Radiotherapy (RT) remains a cornerstone of lung cancer (LC) management, serving as either a definitive treatment or an adjuvant modality following surgical resection. Nevertheless, a major challenge for radiation oncologists is the emergence of radioresistance, whether intrinsic or acquired, which contributes to therapeutic failure, tumor recurrence, metastasis and ultimately to increased patient mortality. Radioresistance is a multifactorial process driven by genetic and epigenetic alterations that dysregulate key signal transduction pathways, enabling cancer cells to survive and adapt under radiotherapeutic stress. A deeper understanding of the molecular mechanisms underlying radioresistance is therefore essential to identify robust biomarkers for patient stratification, prognostication and therapeutic targeting. Such insights could enable individualized treatment strategies within the framework of precision oncology and inform the development of novel radiosensitization approaches to overcome resistance in LC. The present review synthesized current evidence on molecular biomarkers associated with RT resistance in LC.

Innate lymphoid cells type 2 (ILC2s) are key regulators of tissue homeostasis and inflammation. In cancer, ILC2s can exhibit pro-tumoral functions by increasing the myeloid derived suppressor cells (MDSC)/T-cell ratio. Nevertheless, the upstream ILC2 triggers remain poorly defined. Here, we identify nerve growth factor (NGF) as the driver of ILC2 pro-tumoral functions in patients with bladder cancer. We show that ILC2s express the NGF receptor TrkA and respond to NGF by secreting type-2 cytokines. In the tumor microenvironment, NGF-producing mast cells accumulate and activate ILC2s to induce regulatory T cells (Tregs), ultimately fostering tumor growth. In patients, NGF levels inversely correlate with survival in ILC2-rich tumors, underscoring the clinical significance of this axis. In vivo administration of a selective TrkA inhibitor improves survival in orthotopic tumor-bearing female mice and sensitizes them to immune checkpoint blockade (ICB). Overall, we identify NGF as an ILC2 activator that shapes pro-tumoral ILC2 functions. The blockade of TrkA+ ILC2s might represent a targetable strategy to improve survival, particularly in ICB-resistant patients.

Cancer remains a leading cause of mortality worldwide, presenting a major challenge to global health. Quinolines, a class of nitrogen-containing heterocycles, have proven to be promising compounds for anticancer therapeutic development due to their diverse pharmacological properties, including cytotoxic, antiproliferative, pro-apoptotic, and immunomodulatory effects. This systematic review provides an updated synthesis of the anticancer applications of quinoline-based compounds, including their chemical synthesis, cytotoxic potential, clinical relevance, and biological mechanisms of action. Rigorous literature searching was conducted across multiple databases, identifying studies that evaluated quinoline derivatives using a range of methodologies, including computational modeling, cell-based cytotoxicity assays, 3D tumor spheroid models, and animal models. Quinoline-based compounds express broad-spectrum anticancer potential by acting on multiple cellular targets and pathways. Their mechanisms include inducing mitochondrial apoptosis, inhibiting key oncogenic kinases, modulating epigenetic regulators, damaging DNA, regulating autophagy, and triggering ferroptosis. Overall, this review highlights quinolines as a versatile and promising chemical scaffold for developing multi-targeted anticancer agents. Continued preclinical and clinical research is essential to optimize their efficacy and expand their therapeutic applications in oncology.

