Background Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS, NIH category Ⅲ) remains a challenging condition with no universally accepted treatment. Although alpha-blockers and antibiotics are commonly used, their efficacy is inconsistent. Purpose In this study, we aimed to evaluate the efficacy and safety of Qianlieshutong Capsules (QLSTCs, a standardized traditional Chinese medicine) combined with tamsulosin versus tamsulosin alone in patients with CP/CPPS. Methods In this post-marketing, multicenter, randomized, double-blind, single-dummy clinical trial, 240 male patients aged 18–50 years diagnosed with CP/CPPS were randomly assigned (1:1) to receive either QLSTCs (0.4 g/capsule, 3 capsules, three times daily) plus tamsulosin (0.2 mg nightly) or a matching placebo plus tamsulosin for 8 weeks. The primary endpoint was the change in the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) total score from baseline to week 8. Secondary outcomes included changes in the NIH-CPSI score at week 4, domain-specific scores (pain, urinary symptoms, quality of life), and treatment response rates. Safety was assessed through adverse events (AEs), laboratory tests, vital signs, and ECG. Results Of the 240 randomized patients, baseline characteristics were comparable. At week 8, the combination group showed a significantly greater reduction in the total NIH-CPSI score than the control group (−14.30 ± 0.53 vs. −10.60 ± 0.54; mean difference = 3.70, 95% CI: 2.36–5.04; P < 0.0001). The effective response rate and marked improvement rate were significantly higher in the combination group. Improvements were also significant in all NIH-CPSI domains at week 8. AE incidences were low and comparable between groups (10.00% vs. 9.24%), with no serious AEs reported. Conclusion The combination of QLSTCs and tamsulosin is a safe and more effective treatment than tamsulosin alone for CP/CPPS, offering superior symptom relief, particularly in pain, urinary symptoms, and quality of life. This approach may serve as a promising multimodal therapeutic option in clinical practice.

IntroductionMatrix stiffening during idiopathic pulmonary fibrosis (IPF) creates a mechanically altered microenvironment that promotes fibroblast activation, yet the metabolic consequences of these mechanical cues remain incompletely defined. Pyruvate kinase M2 (PKM2) catalyzes the rate-limiting step of glycolysis, but whether it serves as a mechanosensitive link coupling matrix stiffness to fibroblast activation has not been clarified. This study examined whether substrate stiffness drives glycolytic reprogramming through PKM2 upregulation and whether this metabolic adaptation is required for mechanically driven fibroblast activation.MethodsPKM2 expression was analyzed in the NCBI GEO dataset GSE24206, human IPF lung tissues, and the bleomycin-induced mouse pulmonary fibrosis model. Primary mouse lung fibroblasts were cultured on collagen I–coated polyacrylamide hydrogels mimicking normal (2 kPa) or fibrotic (25 kPa) stiffness with or without TGF-β1 treatment. Glucose uptake, lactate secretion, pyruvate kinase activity, LDH activity, NAD+/NADH ratio, and oxygen consumption were measured; PKM2 oligomeric states were resolved by DSS cross-linking; and PKM2 was depleted by lentiviral shRNA.ResultsPKM2 transcripts were progressively elevated in early- and advanced-stage IPF, and corresponding increases in protein and mRNA were confirmed in human IPF lungs and in bleomycin-treated mouse lungs. Stiff substrates upregulated PKM2 expression and reprogrammed fibroblast metabolism, with TGF-β1 eliciting increases in glucose uptake, lactate secretion, and oxygen consumption that were predominantly observed on stiff substrates. Cross-linking analysis showed that soft substrates favored catalytically active PKM2 tetramers, whereas stiff substrates constrained tetramer assembly and promoted lower-order species, providing a mechanistic basis for the dissociation between increased PKM2 expression and unchanged pyruvate kinase activity. PKM2 knockdown attenuated stiffness-induced increases in glucose uptake, lactate secretion, and LDH activity, reduced the cellular NAD+/NADH ratio, and decreased α-SMA–positive stress fiber formation under combined mechanical and TGF-β1 stimulation.DiscussionThese findings indicate that PKM2 contributes to a mechanosensitive metabolic program coupling matrix stiffness to fibroblast activation, with substrate stiffness regulating both PKM2 expression and oligomeric state. Targeting PKM2-mediated metabolic adaptation may interrupt the self-reinforcing cycle of matrix stiffening and fibroblast activation in pulmonary fibrosis.

