Myiasis is the infestation of living or necrotic tissues of humans and animals by dipteran larvae. It is endemic to tropical and subtropical regions of the Americas and Africa. It occurs most frequently in vulnerable populations, and it is associated with open wounds, poor hygiene, and predisposing medical conditions. The objective was to describe 2 clinical cases of cutaneous myiasis in humans confirmed in Mexico.

The first case occurred in a 77-year-old woman, and it was secondary to mild traumatic brain injury according to the World Health Organization (WHO) classification. The second in a 74-year-old man with advanced basal cell carcinoma on the right side of his face. In both cases, samples were sent to the State Public Health Laboratory (LESP) and the National Service for Agrifood Health, Safety and Quality (SENASICA), where the taxonomic diagnosis of Cochliomyia hominivorax was confirmed.

Myiasis is a preventable disease of epidemiological importance which was considered eradicated in Mexico since 1991. Early diagnosis and comprehensive medical-surgical treatment allow for a favorable evolution and prognosis, with the prevention of serious complications.

The incidence of cancer continues to rise globally, with many tumor types remaining difficult to treat effectively. While existing drugs can alleviate symptoms or slow disease progression, their efficacy varies considerably between patients. To explore this challenge, we present a computational approach for identifying patient-specific candidate compounds. Our approach was developed for glioblastoma, but it can be applied to other types of cancer. Our study involves identifying possible disease-relevant proteins specific to each patient that underlie the generated networks, together with drug targets and proteins associated with cancer dependency. These networks are analyzed using centrality measures and Louvain community detection method. Then, further investigating the individual networks, network controllability analysis is applied to identify key regulatory targets within the network. These targets are filtered and ranked to prioritize candidate drugs for individualized treatment. By comparing results across patients and against networks based on generic data, we show substantial differences between patient-specific and generic network representations. Additionally, we track changes in patient-specific networks over time in five glioblastoma cases, exploring how molecular differences between primary and recurrent tumors may influence network structure and computational drug prioritization.

BACKGROUND Postsurgical pyoderma gangrenosum is a rare neutrophilic dermatosis that can mimic infection, wound dehiscence, malignancy, foreign-body reaction, or impaired surgical healing. Diagnostic delay is common and may lead to repeated debridement, which can worsen ulceration through pathergy. This case highlights the diagnostic challenge of multifocal postsurgical pyoderma gangrenosum involving anatomically distinct sites after procedures initially performed for presumed benign lesions. CASE REPORT A 70-year-old woman with celiac disease and prior left breast cancer treated with lumpectomy, chemotherapy, radiation, and implant reconstruction developed nonhealing ulcers of the left superior breast and left lower back after surgical treatment of benign lesions. Initial evaluation favored retained cyst lining, foreign-body reaction, infection, impaired wound healing, and possible implant-related complications. Despite advanced wound therapies, antimicrobials, and biologic wound products, both lesions progressively enlarged. Biopsies demonstrated abscess formation, multinucleated giant cells, and sinus tract formation without malignancy. Wound cultures and pulmonary findings complicated the diagnostic course, but neither targeted antimicrobial nor prolonged antifungal therapy produced sustained improvement. The diagnosis was clinically supported by worsening after procedural intervention, exclusion of malignancy and persistent infection, multifocal involvement, and rapid response after initiation of topical and intralesional corticosteroid therapy. CONCLUSIONS This case supports considering postsurgical pyoderma gangrenosum in refractory postsurgical wounds that worsen despite local wound-directed interventions, particularly when lesions involve multiple anatomically distinct surgical sites. The complete resolution of both lesions after topical and intralesional corticosteroid therapy further supports the importance of recognizing an inflammatory, pathergy-driven process once infection, malignancy, and other local causes have been reasonably excluded. Earlier recognition may help avoid repeated procedural trauma, unnecessary treatment escalation, and prolonged morbidity.

Acute myeloid leukemia (AML) primarily affects older adults, many of whom are unsuitable for intensive chemotherapy. Hypomethylating agents (HMA) -intravenous (IV) decitabine and subcutaneous (SC) azacitidine- are standard therapeutic options but require frequent hospital visits and substantial healthcare resource use. Oral decitabine/cedazuridine (DEC-C) offers a therapeutically equivalent alternative that may reduce hospital resource burden and improve patient convenience. This study estimated and compared the economic and organizational impact of IV, SC, and oral HMA administration in AML patients unfit for standard intensive chemotherapy, from the perspective of the Spanish National Health System. A micro‑costing model quantified direct non‑pharmacological costs associated solely with the administration route across five domains: drug preparation and administration, treatment‑related hospitalizations, medical transportation, catheter management, and infections. Resource use was derived from a survey of 30 healthcare professionals across 16 hospitals and valued using official tariffs. Costs were calculated separately for induction and subsequent cycles; drug acquisition costs were excluded. Non‑pharmacological costs per patient were €9,998 for IV decitabine, €12,177 for SC azacitidine, and €1,306 for oral DEC‑C, representing cost reductions of 87% and 89% for oral therapy versus IV and SC, respectively. Savings were driven mainly by reductions in hospitalization (58-61%), transport (13-22%), infections (9%-12%), administration‑related activities (11-12%) and the avoidance of catheter-related costs. Oral therapy also markedly reduced resource utilization, including 40-50 fewer hours of healthcare professional time, 8-9 fewer inpatient days, and 4-8 fewer ambulance transfers per patient. Catheter use decreased by 33%, and infection risk declined by 87% versus IV and 54% versus SC. Oral administration substantially reduces direct non‑drug costs and frees hospital capacity, offering meaningful organizational efficiencies and contributing to the sustainability of AML care within a resource‑constrained health system. These findings reinforce the value of integrating oral HMAs into clinical pathways.