Cancer remains a leading cause of morbidity and mortality worldwide, and the effectiveness of current therapeutic strategies is often limited by drug resistance, tumor heterogeneity, and suboptimal clinical responses. Consequently, multi-target drug design has gained increasing attention as a promising strategy to simultaneously modulate several interconnected pathways involved in tumor progression. In this context, the present study evaluated 7-phenyl-5-(p-tolyl)pyrido[2,3-d]pyrimidin-4-amine as a potential multitarget scaffold for anticancer drug discovery using an integrated computational framework. To explore its possible polypharmacological profile, network pharmacology was first applied to identify cancer-associated targets linked to the compound, after which four representative proteins involved in complementary oncogenic mechanisms, namely telomerase reverse transcriptase (TERT), murine double minute 2 (MDM2), epidermal growth factor receptor (EGFR), and cyclin-dependent kinase 2 (CDK2), were selected for further investigation. Subsequently, molecular docking was performed to predict ligand-target interactions, while 100 ns molecular dynamics simulations were conducted to assess the structural stability of the resulting complexes. In parallel, in silico ADMET analysis was used to evaluate the pharmacokinetic and toxicity profile of the compound. The docking results showed favorable predicted binding affinities across the selected targets, ranging from -8.1 to -9.7 kcal/mol, suggesting potential interactions with multiple cancer-related proteins. Consistently, molecular dynamics simulations supported the stability of the ligand-protein complexes during the simulation period, as reflected by RMSD, RMSF, radius of gyration, and hydrogen-bond analyses. Moreover, ADMET predictions indicated acceptable drug-like properties; however, toxicity alerts, including possible hepatotoxicity, neurotoxicity, blood-brain barrier penetration, and cytochrome P450 inhibition, highlight the need for further structural optimization. Overall, these findings suggest that this pyrido[2,3-d]pyrimidine derivative may represent a preliminary scaffold for multitarget anticancer investigation, although experimental validation remains essential to confirm its biological activity, tumor selectivity, safety, and therapeutic relevance.

Introduction: Colorectal cancer (CRC) is a heterogeneous and multifactorial malignancy driven by a series of genetic and epigenetic alterations. In this field, telomere/telomerase dysfunction contributes to CRC carcinogenesis by impairing genomic stability and cellular replication. Objective: This study aimed to evaluate genetic and epigenetic alterations in CRC by examining mutation rates in the human telomerase reverse transcriptase (hTERT) promoter region, relative telomere length (RTL), hTERT gene expression, and DNA methylation in the TERT hypermethylated oncological region (THOR). Methods: A total of 45 CRC and 34 adjacent normal tissue samples from Moroccan patients were analyzed using molecular approaches, such as Sanger sequencing, quantitative PCR (qPCR), reverse transcription qPCR (RT-qPCR), and methylation-specific PCR (MSP). Results: No mutations in the hTERT promoter region were identified. However, hypermethylation in the THOR region was reported in 82.2% of CRC samples and 79.4% of adjacent normal tissues. High hTERT expression was detected in 50% of CRC patients. In addition, telomere length was significantly shorter (p=0.002) in cancerous tissues (1.41 [1.36 – 1.43]) compared to normal mucosa (1.559 [1.46 – 1.63]), with an RTL ratio less than 1 (0.90 [0.86 – 0.95]). No significant differences were found between clinicopathological features and hTERT expression, THOR methylation, or RTL, except for a significant correlation between THOR hypermethylation and smaller tumor size (p=0.017) and between THOR methylation and RTL in CRC tissues (p=0.034). Conclusion: These results suggest that telomere lengthening is crucial for CRC initiation and progression, and cancer cells tend to shorten telomeres to maintain the chromosomal instability (CIN) required for tumor progression. Further research is needed to elucidate the mechanisms underlying telomere shortening in CRC and understand the role of telomerase/telomere complex in CRC initiation and progression, which could provide new diagnostic, prognostic, and therapeutic targets.