Fibroblast survival and dysregulated activation drive fibrotic diseases, including idiopathic pulmonary fibrosis (IPF). During physiological wound repair, fibroblasts are transiently activated to restore tissue integrity and are subsequently cleared by programmed cell death. In fibrotic disease, however, fibroblasts evade apoptosis and persist in a pathologically activated state. Although S100A4 has been implicated in fibrotic lung disease, the mechanisms by which S100A4 governs fibroblast fate and sustains profibrotic behavior remain unclear. Here, we identify S100A4 as a key regulator of apoptosis-resistant, profibrotically activated fibroblasts through engagement of extracellular signal-regulated kinase (ERK) signaling. In primary murine lung fibroblasts, S100A4 activates ERK, resulting in a coordinated program of fibroblast activation, including increased migration, extracellular matrix (ECM) contractility, stress fiber formation, and alpha-smooth muscle actin (α-SMA) induction. Functionally, S100A4 confers resistance to apoptosis induced by pro-apoptotic and oxidative stress stimuli, as evidenced by reduced cleaved caspase-3 and preserved cell viability. Pharmacological blockade of ERK signaling attenuates these responses, supporting ERK as an important downstream mediator of S100A4-driven fibroblast activation and survival programs. Extending these findings to disease-relevant contexts, bleomycin (BLM)-induced lung injury in mice induces robust fibrotic remodeling, excessive collagen deposition, and transcriptional upregulation of S100A4. Consistently, primary lung fibroblasts from IPF patients exhibit elevated S100A4 expression, enhanced ERK activation, and increased α-SMA expression, demonstrating conservation of this signaling axis across experimental models and human disease. Importantly, siRNA-mediated knockdown of S100A4 in IPF fibroblasts suppresses ERK activation and attenuates expression of key profibrotic genes, indicating that S100A4 contributes to maintaining the fibrotic program in IPF fibroblasts. Collectively, these findings define a mechanistic link between S100A4-mediated fibroblast survival and activation that drives pathological matrix remodeling and identify S100A4 and ERK as potential therapeutic targets in pulmonary fibrosis.

Esophageal squamous cell carcinoma (ESCC) is a common and aggressive cancer with limited responses to immunotherapy. High mobility group A1 (HMGA1), a chromatin remodeling protein, plays a key role in tumor progression, but its impact on anti-tumor immunity in ESCC remains unclear. Here we show that HMGA1 suppresses the stimulator of interferon genes (STING), inhibiting type I interferon secretion, downregulating interferon-stimulated genes, and impairing tumor-infiltrating lymphocyte (TIL) recruitment. HMGA1 inhibits STING transcription by competing with the coactivator CBP/p300 for binding to CREB. ESCCs from genetically modified mouse models with altered HMGA1 and STING expression exhibit varying TIL levels and sensitivity to STING agonists. Additionally, we design and synthesize a series of HMGA1 inhibitors, including a perylene-based nanoparticle, PDIC-DPC, which effectively inhibits HMGA1 and enhances TIL infiltration. Our findings identify HMGA1 as a critical immune checkpoint in ESCC and suggest that targeting HMGA1 could improve immunotherapy outcomes.

INTRODUCTION:The Parent Tic Questionnaire (PTQ) is a tool for parents to assess their child's tic severity, but its effectiveness in non-Western contexts like China has not been thoroughly examined. This study aimed to evaluate the psychometric properties of the PTQ in assessing motor and vocal tic severity among Chinese children diagnosed with tic disorders. METHOD:Parents of 268 Chinese children and adolescents aged 6-17 years, diagnosed with tic disorders, completed the PTQ. The study assessed tic severity using the Yale Global Tic Severity Scale (YGTSS) and PTQ. Additionally, obsessive-compulsive symptoms were measured using the Children Yale-Brown Obsessive Compulsive Scale (CY-BOCS), and other behavioral problems were evaluated using the Conners' Parent Rating Scale (CPRS-48). RESULTS:The PTQ showed acceptable to good internal consistency (Cronbach's alpha = 0.67 for motor, 0.77 for vocal, and 0.79 for total tic scores) and acceptable to good two-week test-retest reliability (intraclass correlations, ICC = 0.74 for motor, 0.81 for vocal, and 0.79 for total tic scores). It demonstrated good convergent validity with the YGTSS and effective discriminant validity from obsessive-compulsive and internalizing symptoms (i.e., anxiety and psychosomatic). Furthermore, our analysis revealed significant variability in item difficulty across the questionnaire, indicating differences in how various tics are perceived and reported by Chinese parents, which may influence the assessment's accuracy and reliability. DISCUSSION:The findings indicate that the Chinese version of the PTQ is a reliable and valid tool for assessing tic severity in Chinese children with tic disorders, offering significant implications for clinical assessment in diverse cultural contexts. Additionally, our findings on item difficulty highlight the need for further cultural adaptations of the PTQ.

