Facial numbness typically arises from disorders affecting the facial or trigeminal nerves, yet chemotherapy-induced facial numbness is exceedingly rare. Herein, we present a CARE-compliant case of a patient with oxaliplatin-induced facial numbness who experienced symptom improvement following electroacupuncture (EA) treatment.

A 73-year-old patient with rectal cancer developed severe bilateral facial numbness, affecting the periorbital, perinasal, and perioral regions after oxaliplatin-based chemotherapy.

The patient was diagnosed with facial numbness secondary to oxaliplatin-induced peripheral neuropathy.

The patient was treated with EA therapy to improve facial numbness symptoms.

After 3 EA sessions, the patient's facial numbness improved significantly; a subsequent 3-session course resulted in complete resolution of symptoms.

The case suggests that EA may serve as an effective alternative treatment for chemotherapy-induced facial numbness.

Endometrial polyps are common, localized overgrowths of endometrial glands and stroma that protrude into the uterine cavity. These tumor-like lesions can cause symptoms like abnormal uterine bleeding and infertility, and they may undergo malignant transformation. The etiology of endometrial polyps remains largely unknown.

Here, we conducted whole-genome sequencing and global gene expression profiling on 23 polyps. Major findings were validated with targeted DNA (Sanger sequencing) and protein (immunohistochemistry) level analyses. Sanger sequencing was also utilized to validate the observed novel alterations in an additional set of 54 polyp samples.

The most common alterations were chromosomal rearrangements affecting HMGA1 and HMGA2, identified in 74% (17/23) of the polyps. These rearrangements involved LRMDA, RAD51B, TRAF3IP2, and 7p15.2 as recurrent rearrangement partners. 3'RNA sequencing indicated corresponding overexpression of HMGA1 and HMGA2 as well as a downstream target PLAG1. Elevated protein level expression of HMGA1 and HMGA2 was further shown using immunohistochemistry. In addition to frequent HMGA1 and HMGA2 alterations, we found UBE2A as a novel candidate driver gene with highly specific recurrent mutations. We also identified recurrent low-allelic fraction mutations in well-established cancer genes KRAS, PIK3CA, PIK3R1, and PTEN.

Here, we have characterized the genomic landscape of endometrial polyps. We show that chromosomal alterations affecting HMGA1 and HMGA2 are a major underlying cause for polyp development. In addition, we present UBE2A as a novel candidate gene for human tumorigenesis. Our results contribute to a better understanding of endometrial polyp development and pave the way towards the development of targeted, non-invasive treatment options.

Genitourinary mesenchymal neoplasms (GMNs) encompass diverse tumors with limited research on clinicopathologic and genetic characteristics across different organs and age groups. We investigated 71 GMNs with tumor-defining genetic alterations (GMN-TDGA), categorizing tumors into spindle, round, or epithelioid based on predominant patterns. Pediatric GMN-TDGAs primarily involved the kidney, with six congenital mesoblastic nephromas showing spindly histology, including three cellular variants with ETV6::NTRK3 fusion, two classical variants with EGFR exon 18-25 duplications, and one novel TFG::NTRK3-positive case. Four renal clear cell sarcomas exhibited spindly and round cell patterns, harboring BCOR exon 15 duplications (n = 3) or YWHAE rearrangement (n = 1). Two renal EWSR1::FLI1-positive Ewing sarcomas (EWS) and one vesical ALK-rearranged inflammatory myofibroblastic tumor (IMT) occurred in children. In adults, recurrent histotypes included vesical IMTs (n = 15: 14 ALK-rearranged/positive, 1 RET-rearranged), renal synovial sarcomas (SS, n = 13: 7 poorly differentiated, 5 monophasic, 1 biphasic), renal EWS (n = 4, including one unreported EWSR1::ERG-positive atypical variant), renal sclerosing epithelioid fibrosarcomas (SEF, n = 3, all with EWSR1::CREB3L1), renal and vesical TFE3-rearranged PEComas (n = 3, 1 malignant), renal and preputial CIC-rearranged sarcomas (CICRS, n = 3), and multi-organ NAB2::STAT6-positive solitary fibrous tumors (SFTs, n = 10). Event-free survival varied significantly across adult GMN-TDGAs (P < 0.001), with CICRS (100 %), SS (61.5 %), and EWS (50 %) showing higher event rates compared to SEF (33.3 %), PEComa (33.3 %), SFT (20 %), and IMT (0 %). Ultra-rare GMN-TDGAs included a PTCH1::GLI1-positive renal epithelioid mesenchymal neoplasm, a BRAF-deleted renal spindle cell tumor, and a MYOD1-mutated prostatic spindle cell rhabdomyosarcoma. Conclusively, molecular profiling highlights the histologic and genetic diversity of GMNs, supporting challenging diagnoses and informing personalized therapies.

