Unfavorable Prognosis Research Articles

Lentinan suppresses the progression of neuroblastoma by inhibiting FOS-mediated transcription activation of VRK1 to stabilize p53 protein

Neuroblastoma (NB) is a common malignant and solid pediatric tumor with unfavorable prognosis. Although studies have shown the anti-tumor efficacy of lentinan (LNT), molecular mechanism that contribute to the anti-tumor effect on NB remains unclear. The aim of this study is to unmask the anti-tumor role of LNT in NB and the specific molecular mechanism. At first, the in vivo experiments were conducted and the results indicated that LNT could suppress tumor growth in NB. Subsequent cellular functional assays unveiled that LNT treatment could efficiently decrease NB cell viability, induce cell cycle stagnation at G0/G1 phase, increase the apoptosis rate, and weaken the migrating and invasive abilities. Furthermore, LNT resulted in a significant downregulation of FOS expression. FOS overexpression recovered the growth, migration and invasion of NB cells suppressed by LNT treatment. Mechanism investigations revealed that FOS interacted with JUND to transcriptionally activate VRK1. Moreover, VRK1 downregulated p53 protein via inducing the phosphorylation of p53 at site 291–393. In summary, this study reveals a novel molecular pathway by which LNT exerts tumor-suppressing functions in NB.

A Case of Acute Massive Pulmonary Embolism with Multiple Cardiac Arrests and Successful Systemic Thrombolysis.

Massive pulmonary embolism (PE) is a potential noncardiac cause of cardiac arrest with unfavorable prognosis. Maintaining a high degree of clinical suspicion, use of bedside focused cardiac ultrasound and computed tomography pulmonary angiography (CTPA) aid in rapid management. Thrombolytic therapy with anticoagulation is indicated in treatment of massive PE provided that there are no contraindications and there is low risk of bleeding. We present a case of massive PE with multiple cardiac arrests who successfully responded to systemic thrombolysis along with anticoagulation, barring a moderate bleeding complication.

Prediction of prognosis and immune response in lung adenocarcinoma by peroxisome related-lncRNA.

Prediction of prognosis and immune response in lung adenocarcinoma by peroxisome related-lncRNA.

Favorable trends in lung cancer incidence with unfavorable survival prognosis: A spatiotemporal analysis by histology in Córdoba, Argentina.

Favorable trends in lung cancer incidence with unfavorable survival prognosis: A spatiotemporal analysis by histology in Córdoba, Argentina.

Liquid Biopsies in the Early Diagnosis, Prognosis, and Tailored Treatment of Colorectal Cancer

Introduction: Liquid biopsies provide a less-invasive option to tissue biopsies for the early diagnosis, prognosis, and tailored therapy of colorectal cancer (CRC). CRC is a major cause of cancer-related death, and early identification is essential for improving patient outcomes. Review: Conventional diagnostic techniques, including colonoscopy and tissue biopsy, may be enhanced by liquid biopsies that examine circulating tumor cells (CTCs), circulating tumor DNA (ctDNA), extracellular vesicles (EVs), and other indicators present in body fluids. These markers provide significant insights into tumor biology, heterogeneity, and therapeutic response. CTCs detected in early-stage CRC have prognostic significance for disease recurrence and survival, while ctDNA investigation may uncover genetic mutations, epigenetic alterations, and tumor development. The identification of ctDNA in minimal residual disease (MRD) postsurgery correlates with an elevated risk of recurrence and unfavorable prognosis, underscoring its use in assessing treatment effectiveness. Furthermore, non-coding RNAs (ncRNAs) contained inside EVs provide potential prospective biomarkers and therapeutic targets, facilitating diagnosis and treatment assessment. Notwithstanding the potential of liquid biopsies, obstacles persist in assay standardization, sensitivity enhancement, and the management of tumor heterogeneity. Additional extensive research is required to determine their function in clinical practice. Conclusion: Overall, liquid biopsies serve as a potential instrument for real-time monitoring, evaluating therapy responses, and directing individualized therapeutic strategies in CRC patients.