Objective Increasing evidence has shown that dietary behaviors are closely correlated with the carcinogenesis and progression of many types of cancer. However, few studies have assessed the global diet-related burden of cancer. This study aimed to estimate the pooled burdens and trends of five types of cancers attributable to dietary behaviors. Methods Data regarding cancer attributable to dietary behaviors were extracted from the Global Burden of Disease study 2019, including the death cases and age-standardized death rates, and disability-adjusted life years (DALYs) estimated according to diseases, age, sex, the socio-demographic index (SDI) and location. Results According to the Global Burden of Disease study 2019, five types of cancer were affected by dietary behaviors: colon and rectum cancer; tracheal, bronchus and lung cancer; stomach cancer; esophageal cancer and breast cancer. Unhealthy dietary behaviors for cancer caused a total of 605.4 thousand deaths and 13951.3 thousand DALYs globally. The burden of cancer attributable to dietary risks was higher for men than for women. The highest age-standardized death rates in 2019 were observed in southern Latin America, and the lowest rates were observed in North Africa and the Middle East. The greatest increases in the age-standardized death rates, from 1990 to 2019, were found in Western Sub-Saharan Africa, with the greatest decreases in Central Asia. The highest attributable proportions of death or DALYs were colon and rectum cancer. The greatest diet-related cancer burden was observed in regions with a high-middle SDI. Conclusion Global age-standardized deaths and DALYs rates attributable to diet-related cancer are considerable and cause a substantial burden. Successful population-wide initiatives targeting unhealthy dietary behaviors would reduce this burden.

Several risk models for esophageal stricture after endoscopic submucosal dissection have been developed. However, some of them did not include the use of steroids in the risk analysis. Glucocorticoid sensitivity mediated by glucocorticoid receptor expression has not been discussed in this condition. Clinical and endoscopic characteristics were included in the logistic regression model to establish a nomogram for stenosis prediction. The score for each risk factor was estimated. Risk factors of ineffective oral steroid prophylaxis were analyzed and glucocorticoid receptor expressions were detected by immunohistochemistry. Three hundred fourteen patients of endoscopic submucosal dissection for esophageal superficial neoplasms were included to develop the nomogram. The circumferential range(≤ 3/4, 3/4–1 or the whole circumference), longitudinal diameter reached 4 cm (yes or not) and lesion location (the cervical and upper thoracic part, the middle thoracic part or the lower thoracic part) consisted of the nomogram. Patients have a high risk of esophageal stricture if they have a total point greater than 36. In the simplified risk score model, the corresponding cutoff score was 1. 92 patients with oral steroid prophylaxis were separately analyzed and the circumferential mucosal defect involving 7/8 or more was an independent risk factor of ineffective prevention (OR 12.2, 95

Abstract Background The Premonitory Urge for Tics Scale (PUTS) is a common self-report measure of premonitory urges for patients with tic disorders. This study aims to evaluate the Chinese version of the PUTS (PUTS-C) and to explore its association with psychiatric symptoms in Chinese children diagnosed with tic disorders. Methods The psychometric evaluation involved 204 outpatients with tic disorders, aged 7–16 years, who were divided into two age groups: (7–10 years, n = 103; 11–16 years, n = 95). Results The PUTS-C demonstrated good internal consistency (McDonald’sω = 0.84) and two-week test-retest reliability (0.76). We observed a statistically significant correlation between the total PUTS-C score and various Yale Global Tic Severity Scale (YGTSS) subscales and total tic severity scores. The PUTS-C score also showed significant correlations with the Children Yale-Brown Obsessive Compulsive Scale (CY-BOCS), Screening Child Anxiety-Related Emotional Disorders (SCARED), and Children’s Depression Inventory (CDI). Notably, premonitory urges independently predicted tic severity, beyond the influence of comorbid symptoms. A two-factor structure of the PUTS-C was identified in the total sample through factor analysis. Conclusions The PUTS-C possesses acceptable validity and good reliability. It appears that premonitory urges in Chinese patients with tic disorders are associated with obsessive-compulsive symptoms, anxiety, and depression, but can independently predict tic severity. Specific PUTS-C factors possibly related to motor and vocal tics. Future research should continue to investigate age-related differences and the association with tics and other sensory symptoms.

