounting for less than 1% of all breast tumors and approximately 2-3% of breast fibroepithelial tumors. They can be benign, borderline, or malignant, depending on cellular atypia and stromal invasion. Although most display local behavior, malignant forms can metastasize hematogenously, most frequently to the lungs, bones, and liver, with lymph node metastases being exceptional. Case Presentation: We analyzed the case of a 47-year-old woman with a phyllodes breast tumor weighing approximately 5 kg. The tumor evolved slowly over five years, followed by accelerated growth, cutaneous necrosis, superinfection, and severe anemia. Total mastectomy was performed, and histopathological examination confirmed the diagnosis of a malignant phyllodes tumor. Five months after surgery and adjuvant radiotherapy, the patient developed laterocervical metastases with thyroid invasion and life-threatening tracheal compression, an extremely rare presentation for this type of tumor in adults. Discussion/Conclusions: This case illustrates the aggressive and unpredictable behavior of malignant phyllodes tumors and underscores the necessity of careful oncological monitoring and a multidisciplinary approach, given their potential for dissemination to unusual locations.