MiR-183-5p-enriched extracellular vesicles promote the crosstalk between hepatocellular carcinoma cell and endothelial cell via SIK1/PI3K/AKT and CCL20/CCR6 signaling pathways

BackgroundThe cancer-related mortality of primary liver cancer ranks third globally, and hepatocellular carcinoma (HCC) is predominant, posing a serious threat to patients’ health. Understanding HCC’s pathogenesis and target molecules is crucial for early diagnosis and prognosis. Extracellular vesicles (EVs) and their carried miRNAs impact tumor progression. This study aims to investigate miR-183-5p in HCC cell-derived EVs on angiogenesis, progression, and metastasis, and provide diagnostic and therapeutic evidence.MethodsqRT-PCR was used to evaluate the expression of miR-183-5p in HCC tissue and plasma EV samples. Contrast-enhanced ultrasound and The Cancer Genome Atlas evaluated its correlation with angiogenesis and prognosis. In vitro, cell counting kit-8 (CCK-8), colony formation, transwell, tube formation, and permeability assays examined the effect of HCC cell-derived EVs on human umbilical vein endothelial cells (HUVECs). Subcutaneous tumor and lung metastasis models in nude mice verified it in vivo effects. RNA sequencing and databases predicted downstream genes and pathways, and dual luciferase and western blotting assays verified binding and activation. Conditioned medium from treated HUVECs was used on HCC cells, and chemokine levels measured. The CCL20/CCR6 axis effect was studied in vitro and in vivo by knocking down CCR6.ResultsThis study revealed the abnormal upregulation of miR-183-5p in both tissues and plasma EVs from patients with HCC, and its association with unfavorable prognosis. In vivo experiments, the promoting effects of miR-183-5p in HCC cell-derived EVs on the progression, metastasis and angiogenesis were verified by employing subcutaneous tumor formation models and lung metastasis models in nude mice. We demonstrated that miR-183-5p in HCC cell-derived EVs induced HUVECs proliferation, migration, angiogenesis and permeability by downregulating SIK1 expression and activating the PI3K/AKT signaling pathway in vitro. Moreover, stimulated HUVECs could secrete the chemokine CCL20 and induce HCC progression and metastasis through the CCL20/CCR6 signal pathway in vitro and in vivo.ConclusionThe findings indicated that miR-183-5p delivered by EVs from HCC cells is crucial in mediating the communication between HUVECs and HCC cells by modulating the SIK1/PI3K/AKT and CCL20/CCR6 signaling pathways, and EVs-miR-183-5p might be a potential therapeutic target for HCC patients.

Early NCCT imaging signs for prognostication in intracerebral hemorrhage: a retrospective cohort study with long follow up results.

This study intends to investigate the connection between non-contrast computed tomography (NCCT) imaging findings and neurological function scores in patients with intracerebral hemorrhage (ICH) in a long follow up of 451 patients. Between January 2020 and October 2021, a retrospective review was undertaken on patients with ICH. The NCCT imaging results within 24h of symptom onset, clinical information, biochemical markers and the one-year outcome post-discharge were collected and analyzed. Subsequently, a prognostic model was devised to predict poor outcomes. A cohort of 451 patients diagnosed with ICH was analyzed in this study. Adverse prognostic outcomes at three months were found to be independently associated with several factors, including the presence of the swirl sign (P = 0.010), advanced age (P = 0.003), post-ICH modified Rankin Scale (mRS) score (P = 0.003,), time elapsed from symptom onset to NCCT scan (P = 0.018), and the presence of ventricular hemorrhage (P = 0.003). Unfavorable prognosis at 12months was independently associated with the presence of the island sign (P = 0.001), older age (P = 0.003), post-ICH mRS score (P = 0.003), and HE (P = 0.014). Additionally, the integration of NCCT imaging signs into the predictive model significantly improved its accuracy in predicting adverse outcomes at both three months (AUC = 0.817 vs. 0.782 in the model without NCCT, NRI = 0.219, P = 0.033, IDI = 0.080, P = 0.006) and 12months (AUC = 0.829 vs. 0.797 in the model without NCCT, NRI = 0.235, P = 0.028, IDI = 0.096, P = 0.003). The early imaging features of patients suffering from ICH can provide a more precise prognosis from the analysis of the 12-month follow up results.