This study aims to compare the efficiency and clinical outcomes between the suctioning ureteral access sheath (UAS) group and the traditional UAS group during retrograde intrarenal surgery (RIRS) for kidney stones and explore the impact of suctioning UAS on postoperative infectious complications. We retrospectively reviewed the clinical data of 162 patients with kidney stones who underwent RIRS with a traditional UAS (n = 74) or a suctioning UAS (n = 71) between March 2021 and May 2023. The mean operative time in suctioning UAS group (39.03 ± 18.01 s) was significantly shorter than that (49.73 ± 20.77 s) in the traditional UAS group (P = 0.037). The mean postoperative hospital stay was significantly shorter in the suctioning UAS group (1.57 ± 0.82d) compared with the traditional UAS group (2.30 ± 1.6 2 d) (P = 0.032). The instant SFRs were significantly higher in the suctioning UAS group (88.73

Gut microbiota-derived extracellular vesicles (mEVs) are reported to regulate inflammatory response by delivering bacterial products into host cells. The complement receptor of the immunoglobulin superfamily macrophages (CRIg+ Mφ) could clear invading bacteria and their derivatives. Here, we investigate the role of CRIg+ Mφ and the mechanism by which mEVs regulate intestinal inflammation. We found that it is exacerbated in IBD patients and colitis mice by mEVs’ leakage from disturbed gut microbiota, enriching microbial DNA in the intestinal mucosa. CRIg+ Mφ significantly decrease in IBD patients, allowing the spread of mEVs into the mucosa. The microbial DNA within mEVs is the key trigger for inflammation and barrier function damage. The cGAS/STING pathway is crucial in mEVs-mediated inflammatory injury. Blocking cGAS/STING signaling effectively alleviates inflammation caused by mEVs leakage and CRIg+ Mφ deficiency. Microbial DNA-containing mEVs, along with CRIg+ Mφ deficiency, stimulate inflammation in IBD, with the cGAS/STING pathway playing a crucial role.

PURPOSE:Calcium-sensing receptor (CASR) influences the expression pattern of multiple genes in renal tubular epithelial cells. The objective of this inquiry was to explore the molecular mechanisms of CASR in renal tubular epithelial cells and nephrolithiasis.METHODS:HK-2 cells were transfected with lentiviruses carrying either CASR (named CASR) or an empty vector negative control (named NC), as well as shRNA intended to target CASR (named shCASR) or its corresponding negative control (named shNC). CCK-8 assay was used to detect the effect of CASR on the proliferation of HK-2 cells. RNA-Sequencing was applied to explore potential pathways regulated by CASR in HK-2 cells.RESULTS:PCR and western blot results showed that CASR expression was significantly increased in CASR cells and was decreased in shCASR cells when compared to their corresponding negative control, respectively. CCK-8 assay revealed that CASR inhibited the proliferation of HK-2 cells. RNA-Sequencing results suggested that the shCASR HK-2 cells exhibited a significant up-regulation of 345 genes and a down-regulation of 366 genes. These differentially expressed genes (DEGs) were related to cell apoptosis and cell development. In CASR HK-2 cells, 1103 DEGs primarily functioned in mitochondrial energy metabolism, and amino acid metabolism. With the Venn diagram, 4 DEGs (Clorf116, ENPP3, IL20RB, and CLDN2) were selected as the hub genes regulated by CASR. Enrichment analysis revealed that these hub genes were involved in cell-cell junction, and epithelial cell development.CONCLUSIONS:In summary, our investigation has the potential to offer novel perspectives on CASR regulating cell-cell junction in HK-2 cells.

Dear Editor, Here,we report the association of mutations in the prostate cancer cluster region(PCCR;c.7914 to 3')and non-PCCR(5'to c.7914)in breast cancer susceptibility gene 2(BRCA2)with prostate cancer(PCa)risk at the population level in Caucasian and Chinese cohorts.Pathogenic mutations of BRCA2 have been reported to significantly increase the risk of PCa and disease aggressiveness.