Aim: Angiogenesis is a universal hallmark of all cancers involving a variety of proteins including vascular endothelial growth factor (VEGF). Extensive studies have explored the potential implications of single nucleotide polymorphisms (SNPs) within VEGF-A in lung cancer (LC) susceptibility, tumor growth, and their effect on the gene expression level. Accordingly, we have planned in the present study to evaluate the prevalence of the -460T/C (rs833061), the -2578C/A (rs699947), and the -2549I/D (rs35569394) SNPs and their association with clinicopathological parameters and to assess their impact on the expression of VEGF-A, VEGFR-1, and VEGFR-2 to be used in the accurate management of LC in Morocco. Methods: A total of 60 fresh biopsies were collected from patients with primary LC and were subjected to polymerase chain reaction (PCR)-DNA sequencing of VEGF-A to detect -460T/C (rs833061), -2578C/A (rs699947), and -2549I/D (rs35569394) SNPs. Reverse transcription (RT)-PCR was used to evaluate VEGF-A, VEGFR-1, and VEGFR-2 expression levels. Results: Sequencing analysis revealed the occurrence of -460T/C, -2578C/A, and -2549I/D polymorphisms with different frequencies. VEGF-2549I/D polymorphism was associated with cancer staging for both genotypes and alleles distributions (p < 0.05). Overall, gene expression analysis revealed an overexpression of VEGF-A, VEGFR-1, and VEGFR-2. The expression of VEGFR-1 and VEGFR-2 was significantly associated with histological types (p = 0.0114). Of note, no significant correlation was obtained between VEGF-A expression and VEGF-A gene polymorphisms (p > 0.05). Conclusions: This study is very informative providing the first insight into polymorphisms and expression of VEGF ligand and its receptors in LC patients from Morocco. Globally, -2549I/D SNP and VEGFR-1 and VEGFR-2 expressions appear to be promising prognostic biomarkers and are likely potential keys for better management of LC.

Recently, the World Health Organization recommended integrating HPV testing into cervical cancer screening programs globally. This study aimed to compare the GeneXpert assay with PCR-sequencing for HPV detection and genotyping to assess the feasibility of incorporating HPV molecular testing into cervical cancer screening. A total of 1000 women aged 30 or 40 from rural and urban areas across four regions in Morocco with high sexually transmitted infection prevalence were recruited. After excluding 21 invalid tests, DNA testing on the remaining 979 samples showed an HPV prevalence of 4.0 % (39/979) by PCR and 5.0 % (49/979) by Xpert, with an overall prevalence of 5.7 % (56/979) when combining both techniques. The concordance rate between the tests was 97.5 %. Notably, the Xpert HPV assay was highly efficient in detecting HPV, with nearly all identified HPVs being high-risk oncogenic types, predominantly HPV16, 18, 31, 35, and 45. The Xpert HPV assay has demonstrated excellent analytical performance, making it a reliable option for HPV detection in vaginal and cervical swabs. Its integration into primary cervical cancer screening programs could significantly enhance the early detection of HPV-positive cases, thereby strengthening the screening framework and potentially reducing both the incidence and mortality of cervical cancer. Future studies should focus on confirming these results and exploring the utility of this method in conjunction with other diagnostic tools such as visual inspection with acetic acid (VIA) for a comprehensive assessment of its effectiveness in real-world settings.

Signal transducer and activator of transcription (STAT) proteins are cytoplasmic transcription factors known to play key roles in numerous physiological and pathological processes, from pathogen response to cancer modulation. However, the roles of some STAT family members, particularly STAT1 and STAT4, in the initiation and progression of bladder cancer (BC) have not been comprehensively studied. The present study investigated the expression pattern of STAT1 and STAT4 in the prognosis and survival of BC taking advantage of patients' specimens and cell lines. In our cohort, high mRNA expression of STAT1 was significantly associated with tumor invasiveness, recurrence and progression, and was shown to increase according to tumor stage in BC cell lines. However, it did not affect patient survival. By contrast, STAT4 exhibited its highest expression in early-stage tumors, without a significant link to the tumor stage. Moreover, it was found that increased STAT4 mRNA expression was associated with improved disease-free survival and overall survival in our cohort. Collectively, these findings suggest that STAT1 and STAT4 could be promising prognostic markers to enhance BC management.