Iris melanoma: correlation of clinical, morphometric, pathomorphological features and infectious status

To identify clinical, morphometric, and pathomorphological correlations with infectious status in patients with iris melanoma and to determine predictors of unfavorable prognosis. Sixteen patients with iris melanoma were examined. Anterior segment optical coherence tomography (AS-OCT) was performed using the RS-3000 Advance system (Nidek, Japan) with OCT-Angiography software. The specific humoral response to herpesviruses was assessed by detecting IgG and IgM antibodies in blood serum via enzyme-linked immunosorbent assay (ELISA) using an automated immunoassay analyzer LAZURITE (Dynex Technologies Inc., USA). Statistical analysis employed Spearman's rank correlation coefficient (rs). Iris melanoma was predominantly observed in female patients (n=11) of advanced age (n=8). Biomicroscopy revealed 10 pigmented, 1 hypopigmented, and 5 non-pigmented tumors. The mean prominence on OCT was 1461.7±740.5 μm, the basal diameter was 3409.6±1822.8 μm, and the volume was 4.7±3.7 mm3. Ciliary body involvement was detected in 10 patients. Iris melanomas were classified as epithelioid-cell (n=1), spindle-cell (n=12), and mixed-cell (n=3) types. Extrabulbar growth was noted in three patients. Serological markers of viral reactivation were identified: herpes simplex virus type 1 (n=11) and type 2 (n=5), and cytomegalovirus (n=3). The findings of this study demonstrated a correlation between herpesvirus reactivation and unfavorable prognostic features of iris melanoma. Further research is needed to deepen the understanding of the role of herpesviruses in the pathogenesis of iris melanoma and to develop personalized approaches to prevention and treatment.

Aspartate beta-hydroxylase is a prognostic factor in gallbladder cancer with the function of promoting tumorigenesis and chemoresistance

AimsGallbladder cancer is characterized by a dismal prognosis, with a limited number of biological markers currently identified for the carcinogenesis, progression and prognosis of gallbladder cancers (GBCs). The discovery of efficacious biomarkers is crucial for enhancing the prognosis of gallbladder cancer.MethodsAnalysis of RNAseq datasets from gallbladder cancer allowed the identification of differential genes between gallbladder cancer and adjacent tissues. Subsequent application of Mendelian randomization extracted target gene known to promote gallbladder cancer from these differentially expressed genes. Immunohistochemistry was then conducted to evaluate the expression of these target gene in a cohort of 215 patients with gallbladder cancer, utilizing follow-up information to determine their prognostic value. Moreover, single-cell sequencing data of gallbladder cancer elucidated the role of target genes within the immune microenvironment of this cancer type. The Genomics of Therapeutics Response Portal (CTRP) database enabled the assessment of the impact of target genes on the IC50 of chemotherapy drugs. Lastly, network pharmacology and analytical methodologies were employed to investigate the effects of traditional Chinese medicine active ingredients targeting these specific genes.ResultsASPH expression is notably elevated in gallbladder cancer tissues, correlating with an unfavorable prognosis for patients afflicted with this disease. Results from Mendelian randomization studies suggest that heightened ASPH levels play a significant role in the development of gallbladder polyps and stones, which are established clinical risk factors in gallbladder cancer. Analysis of clinical samples demonstrates a positive association between ASPH expression and indicators of poor differentiation, increased tumor size, advanced TNM stage, lymph node metastasis, and invasion. The single-cell immune microenvironment reveals that ASPH not only enhances the expression of immune checkpoints, namely PDL1 and PVR, in the gallbladder cancer epithelium, resulting in immune evasion, but also triggers epithelial-mesenchymal transition and migration, promoting metastasis. Furthermore, ASPH contributes to heightened tumor drug metabolism, hence raising the IC50 values for gemcitabine and paclitaxel. Utilizing network pharmacology and molecular docking techniques, this study pinpointed six bioactive compounds derived from traditional Chinese medicine with a targeted effect on the ASPH protein, comprising Sebacic acid, Suberic acid, Azelaic acid, Dimelic acid, Succinic acid, and D-Asparaginsaeure.ConclusionsASPH plays a role in promoting the development of gallbladder cancer and resistance to chemotherapeutic agents, rendering it a promising target for therapeutic interventions. Active therapeutic compounds targeted on ASPH can be identified among the active ingredients present in traditional Chinese medicine.