The aim of this study was to assess the narrow-sense validity of polygenic risk score (PRS) for prostate cancer (PCa) in a Chinese prostate biopsy cohort. We performed an observational prospective study with 2640 men who underwent prostate biopsy. Germline DNA samples were genotyped and PRS was calculated for each subject using 17 PCa risk-associated genetic variants. Additional GWAS data of the ChinaPCa dataset was also used to compliment the evaluation process. The mean PRS was 1.02 in patients with negative biopsy results, which met the baseline benchmark. The mean PRS was significantly higher in the PCa cases (1.32 vs. 1.02, p = 5.56 × 10-17 ). Significant dose-response associations between PRS values and odds ratios for PCa were observed. However, the raw calibration slope was 0.524 and the average bias score between the observed risk and uncorrected PRS value was 0.307 in the entire biopsy cohort. After applying a correction factor derived from a training set, the corrected calibration slope improved to 1.002 in a testing set. Similar and satisfied results were also seen in the ChinaPCa dataset and two datasets combined, while the calibration results were inaccurate when the calibration process were performed mutually between two different study populations. In conclusion, assessing the narrow-sense validity of PRS is necessary prior to its clinical implementation for accurate individual risk assessment.

Supplemental Methods and References, Supplemental Tables S1-S10, Supplemental Figures S1-S11

To date, the combined effect of polygenic risk score (PRS) and prostate health index (phi) on PCa diagnosis in men undergoing prostate biopsy has never been investigated. A total of 3166 patients who underwent initial prostate biopsy in three tertiary medical centers from August 2013 to March 2019 were included. PRS was calculated on the basis of the genotype of 102 reported East-Asian-specific risk variants. It was then evaluated in the univariable or multivariable logistic regression models that were internally validated using repeated 10-fold cross-validation. Discriminative performance was assessed by area under the receiver operating curve (AUC) and net reclassification improvement (NRI) index. Compared with men in the first quintile of age and family history adjusted PRS, those in the second, third, fourth, and fifth quintiles were 1.86 (odds ratio, 95% confidence interval (CI): 1.34–2.56), 2.07 (95%CI: 1.50–2.84), 3.26 (95%CI: 2.36–4.48), and 5.06 (95%CI: 3.68–6.97) times as likely to develop PCa (all p < 0.001). Adjustment for other clinical parameters yielded similar results. Among patients with prostate-specific antigen (PSA) at 2–10 ng/mL or 2–20 ng/mL, PRS still had an observable ability to differentiate PCa in the group of prostate health index (phi) at 27–36 (Ptrend < 0.05) or >36 (Ptrend ≤ 0.001). Notably, men with moderate phi (27–36) but highest PRS (top 20% percentile) would have a comparable risk of PCa (positive rate: 26.7% or 31.3%) than men with high phi (>36) but lowest PRS (bottom 20% percentile positive rate: 27.4% or 34.2%). The combined model of PRS, phi, and other clinical risk factors provided significantly better performance (AUC: 0.904, 95%CI: 0.887–0.921) than models without PRS. Adding PRS to clinical risk models could provide significant net benefit (NRI, from 8.6% to 27.6%), especially in those early onset patients (NRI, from 29.2% to 44.9%). PRS may provide additional predictive value over phi for PCa. The combination of PRS and phi that effectively captured both clinical and genetic PCa risk is clinically practical, even in patients with gray-zone PSA.