The environmentally sustainable synthesis of nanoparticles has arisen as a viable alternative to traditional methods, tackling ecological and economic issues. This research investigates the green synthesis of ZnO nanoparticles utilizing an aqueous extract of Echinops Spinosus L. roots (ESRE), abundant in bioactive chemicals, as a natural reducing agent. The impacts of different quantities of precursors and reducing agents were methodically examined. The synthesized ZnO nanoparticles were characterized by zeta potential measurements (-15.2 mV), transmission electron microscopy (TEM), which indicated spherical and hexagonal morphologies with an average size of 20.47-48.22 nm, and energy-dispersive X-ray spectroscopy (EDX), confirming zinc and oxygen as the principal elements. Fourier transform infrared spectroscopy (FTIR) underscored plant-derived compounds' contribution to nanoparticle stabilization. Cytotoxicity was assessed using the MTT assay on two cancer cell lines, HepG2 (hepatocellular carcinoma) and MCF-7 (breast cancer). The green-synthesized ZnO nanoparticles had substantial anticancer efficacy, with the ZnO nanoparticles exhibiting the most pronounced anti-proliferative effect on HepG2 cells (10.4 folds) and 5.4 folds more effective in MCF-7 cells compared to ESRE, with HepG2 cells IC50 value of 19.94 ± 0.11 µg/mL while the IC50 for MCF-7 cells was 75.65 ± 0.16 µg/mL. The results indicate that ZnO-NPs produced by green technologies exhibit significant potential as anticancer agents, especially for hepatocellular carcinoma treatment.

Advances in the prognostication, monitoring, and treatment of both the acute and chronic leukemias have led to drastically improved outcomes over the past 2 decades. With the advent of targeted therapies, including antibodies such as blinatumomab and inotuzumab and small molecule inhibitors, such as the BCR::ABL1 tyrosine kinase inhibitors, Bruton tyrosine kinase inhibitors, and venetoclax, the treatment landscape of leukemia has drastically changed, improving survival outcomes while relying less on overall chemotherapy intensity in many leukemia types. This progress has allowed the categorization of more leukemia types as favorable (i.e., chronic lymphocytic leukemia, younger acute lymphoblastic leukemia [patients younger than 60 years], and Philadelphia chromosome-positive acute lymphoblastic leukemia) in addition to the traditional favorable subtypes of acute promyelocytic leukemia, core-binding factor acute myelocytic leukemia, chronic myelocytic leukemia, and hairy cell leukemia. Advancements in the treatment of TP53-mutated, MECOM-rearranged, and treated secondary AML are still needed to improve outcomes in these adverse risk groups. The authors also review the recent progress in the treatment of the acute and chronic leukemias.

TP53 gain-of-function (GOF) effects lead to cellular responses beyond the capabilities of wild-type TP53 and are known to promote cancer progression, resulting in poorer outcomes in cancer.

A total of 486 patients diagnosed with non-small cell lung cancer (NSCLC) with baseline DNA sequencing data were enrolled in our study cohort. In addition, clinical and sequencing data from external NSCLC cohorts, including a cohort with histologic data (N = 219), a combined cohort from two studies treated with immunotherapy (N = 315), and a cohort treated with ROS1 tyrosine kinase inhibitor (TKI) (N = 50), were analyzed to assess the relationships between TP53 GOF mutations and histologic subtypes, immunotherapy outcomes, and ROS1-TKI treatment efficacy.