Narrative review.

To synthesize current evidence on diagnostics and clinical decision-making for patients with cervical spine neoplasms.

Although the cervical spine is disproportionately affected by primary spinal tumors and is the predominant site for intramedullary spinal cord tumors, there remains a relative paucity of reviews focused specifically on cervical spine neoplasms.

PubMed and Scopus were searched using a combination of terms related to cervical spine neoplasms, classification schemas, diagnostic evaluation, staging, and clinical decision-making. Supplemental targeted searches evaluated spinal oncology staging and treatment frameworks. Reference lists of articles and major reviews were screened for additional studies.

Cervical spinal tumors are classified by anatomic compartment as intramedullary, intradural extramedullary, or extradural, with pathologic diagnosis described by the 2021 World Health Organization (WHO) Classification of Tumors of the Central Nervous System and the 2020 WHO Classification of Soft Tissue and Bone Tumors. Diagnosis integrates clinical symptoms with a multimodal imaging approach that incorporates magnetic resonance imaging, computed tomography, positron emission tomography/computed tomography, vascular imaging, and adjunctive modalities such as diffusion tensor imaging tractography. Tissue biopsy remains central to diagnosis, with indications, contraindications, and technique selection guided by lesion characteristics and compartment. Liquid biopsy through cerebrospinal fluid-based circulating tumor DNA analysis has also emerged as a promising minimally invasive alternative for intramedullary lesions. Clinical decision-making frameworks have evolved considerably, from early anatomic staging systems through neurological and instability assessments to modern comprehensive treatment algorithms. Multidisciplinary tumor boards are essential for integrating medical, surgical, and radiation oncology expertise and individualizing care for these patients.

Cervical spine neoplasms are a diagnostically and therapeutically challenging subset of spinal tumors, encompassing a heterogeneous spectrum of primary and metastatic lesions. A multimodal, multidisciplinary approach is essential to optimize diagnostic accuracy, clinical decision-making, and individualized patient care.

Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal solid tumors due to its dense desmoplastic stroma, poor vascular perfusion, and the limited intratumoral delivery of chemotherapeutic agents such as oxaliplatin (OXA). Extracellular vesicles (EVs) offer a biocompatible platform for drug delivery, yet their intrinsic lack of tumor specificity constrains therapeutic efficacy. Ephrin type-A receptor 2 (EphA2), which is highly expressed and efficiently internalized in PDAC, represents an attractive molecular target for guiding EVs into tumor cells. In this study, we engineered HEK293T-derived EVs to display membrane-anchored anti-EphA2 Fab fragments and encapsulate OXA (EVs-EphA2/OXA) as a targeted delivery system for PDAC therapy. Stable producer cells expressed the engineered Fab on the plasma membrane and released vesicles that retained canonical EV markers and robust antigen-binding capability. EVs-EphA2 demonstrated selective uptake into EphA2-positive AsPC-1 and BxPC-3 cells and induced significantly greater cytotoxicity than free OXA or untargeted EVs/OXA in vitro. In xenograft models, EVs-EphA2/OXA achieved the most pronounced tumor suppression, accompanied by increased γH2AX-associated DNA damage, enhanced TUNEL-positive apoptosis, and preferential tumor accumulation in biodistribution imaging. These findings demonstrate that EphA2-targeted EVs can substantially improve intratumoral delivery of OXA and amplify antitumor efficacy, supporting EVs-EphA2/OXA as a promising platform for receptor-guided chemotherapy in PDAC.