RBPMS inhibits bladder cancer metastasis by downregulating MYC pathway through alternative splicing of ANKRD10

RNA-binding proteins (RBPs) are pivotal mediators of the alternative splicing (AS) machinery of pre-mRNA. Research has demonstrated that the AS process is significantly dysregulated and plays a crucial role in bladder cancer (BLCA). We conducted comprehensive screening and analysis of the TCGA-BLCA cohort, specifically focusing on genes with significant differences in expression levels between carcinoma and adjacent non-cancerous tissues. Among the 500 differentially expressed genes, 5 RNA-binding proteins were identified. Only the RNA-binding protein with multiple splicing (RBPMS) demonstrated a consistent downregulation in BLCA and was correlated with an unfavorable prognosis for affected patients. Subsequent experiments revealed that RBPMS exerted inhibitory effects on the epithelial-mesenchymal transition (EMT) pathway and the migratory potential of BLCA cells. RNA-Seq analysis identified ANKRD10 as a key target mRNA regulated by RBPMS in BLCA. RBPMS depletion in BLCA cells resulted in AS of ANKRD10 and increased ANKRD10-2 expression. ANKRD10-2 functioned as a transcriptional co-activator of MYC proteins, thereby augmenting their transcriptional activity. Furthermore, ANKRD10-2 knockdown significantly rescued the migration enhancement induced by RBPMS depletion in BLCA cells. Taken together, this study revealed a mechanism whereby RBPMS suppresses the migration and invasion of BLCA cells by attenuating MYC pathway activity via the AS of ANKRD10.

LncRNA LINC01128 promotes prostate cancer cell proliferation, metastasis, and epithelial-mesenchymal transition by modulating miR-27b-3p

BackgroundProstate cancer (PCa) is a prevalent malignancy within the male reproductive system that poses a significant threat to patients’ lives. The function of long non-coding RNA LINC01128 in PCa progression remains to be elucidated.ObjectiveThe objective was to evaluate the significance of LINC01128 in PCa and to elucidate the underlying mechanisms, thereby identifying a potential target for PCa treatment.MethodsThe clinical significance of LINC01128 in PCa was investigated by bioinformatics methods and data analysis. The expression of LINC01128 was quantified using real-time quantitative PCR. The impact of LINC01128 on PCa cell viability and metastasis was evaluated through Cell Counting Kit-8 and Transwell assays. The expression of epithelial-mesenchymal transition markers was analyzed by Western blot analysis. Bioinformatics methods and dual-luciferase reporter assay were employed to explore the mechanisms underlying the role of LINC01128 in PCa progression.ResultsLINC01128 demonstrated significant upregulation in PCa and exhibited a strong correlation with tumor-node-metastasis (TNM) stage, Gleason score, and lymph node metastasis. The upregulation of LINC01128 was found to be linked to a poorer prognosis for PCa. In PCa cells, silencing LINC01128 resulted in the suppression of cell proliferation, migration, and invasion. Furthermore, the knockdown of LINC01128 enhanced the expression of E-cadherin while concurrently repressing the expression of N-cadherin and Vimentin. Mechanistically, the negative regulation of miR-27b-3p by LINC01128 mediated the role of LINC01128 in PCa progression.ConclusionsIn PCa, high expression of LINC01128 may predict patients’ unfavorable prognosis. LINC01128 promoted PCa cellular processes by negatively regulating miR-27b-3p.

Leiomyosarcoma Arising in Angiomyolipoma 5 Years Post-Embolisation: A Case Report and Literature Review

Renal angiomyolipoma is a benign tumour characteristically composed of fat, smooth muscles, and thick-walled blood vessels. In extremely rare instances, transformation into the more sinister leiomyosarcoma causes potentially drastic differences in both management strategies and prognosis. In most cases, radical nephrectomy remains the standard modality of choice for these tumours as they exhibit aggressive biological behaviour with unfavourable prognosis. Herein, the authors describe a rare case of renal angiomyolipoma in a 33-year-old male, which showed malignant transformation into leiomyosarcoma 5 years post angioembolisation and was managed with radical nephrectomy.

TP53-Mutated Acute Myeloid Leukemia: Review of Treatment and Challenges.

Patients with acute myeloid leukemia (AML) harboring mutations in TP53 (TP53-MT) have poor responses to current therapies and unfavorable prognoses. Despite the recognition of variant TP53 as an adverse feature of AML, an optimal treatment regimen has not yet been established, underlining a critical need for new, more effective therapeutic combinations and novel treatments. We present the case of a patient with TP53-MT AML and marked myelodysplasia who developed primary refractory disease after induction therapy with the intensive chemotherapy regimen of liposomal daunorubicin and cytarabine. Our patient's optimal response to second induction chemotherapy with FLAG-Ida prompted an exploration of established and investigational treatment regimens for this specific high-risk AML subtype. Therefore, we performed a comprehensive literature review of findings from studies exploring AML therapies, focusing on outcomes for patients with TP53-MT AML. The summary provided here reveals the complexity of defining the therapeutic responses of patients with the heterogeneous TP53-MT genetic background and the challenges in treating this high-risk form of AML. Future work must continue to investigate novel therapies and combinations to improve patient outcomes in this vulnerable population.