Background: The clinical implementation of immune-checkpoint inhibitors (ICIs) targeting CTLA4, PD-1, and PD-L1 has revolutionized the treatment of cancer. However, the majority of patients do not derive clinical benefit. Further development is needed to optimize the approach of ICI therapy. Immunotherapy combined with other forms of treatment is a rising strategy for boosting antitumor responses. CD93 was found to sensitize tumors to immune-checkpoint blocker therapy after the blockade of its pathway. However, its role in immune and ICB therapy across pan-cancer has remained unexplored. Methods: In this study, we provide a comprehensive investigation of CD93 expression in a pan-cancer manner involving 33 cancer types. We evaluated the association of CD93 expression with prognosis, mismatch repair, tumor mutation burden, and microsatellite instability, immune checkpoints, tumor microenvironment, and immune using multiple online datasets, including The Cancer Genome Atlas, Cancer Cell Line Encyclopedia, Genotype Tissue-Expression, cBioPortal, Tumor Immune Estimation Resource database, and Tumor Immune Single-cell Hub. Results: CD93 expression varied strongly among cancer types, and increased CD93 gene expression was associated with poor prognosis as well as higher immune factors in most cancer types. Additionally, the level of CD93 was significantly correlated with MMR, TMB, MSI, immune checkpoints, TME, and immune cell infiltration. Noticeably, our results mediated a strong positive contact between CD93 and CAFs, endothelial cells, myeloid dendritic cells, hematopoietic stem cells, mononuclear/macrophage subsets, and neutrophils while a negative correlation with Th1, MDSC, NK, and T-cell follicular helper in almost all cancers. Function analysis on CD93 revealed a link between itself and promoting cancers, inflammation, and angiogenesis. Conclusion: CD93 can function as a prognostic marker in various malignant tumors and is integral in TME and immune infiltration. Inhibition of the CD93 pathway may be a novel and promising strategy for immunotherapy in human cancer. Further explorations of the mechanisms of CD93 in the immune system may help improve cancer therapy methods.

Endoplasmic reticulum membrane protein complex subunit 10 (EMC10) is an evolutionarily conserved and multifunctional factor across species. We previously reported that Emc10 knockout (KO) leads to mouse male infertility. Emc10-null spermatozoa exhibit multiple aspects of dysfunction, including reduced sperm motility. Two subunits of a Na/K-ATPase, ATP1A4 and ATP1B3, are nearly absent in Emc10 KO spermatozoa. Here, two isoforms of EMC10 were characterized in the mouse testis and epididymis: the membrane-bound (mEMC10) and secreted (scEMC10) isoforms. We present evidence that mEMC10, rather than scEMC10, is required for cytoplasm sodium homeostasis by positively regulating ATP1B3 expression in germ cells. Intra-testis mEMC10 overexpression rescued the sperm motility defect caused by Emc10 KO, while exogenous recombinant scEMC10 protein could not improve the motility of spermatozoa from either Emc10 KO mouse or asthenospermic subjects. Clinically, there is a positive association between ATP1B3 and EMC10 protein levels in human spermatozoa, whereas no correlation was proven between seminal plasma scEMC10 levels and sperm motility. These results highlight the important role of the membrane-bound EMC10 isoform in maintaining cytoplasm sodium homeostasis and sperm motility. Based on the present results, the mEMC10-Na, K/ATPase α4β3 axis is proposed as a novel mechanism underlying the regulation of cytoplasmic sodium and sperm motility, and its components seem to have therapeutic potential for asthenospermia.

Background Chromosomal translocation has been detected in many human cancers including gliomas and is considered a driving force in tumorigenesis. Co-deletion of chromosome arms 1p and 19q is a hallmark for oligodendrogliomas. On the molecular level, 1p/19q co-deletion results from t(1;19)(q10;p10), which leads to the concomitant formation of a hybrid chromosome containing the 1q and 19p arms. A method to generate 1p/19q co-deletion is lacking, which hinders the investigation of how 1p/19q co-deletion contributes to gliomagenesis. Methods We hypothesized that chromosomal translocation, such as t(1;19)(q10;p10) resulting in the 1p/19q co-deletion, may be induced by simultaneously introducing DNA double-strand breaks (DSBs) into chromosomes 1p and 19q using CRISPR/Cas9. We developed a CRISPR/Cas9-based strategy to induce t(1;19)(q10;p10) and droplet digital PCR (ddPCR) assays to detect the hybrid 1q/19p and 1p/19q chromosomes. Results After translocation induction, we detected both 1p/19q and 1q/19p hybrid chromosomes by PCR amplification of the junction regions in HEK 293T, and U-251 and LN-229 glioblastoma cells. Sequencing analyses of the PCR products confirmed DNA sequences matching both chromosomes 1 and 19. Furthermore, the 1p/19q hybrid chromosome was rapidly lost in all tested cell lines. The 1q/19p hybrid chromosome also become undetectable over time likely due to cell survival disadvantage. Conclusion We demonstrated that t(1;19)(q10;p10) may be induced by CRISPR/Cas9-mediated genomic editing. This method represents an important step toward engineering the 1p/19q co-deletion to model oligodendrogliomas. This method may also be generalizable to engineering other cancer-relevant translocations, which may facilitate the understanding of translocation roles in cancer progression.