Lung cancer (LC) mutations in the epidermal growth factor receptor (EGFR), phosphoinositide 3-kinase catalytic subunit alpha (PIK3CA), and human epidermal growth factor receptor 2 (HER2) genes represent promising targets for personalized treatment strategies. This study aims to investigate the mutation profiles of these genes in Moroccan LC patients and examine their correlation with clinicopathological features. In this prospective study, LC specimens were collected from 60 patients. Mutations in specific regions of EGFR (exons 18 – 21), PIK3CA (exons 9 and 20), and HER2 (exon 20) were assessed using polymerase chain reaction and sequencing. Correlation with clinicopathological features was analyzed using Jamovi software. Overall, 25 patients (41.7%, 25/60) harbored mutations in EGFR, and five patients (8.3%, 5/60) had alterations in PIK3CA, while no mutation was found in HER2. Most EGFR mutations were located in exon 21 (19/27), and PIK3CA mutations were found in exons 9 and 20. Interestingly, 3.4% of cases exhibited co-occurring PIK3CA and EGFR mutations. EGFR mutations were observed across multiple histological types, whereas PIK3CA mutations were associated with adenocarcinoma and squamous cell carcinoma. No notable correlations were found between EGFR mutations and clinicopathological parameters, but a significant association between PIK3CA mutations and age was observed. The occurrence of EGFR and PIK3CA mutations highlights their potential as biomarkers for personalized LC therapy. The absence of HER2 mutations in this cohort warrants further investigation. These findings highlight the importance of expanding molecular profiling to identify additional actionable mutations for tailored treatment in LC patients.

Bladder cancer (BC) is a prevalent malignancy with poor prognosis in advanced stages. While immune checkpoint blockade has revolutionized immunotherapy, its efficacy remains limited for most advanced BC patients. The detailed characterization of BCs tumor microenvironment (TME) is a prerequisite to understand these mechanisms of resistance and to develop new therapeutic strategies. In this study, we used a genetically engineered BC mouse model resistant to anti-PD1 treatment, and BC patient samples, to investigate the evolution of tumor-associated macrophages (TAMs) during BC progression. We identified a subset of pro-tumor TAMs expressing CXCR4, predominantly found in advanced stages of BC-bearing mice and in half of muscle-invasive BC patients from the studied cohort. Interestingly, CXCR4+ TAM-rich regions were associated with CD8 T cell-excluded areas in both mice and patients. Administration of a small molecule CXCR4 inhibitor significantly reduced the number of pro-tumor TAMs within the tumor and markedly prolonged mouse survival. Incorporating this inhibitor into a tri-immunotherapy regimen further enhanced survival, highlighting the potential of targeting multiple pathways to strongly enhance anti-tumor effects and offering new hope for improving immunotherapy in advanced BC.  ### Competing Interest Statement The authors have declared no competing interest.

Ethnopharmacological relevance Modern research has increasingly focused on the traditional use of plants for radioprotection. Plant extracts, rich in bioactive compounds, represent promising candidates for mitigating radiation-induced damage. This ethnopharmacological perspective highlights the value of ancestral knowledge in developing complementary therapeutic strategies. Purpose Radiotherapy remains a cornerstone of cancer treatment, yet it is often accompanied by adverse effects that impair patients' quality of life. The search for effective, safe, and natural radioprotective agents is therefore of high importance. Methods Following PRISMA guidelines, a systematic search was conducted using PubMed and Google Scholar for articles published between April 2019 and February 2025. Keywords included “radioprotective potential” AND (“plant extracts” OR “natural radioprotectors” OR “radioprotection”). Only studies reporting experimental or clinical evidence on the radioprotective effects of plant-derived compounds were selected. Results Numerous studies demonstrate that plant-based compounds may protect against ionizing radiation through mechanisms such as reactive oxygen species scavenging, DNA repair, anti-inflammatory activity, and regulation of apoptosis-related pathways. These effects are primarily attributed to secondary metabolites, including polyphenols, vitamins, terpenoids, alkaloids, and glucosinolates. Conclusion This review compiles recent advances on the use of plant-based natural products for radioprotection. These findings encourage further research into phytomedicine as a supportive approach to reduce radiation-induced side effects and improve cancer care.