Transforming growth factor-beta (TGFβ) has dual roles in cancer, initially suppressing tumors but later promoting metastasis and immune evasion. Efforts to inhibit TGFβ have been largely unsuccessful due to significant toxicity and indiscriminate immunosuppression. Leucine-rich repeat-containing protein 15 (LRRC15) is a TGFβ-regulated antigen expressed by cancer cells of mesenchymal origin and cancer-associated fibroblasts (CAFs). In preclinical studies, ablation of TGFβ-driven LRRC15+ CAFs enhances effector functions of CD8+ T cells. However, the pathobiological mechanisms associated with TGFβ's upregulation of LRRC15 expression in cancer cells remain unclear. Using an integrated approach combining functional compound screening with scRNA-seq, we reveal key genomic features regulating TGFβ's ability to increase LRRC15 expression on cancer cells. Construction of gene regulatory networks converged our analyses on four key genes (MMP2, SPARC, TGFβR2, and WNT5B) central to TGFβ-induced LRRC15 pathobiology in cancer cells. Validation of these genes in cell models and their use in predicting immunotherapy responses highlight their potential in refining immunotherapy strategies and personalizing cotreatment options.

Mucosal melanoma is a rare disease with a poor prognosis, and its clinical signs and symptoms are nonspecific. This study aims to identify histopathological features and immunohistochemical markers of head and neck mucosal melanoma that characterize the tumor immunophenotype and are associated with patient survival.

The study analysed head and neck mucosal melanoma diagnosed at Helsinki University hospital between January 1, 2011, and June 8, 2023. Samples were obtained from the Helsinki Biobank in Finland. New slides were prepared and stained for hematoxylin and eosin (H&E), CD3, CD4, CD8, Granzyme B (GrzB), CD68, CD117, p16INK4a, p53, SOX10 and PRAME.

The study included 23 patients, 10 men and 13 women, aged 60-92 years (mean 75 years). The tumors were predominantly sinonasal. Ulceration was present in 15 cases, also 15 cases were amelanotic. Immunohistochemical staining SOX10 was positive in all tumors. PRAME was strongly positive in majority (20 cases, 87%). Strong p16 positivity was observed in 13 cases (57%), with a longer median survival compared to cases with weakened p16 expression (32.8 vs 13.8 months, p = 0.176). The median survival was also longer in the cases with high score of tumor infiltrating CD3-, CD8- and CD68-positive immune cells, though not statistically significant.

Immunohistochemical markers routinely applied in cutaneous melanoma (SOX-10 and PRAME) are also expressed in head and neck mucosal melanoma. Tumour-infiltrating immune cells showed trend toward better survival, as has been previously found out in cutaneous melanoma. Strong p16 positivity may be an independent predictor of favorable prognosis in head and neck mucosal melanoma, irrespective of disease stage. Larger multicenter studies are warranted to validate these findings in this rare disease.

Glioblastoma (GBM) is characterized by extensive intratumoral heterogeneity and a complex tumor microenvironment that complicate the preclinical evaluation of gene therapy vectors. We investigated how culture model, epidermal growth factor (EGF) supplementation, and adeno-associated virus (AAV) serotype influence vector-mediated gene delivery in patient-derived GBM models. Patient-derived neurospheres (PDNS) and patient-derived tissue slice cultures (PDTC) were transduced with AAV2 or AAV6 vectors encoding green fluorescent protein (GFP). Transduction was evaluated by live confocal imaging, quantitative PCR, flow cytometry, and immunofluorescence under EGF-containing and EGF-free culture conditions. In PDNS, AAV6 produced significantly greater GFP expression than AAV2 and demonstrated a dose-dependent increase in transduction at both 2 and 5 days after vector exposure. EGF supplementation altered transduction patterns and was associated with changes in PDNS growth and marker-defined stem-like cell populations. In contrast, PDTC preserved tissue architecture and stromal, vascular, and immune-associated compartments while revealing substantial interpatient variability in AAV-mediated transduction. AAV-mediated gene delivery in GBM is influenced by culture model, growth factor conditions, and capsid serotype. Patient-derived tissue slice cultures complement neurosphere models by preserving features of the native tumor microenvironment and may improve the preclinical evaluation of gene therapy vectors for GBM.

USP5 is a deubiquitinating enzyme whose role in anti-PD-L1 resistance in breast cancer remains unclear. This study investigated whether USP5 contributes to resistance against the anti‑PD‑L1 antibody (atezolizumab) by regulating the FOXM1/Nectin2 axis. Anti-PD-L1-resistant and lung metastatic mouse models were established, combined with in vitro cellular assays, clinical sample analyses, and bioinformatics approaches. The results showed that USP5 was upregulated in breast cancer and stabilized FOXM1 via deubiquitination, which led to increased Nectin2 expression and resistance to CD8⁺ T cell-mediated killing. Knockdown of USP5 or its pharmacological inhibition with G9 synergized with anti-PD-L1 to suppress tumor growth, an effect that was reversible by Nectin2 overexpression. In conclusion, USP5 promotes breast cancer progression and anti-PD-L1 resistance by deubiquitinating FOXM1, thereby upregulating Nectin2 expression. Targeting USP5 enhances the efficacy of anti-PD-L1 therapy, offering a novel strategy to overcome immunotherapy resistance in breast cancer.