Targeting p70S6K1 Inhibits Glycated Albumin-Induced Triple-Negative Breast Cancer Cell Invasion and Overexpression of Galectin-3, a Potential Prognostic Marker in Diabetic Patients with Invasive Breast Cancer

Background: There is an urgent need to identify new biomarkers for early diagnosis and development of therapeutic strategies for diabetes mellitus (DM) patients who have invasive breast cancer (BC). We previously reported the increased activated form of 70 kDa ribosomal protein S6 kinase 1 (phospho-p70S6K1) in a triple-negative BC (TNBC) cell line MDA-MB-231 exposed to glycated albumin (GA) and in invasive ductal carcinoma tissues from T2DM patients, compared to untreated cells and their non-diabetic counterparts, respectively. Objective: We aimed to explore the function of p70S6K1 in GA-promoted TNBC progression. Methods: By employing small interference (si)RNA technology or blocking its kinase activity using its specific pharmacological inhibitor, we monitored cell invasion using Transwell® inserts and the expression levels of activated signaling proteins and cancer-related proteins using Western blot. Results: In silico analysis revealed that high mRNA levels of p70S6K1 were associated with an unfavorable prognosis and progression to advanced stages of TNBC in DM patients. The downregulation/blockade of p70S6K1 inhibited GA-promoted MDA-MB-231 cell invasion and the phosphorylation of protein S6 and ERK1/2, the p70S6K1 downstream effector, and the key oncogenic signaling protein, respectively. The suppression of the expression of GA-upregulated cancer proteins, including enolase-2, capping protein CapG, galectin-3, and cathepsin D, was observed after p70S6K1 downregulation/blockade. Further in silico validation analyses revealed increased gene expression of galectin-3 in DM TNBC patients, resulting in poor overall survival and disease-free survival. Conclusions: Targeting p70S6K1 may present a valuable therapeutic strategy, while galectin-3 could serve as a potential prognostic biomarker for invasive BC progression in DM patients.

Integrating machine learning and single-cell sequencing to identify shared biomarkers in type 1 diabetes mellitus and clear cell renal cell carcinoma.

Type 1 diabetes mellitus (T1DM), as an autoimmune disease, can increase susceptibility to clear cell renal cell carcinoma (ccRCC) due to its proinflammatory effects. ccRCC is characterized by its subtle onset and unfavorable prognosis. Thus, the aim of this study was to highlight prevention and early detection opportunities in high-risk populations by identifying common biomarkers for T1DM and ccRCC. Based on multiple publicly available datasets, WGCNA was applied to identify gene modules closely associated with T1DM, which were then integrated with prognostic DEGs in ccRCC. Subsequently, the LASSO and SVM algorithms were employed to identify shared hub genes between the two diseases. Additionally, clinical samples were used to validate the expression patterns of these hub genes, and scRNA-seq data were utilized to analyze the cell types expressing these genes and to explore potential mechanisms of cell communication. Overall, three hub genes (KIF21A, PIGH, and RPS6KA2) were identified as shared biomarkers for TIDM and ccRCC. Analysis of clinical samples and multiple datasets revealed that KIF21A and PIGH were significantly downregulated and that PIG was upregulated in the disease group. KIF21A and PIGH are mainly expressed in NK and T cells, PRS6KA2 is mainly expressed in endothelial and epithelial cells, and the MIF signaling pathway may be related to hub genes. Our results demonstrated the pivotal roles of hub genes in T1DM and ccRCC. These genes hold promise as novel biomarkers, offering potential avenues for preventive strategies and the development of new precision treatment modalities.

A Potential Relationship Between HALP Score and In-Hospital Mortality in Acute Heart Failure.