BACKGROUND:The mouse mammary tumor virus (MMTV) has been identified as potentially oncogenic, and its presence in milk was reported and discussed. However, with respect to breast cancer etiology, the transmission routes for these viruses are not known. In this context, the objective of this study is to assess the presence of MMTV-like virus in breast milk and to explore the associated factors of its presence among healthy lactating women in Morocco. METHODS:In this prospective study, milk samples were collected from 44 lactating women recruited from the Souissi Maternity Hospital of Rabat in Morocco. MMTV-like DNA was identified by polymerase chain reaction amplification using specific primers targeting the env gene. RESULTS:The prevalence of the MMTV-like virus was 45.5% (20/44). Statistical analysis revealed a significant association with the use of henna. It seems that it increases the risk of the presence of MMTV-like virus in breast milk. The hypothesis could be the possible contamination of henna sold in bulk in local markets by urine and feces of mice during storage. CONCLUSION:Nevertheless, these results need to be confirmed by multicenter studies to thoroughly investigate the impact of other factors and the potential contamination of henna with the virus through urine and feces of mice during storage.

The transcription factor TWIST1 is a major regulator of Epithelial-Mesenchymal Transition, enhancing cancer cell mobility and invasive potential. Overexpression of TWIST1 is associated with tumor progression and poor prognosis. In our study, we explored the role of TWIST1 as both a prognostic biomarker and a therapeutic target in bladder cancer (BC), as well as the relationship between its promoter methylation and mRNA expression in bladder cancer patients. In cohort of 66 bladder cancer patients, we explored TWIST1 expression levels in tumor samples through RT-qPCR analysis;Our findings revealed a significant correlation between high TWIST1 expression levels and advanced bladder tumor stages, grades, and progression; suggesting its association with aggressive BC phenotypes. Importantly, patients with low TWIST1 expression exhibited significantly prolonged disease-free survival (DFS), indicating its potential as a prognostic marker for stratification and as a therapeutic target in advanced BC. In contrast, there was no direct correlation between TWIST1 promoter methylation status and TWIST1 expression levels in BC tumors.In summary, TWIST1 expression could play an important role as a molecular marker for BC patients’ prognosis and overall survival prediction. Moreover, our results suggest that TWIST1 promoter methylation doesn't affect the gene expression in BC. Furthermore, understanding the molecular mechanisms driving TWIST1 dysregulation may uncover novel therapeutic targets to improve the management of BC.

Background Telomerase activity plays a crucial role in cancer development and progression. Thus, telomerase activation through the interplay of mutations and epigenetic alterations in the telomerase reverse transcriptase (TERT) promoter may provide further insight into bladder cancer induction and progression. Methods In this study 100 bladder tumour tissues were selected, and four molecular signatures were analysed: THOR methylation status, TERT promotor mutation, telomere length, and TERT expression. Results In our study, 88% of bladder cancer patients had an hypermethylation of the THOR region and 60% had mutations in the TERT promoter region. TERT promoter methylation was observed in all stages and grades of bladder cancer. While, TERT promoter mutations were detected in advanced stages and grades. In our cohort, high levels of TERT expression and long telomeres have been found in noninvasive cases of bladder cancer, with a significant association between TERT expression and Telomere length. Interestingly, patients with low TERT expression and cases with long telomeres had significantly longer Disease-free survival and overall survival. Conclusion The methylation and mutations occurring in the TERT promoter are implicated in bladder carcinogenesis, offering added prognostic and supplying novel insight into telomere biology in cancer.