Compared to TP53 non-GOF mutations, patients with TP53 GOF mutations showed higher mutation rates in PIK3CA, STK11, and CTNNB1 but lower in NTRK1; increased VEGFA but decreased DLL3 and HRAS amplification rates. Patients with TP53 GOF mutations exhibited significantly higher tumor mutation burdens compared to those with non-GOF TP53 statuses. Patients with TP53 mutations, both GOF and non-GOF, showed significantly higher expression of immune checkpoints compared to TP53 wild-type patients. GOF-mutated patients also had higher M1 macrophage and CD8+ T cell infiltration, along with elevated B cell receptor signaling. Consistent with our findings, analysis of external cohorts revealed that TP53 GOF mutations were associated with improved prognosis in the context of immunotherapy. Among ROS1 fusion-positive patients treated with ROS1-TKIs, those harboring TP53 GOF mutations had a longer median PFS compared to patients with non-GOF TP53, although both were shorter than those with wild-type TP53. Additionally, TP53 GOF mutations were associated with a relatively lower histologic grade than non-GOF mutations.

TP53 GOF mutations were associated with poorer ROS1-TKI treatment outcomes but improved immunotherapy response in NSCLC, with elevated immune activities and distinct molecular profiles.

Interpreting the functional impact of genomic variants remains a major challenge in precision oncology, particularly in breast cancer, where many variants of unknown significance lack clear therapeutic guidance. Current annotation strategies focus on frequent driver mutations, leaving rare or understudied variants unclassified and clinically uninformative. Here, we present an Artificial Intelligence/Machine Learning (AI/ML)-driven framework that systematically identifies variants associated with key breast cancer phenotypes, including ESR1 and EZH2 activity, by integrating genomic, transcriptomic, structural, and drug response data. Using CCLE/DepMap and TCGA datasets, we analyzed > 12,000 variants across breast cancer genomes, identifying structurally clustered mutations that share functional consequences with well-characterized oncogenic drivers. This approach reveals that mutations in PIK3CA, TP53, and other genes strongly associate with ESR1 signaling, challenging conventional assumptions about endocrine therapy response. Additionally, EZH2-associated variants emerge in unexpected genomic contexts, suggesting new targets for epigenetic therapies. By shifting from frequency-based to structure-informed classification, we expand the set of potentially actionable mutations, enabling improved patient stratification and drug repurposing strategies. This work provides a scalable, clinically relevant method to accelerate variant annotation, offering new insights into drug sensitivity and resistance mechanisms. Future validation efforts will refine these predictions and integrate clinical outcomes to guide personalized treatment strategies. Our findings highlight the transformative potential of AI/ML in redefining cancer variant interpretation, bridging the gap between genomics, functional biology, and precision medicine.

Tumor-associated macrophages (TAMs) promote immunosuppression, hindering immune checkpoint blockade and immunotherapy efficacy. To overcome this, we developed a novel multifunctional nanovaccine based on hepatitis B core virus-like particles (HBc VLP) to synergistically remodel the immunosuppressive tumor microenvironment through integrated TAM reprogramming and B7-H3 checkpoint blockade.

The core VLP co-displayed tumor antigen peptide MAGE-A10 and TAM-targeting peptide M2pep via fusion expression. Immunostimulatory CpG oligodeoxynucleotide 1826 (CpG) was encapsulated within VLP. Anti-B7-H3 antibody (αB7-H3) and polyethylene glycol (PEG) were chemically conjugated to the surface for checkpoint blockade and prolonged circulation, forming CpG@VLP-αB7-H3-PEG.