Acute heart failure (AHF) is associated with a dismal prognosis that is even poorer than the majority of cancer types. Therefore, clinical indicators that can aid in determining the prognosis of heart failure are of interest. Multiple risk prediction tools with varying sensitivity and specificities have been introduced before. In the current study, we aimed to evaluate whether the HALP score could accurately predict in-hospital mortality in patients with AHF. We evaluated the medical records of a total of 153 patients admitted to our institution between August 2016-May 2018 for acute heart failure. The patients were divided into two groups: Group 1 (patients who died during hospital admission) and Group 2 (patients who were discharged from the hospital). The HALP score was calculated as: hemoglobin (g/L) x albumin (g/L) x lymphocytes (/L)/platelets (/L) for each patient. The two groups were compared in terms of HALP scores. The receiver operator characteristic (ROC) curve was utilized to assess the predictive performance of HALP on in-hospital mortality in AHF. Patients who died during admission had lower HALP scores compared with the patients who were discharged uneventfully. A ROC curve analysis was performed to predict the optimal cut-off value of the HALP score. The area under the curve (AUC), sensitivity, specificity, and the cut-off value were 0.650, 43%, 57%, 21,5 respectively (p = 0.014). Despite all evolving treatment modalities, heart failure-related mortality rates remain high. Prompt recognition of patients with an unfavorable prognosis is vital for the timely implementation of disease-modifying therapeutic interventions. The HALP score, being a readily calculable tool, serves as an effective means to pinpoint individuals at a heightened risk of in-hospital mortality. We believe that the HALP score holds promise as a practical tool for predicting in-mortality among patients admitted for AHF.

Arsenene-Vanadene Nanodots Co-Activate Apoptosis/Ferroptosis for Enhanced Chemo-Immunotherapy.

Arsenene-Vanadene Nanodots Co-Activate Apoptosis/Ferroptosis for Enhanced Chemo-Immunotherapy.

Long non‑coding RNA ABHD11‑AS1 inhibits colorectal cancer progression through interacting with EGFR to suppress the EGFR/ERK signaling pathway.

Long non‑coding (lnc)RNAs participate in colorectal cancer (CRC) occurrence and progression. The present study aimed to investigate whether lncRNA ABHD11‑AS1 regulates malignant biological behavior of CRC cells. Bioinformatic analysis, reverse transcription‑quantitative PCR and in situ hybridization revealed that ABHD11‑AS1 expression was decreased in CRC samples and associated with an unfavorable prognosis. ABHD11‑AS1 overexpression significantly decreased proliferation, migration and invasion of CRC cells, whereas ABHD11‑AS1 inhibition had the opposite effects. ABHD11‑AS1 interacted with EGFR to inhibit EGFR phosphorylation and attenuate EGFR/ERK signaling, which in turn suppressed the malignant biological behavior of CRC cells. The tumor suppressor function of ABHD11‑AS1 was attenuated by the EGFR agonist NSC228155. Finally, resveratrol (RSV) inhibited CRC cell proliferation, migration and invasion, which may be associated with RSV‑induced decrease in SPT6 homolog, histone chaperone and transcription elongation factor protein expression and increase in ABHD11‑AS1 transcript levels. ABHD11‑AS1 inhibited the phosphorylation of EGFR and decreased EGFR/ERK signaling by interacting with EGFR, thereby delaying the progression of CRC. The ABHD11‑AS1/EGFR/ERK axis may be a novel therapeutic target for preventing CRC progression.

TERT promoter mutations or protein overexpression define an aggressive subset with favourable immunotherapeutic response in advanced urothelial carcinoma

ObjectiveTelomerase reverse transcriptase (TERT) gene promoter mutation (TPM) is a key non-coding somatic alteration in urothelial carcinoma (UC) that plays a critical role in telomerase activation. Despite its importance, the...

I-motif formation in the promoter region of the B-MYB proto-oncogene.

Understanding the mechanisms of carcinogenesis is essential to combat cancer. The search for alternative targets for anticancer therapy has gained interest, particularly when focused on upstream pathways. This strategy is particularly relevant when the encoded target proteins are known - or believed - to be "undruggable", as has been reported for the B-MYB oncogene. This gene, which regulates survival and cell cycle regulation, is overexpressed in cancer and correlates with an unfavorable prognosis. In this study, we focused on the identification of the i-motif (iM) structures in the promoter region of B-MYB as a possible anticancer target, with a complete biophysical characterization and in cell formation assessment using iM-CUT&Tag. Additionally, the interaction of the iM structures with a library of small molecules was investigated.