Nowadays, cutting-edge Artificial intelligence systems demonstrate exceptional capabilities in comprehending, generating, and manipulate human language, ushering in a new era of understanding, collaboration, and innovation. This systematic review explores the varied applications of ChatGPT within the realm of biomedicine and patient care, aiming to uncover its potential in transforming textual information into actionable insights for improved healthcare outcomes. To conduct this study, we followed PRISMA guidelines that specifically pertain to systematic reviews by targeting two dataset sources “Google Scholar” and “PubMed” and by using the keywords “Chatgpt, Biomedicine, and Health care”. According to our literature surveys conducted from January 2021 to January 2024, we introduce ChatGPT, as a powerful language model, implicated in various tasks, such as interpreting medical literature, extracting meaningful patterns from vast datasets, and enhancing communication between healthcare professionals. It also investigates the model's ability to assist in clinical decision-making, generating hypotheses, and facilitating personalized treatment plans. However, the integration of ChatGPT into healthcare frameworks may bridge ethical concerns, and potential obstacles such as data privacy, bias, hallucination, and interpretability, emphasizing the need for responsible implementation to ensure patient safety and data security.

Background: Lung cancer (LC) is a lethal malignancy with a late diagnosis and poor prognosis. During the last decade, the identification of oncogenic driver alterations has noticeably changed the therapeutic landscape and contributed to the emergence of the “oncogene addiction” concept and precision medicine in oncology. Among these alterations, the spotlight has turned to driver mutations in the KRAS and BRAF genes, which have garnered significant attention due to the emergence of targeted therapies and the potential for personalized treatment strategies. Objective: Hence, the present study aimed to evaluate the mutational landscape of the KRAS and BRAF genes in LC Moroccan patients along with their frequencies and their correlation with clinicopathological features. Methods: A total of 60 fresh biopsies were collected from patients with primary LC and were subjected to PCR-DNA sequencing of exon 2 of KRAS and exon 15 of BRAF genes in order to detect the most common mutations known by their implication in response to targeted therapies. Results: Sequencing analysis revealed that mutations in KRAS and BRAF genes represented respectively 8.3% and 6.7% of cases; one patient had two KRAS mutations (G12A and K5E), and none had simultaneous BRAF and KRAS mutations. The vast majority of patients harboring KRAS mutations were men, formal smokers with adenocarcinomas, and at advanced stage (stage III). BRAF mutations were mainly detected in men and nonsmokers with adenocarcinoma. Statistical analyses showed no significant correlation between KRAS and BRAF substitutions and clinico-pathological features (p>0.05). Conclusion: The presence of these mutations will be used as a valuable molecular biomarker to select potential candidates eligible for effective personalized medicine using available agents targeting these mutations. Much effort is needed to identify other druggable mutations to generalize personalized LC therapy for better management of this devastating disease.

Background/Objectives: This study aimed to identify various risk factors associated with breast cancer and explore different treatment strategies based on socio-economic, hormonal, and clinical perspectives.; Methods: We analyzed socio-economic, hormonal, genetic, and clinical variables using data from 356 questionnaires obtained from breast cancer patients at Hassan II Regional Hospital in Agadir, Morocco ; Results:The study reveals that the average age of breast cancer patients is 50 ± 10.72 years, with a mode of 47 years and an age range from 29 to 94 years. Notably, women aged 38 are most frequently diagnosed with triple-negative breast cancer. Significant socio-economic trends were observed among the participants, with the majority being housewives (91%) and nearly half residing in rural areas (48.60%). High rates of illiteracy (74.72%) and financial difficulties (54.2%) pose challenges in accessing healthcare services. Psychological distress is prevalent, with 40.7% experiencing anxiety and 30.1% experiencing sadness. The use of oral contraceptives varies, with implications for breast cancer risk. Additionally, statistics on menarche and menopause suggest hormonal influences on breast cancer development. Histological analysis indicates a predominance of grade II invasive ductal carcinoma and left breast localization. Metastases are present in nearly 38.20% of cases. Notably, surgery as the primary treatment effectively treats medium-sized tumors while limiting metastasis. Furthermore, a comparison of treatment strategies reveals a preference for letrozole among postmenopausal patients and tamoxifen among premenopausal patients; Conclusions:These findings highlight the complexity of breast cancer risk factors and therapeutic approaches, emphasizing the importance of personalized care and targeted interventions.