Structural characterization using transmission electron microscopy and dynamic light scattering confirmed the hollow spherical self-assembly of VLP. Nanovaccines efficiently targeted TAMs in vitro and in vivo. Following CpG encapsulation (5.60 µg/mg), the nanovaccine reprogrammed M2-like TAMs into an M1-like phenotype. This was achieved by elevating the M1/M2 ratios of CD86/CD206 and MHC II/CD206 to 15.50-fold and 3.11-fold, respectively, as determined by flow cytometry. Further conjugation of αB7-H3 (250 µg/mg) significantly enhanced T-cell activation in TAM-T cell co-culture assays. In B16-F10 melanoma-bearing mice, reprogrammed iNOS⁺ M1-like macrophages triggered robust antitumor immunity, achieving a tumor inhibition rate of 63.47%. These macrophages also function as antigen-presenting cells and increase the proportion of tumor-infiltrating Granzyme B⁺CD8⁺ T cells. αB7-H3 conjugation further boosted infiltrating immune cells, M1-like macrophages, activated CD69⁺CD4⁺/CD8⁺ T cells, and cytotoxic T lymphocytes. PEGylation amplified systemic tumor-specific immunity and increased tumor inhibition by 80.12%.

This HBc VLP-based nanovaccine constitutes a pioneering multifunctional platform designed to overcome TAM-mediated immunosuppression through synergistic integration of three modalities: antigen presentation, TAM phenotype reprogramming, and B7-H3 checkpoint blockade. To the best of our knowledge, this is the first nanovaccine architecture to enable coordinated immunomodulation. Its modular design supports the clinical translation of solid tumors and personalized immunotherapy.

Giant cell tumors (GCTs) of bone are rare, locally aggressive primary neoplasms that account for approximately 3%-7% of all primary bone tumors. They most commonly arise in the epiphyses of long bones in young adults and are seldom seen in the craniofacial skeleton. Involvement of the frontal bone with orbital extension is exceptionally rare, particularly in the pediatric age group. We report a case of a 9-year-old male who presented with a progressively enlarging swelling of the left orbit associated with vision loss with atypical imaging features and an intracranial component with compression of the adjacent brain parenchyma. Histopathological examination subsequently confirmed the diagnosis of GCT. He was managed with a multimodal approach comprising neoadjuvant therapy and surgical excision, which achieved complete tumor removal, with no evidence of recurrence at 1-year follow-up. This case highlights the need for awareness of rare sites of presentation of GCT and the importance of considering it in the differential diagnosis of destructive calvarial masses with orbital involvement in children.

Lumbar discectomy may be considered for lumbar radicular symptoms. There have been recent pushes to reduce opioid use and promote multimodal pain management. This large administrative database study evaluated trends in pain management prescriptions following lumbar discectomy.

Lumbar discectomy patients were identified from the 2010-2021 PearlDiver M165Ortho database. Patients with prior history of substance abuse, neoplasm, or any concomitant anterior or posterior lumbar surgical intervention were excluded. Prescriptions of pain management drugs were evaluated in the 90-days following surgery and manually grouped as opioids and/or other categories of pain management drugs. Prescriptions and morphine milligram equivalents (MMEs) per 1,000 lumbar discectomy surgeries were determined and trended. Multivariable analysis was performed to determine clinical and nonclinical factors independently associated with opioid prescription use.

From a total of 93,252 lumbar discectomies meeting inclusion criteria, opioid prescriptions decreased from 531.7 per 1,000 lumbar discectomy surgeries in 2010 to 97.1 in 2021 (-81.7%). Prescriptions of other pain management drugs on aggregate decreased from 527.9 in 2010 to 174.9 in 2021 (-66.9%). The proportion of all analgesics prescribed postoperatively that were opioids decreased from 50.2% in 2010 to 35.7% in 2021. Among patients who received opioids in the 90-days postoperatively, MMEs prescribed per lumbar discectomy case decreased from 262.8 in 2010 to 24.6 in 2021 (-90.7%). Predictors of postoperative opioid prescriptions by multivariate analysis included clinical factors (younger age [OR 1.20 per decade decrease], male sex [OR 1.40], lower ECI [OR 1.16]) and the nonclinical factor of geographic variation (relative to South, Northeast OR 1.08, Midwest OR 1.09) (p<.05 for each).

Opioid prescriptions following lumbar discectomy have markedly decreased over the past decade. Notably, nonopioid prescriptions have also decreased, likely in favor of nonprescription multimodal pain management medications and strategies.