Introduction: Single nucleotide poly-morphisms (SNPs) in DNA repair genes are mainly correlated with the response to radiotherapy in na-sopharyngeal cancer (NPC). In NPC patients, previous research has stud-ied the association between X-ray re-pair cross-complementing group 1 and 3 (XRCC1 and XRCC3) polymorphisms and radio-therapeutic response. The objective of our study was to test the association between XRCC1 Arg399Gln and XRCC3 Thr241Met polymorphisms and the response to radiotherapy in the NPC Moroccan population.Material and methods: A total of 100 patients with NPC were geno-typed for polymorphisms in XRCC1 and XRCC3 genes.Results: The results revealed that the genotypes and alleles of both SNPs did not show any significant associa-tion with clinical stages (for XRCC1 Arg-399Gln: p [genotype] = 0.559; p [allele] = 0.440) and (for XRCC3 Thr241Met: p [genotype] = 0.638; p [allele] = 0.567). Moreover, in the study of the associa-tion between the polymorphisms and radiotherapy, the response to radia-tion therapy between genotypes and alleles was not statistically significant (for XRCC1 Arg399Gln p [genotype] = 0.583; p [allele] = 0.459) and (for XRCC3 Thr241Met p [genotype] = 0.660; p [allele] = 0.590).Conclusions: The present study sug-gests that XRCC1 Arg399Gln polymor-phism does not have any impact on the radio-therapeutic response in Mo-roccan NPC patients whereas XRCC3 Thr241Met polymorphism may act as a prognostic indicator for NPC patients treated with radiotherapy. However, studies with a larger sample are need-ed to confirm our results.

Les mutations du promoteur de la télomérase inverse humaine (hTERT) sont des événements génétiques fréquents dans les tumeurs de vessie et peuvent servir comme des biomarqueurs potentiels pour le diagnostic précoce. Cette étude a évalué les mutations du promoteur hTERT à la fois dans les biopsies et les urines de patients atteints de tumeur de vessie. Dans une étude de cohorte prospective impliquant 70 patients admis pour la prise en charge de tumeur de vessie à différents stades et grades au service d'urologie. Les mutations du promoteur hTERT ont été identifiées dans les échantillons des biopsies fraîches prélevées lors de la résection trans-urétrale de la vessie et dans les sédiments urinaires par amplification PCR et séquençage de l'ADN. Les mutations du promoteur de l'hTERT ont été signalées dans 60 % des biopsies cancéreuses (42/70), les mutations hotspot C228 T et C250 T ont été identifiées respectivement dans 80,95 % (34/42) et 16,67 (7/42) des cas positifs. Les mutations du promoteur de l'hTERT ont été identifiées dans 30 % des sédiments urinaires appariés (21/70) et ont montré une sensibilité globale de 50 % et une spécificité de 100 %. Chez les patients atteints d'un cancer de la vessie non invasif sur le plan musculaire, aucune association statistiquement significative n'a été détectée entre les mutations du promoteur de l'hTERT et la survie sans récidive (HR : 1,224, 95 % CI : 0,373–4,011, p = 0,739), et la survie globale (HR : 0,363, 95 % CI : 0,041–3,244, p = 0,364). Les mutations du promoteur de l'hTERT sont des événements précoces qui se produisent à des fréquences élevées et peuvent être identifiées dans les cellules exfoliées d'un échantillon urinaire, ce qui pourrait être un biomarqueur non invasif et intéressant pour le diagnostic et le suivi de la tumeur de vessie.