FRAX486, a PAK inhibitor, overcomes ABCB1-mediated multidrug resistance in breast cancer cells.

The overexpression of P-glycoprotein (P-gp/ABCB1) is a leading cause of multidrug resistance (MDR). Hence, it is crucial to discover effective pharmaceuticals that counteract ABCB1-mediated multidrug resistance. FRAX486 is a p21-activated kinase (PAK) inhibitor. The objective of this study was to investigate whether FRAX486 can reverse ABCB1-mediated multidrug resistance, while also exploring its mechanism of action. The CCK8 assay demonstrated that FRAX486 significantly reversed ABCB1-mediated multidrug resistance. Furthermore, western blotting and immunofluorescence experiments revealed that FRAX486 had no impact on expression level and intracellular localization of ABCB1. Notably, FRAX486 was found to enhance intracellular drug accumulation and reduce efflux, resulting in the reversal of multidrug resistance. Docking analysis also indicated a strong affinity between FRAX486 and ABCB1. This study highlights the ability of FRAX486 to reverse ABCB1-mediated multidrug resistance and provides valuable insights for its clinical application.

The therapeutic role of γδT cells in TNBC.

Triple-negative breast cancer (TNBC) is a subtype of breast cancer that presents significant therapeutic challenges due to the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression. As a result, conventional hormonal and targeted therapies are largely ineffective, underscoring the urgent need for novel treatment strategies. γδT cells, known for their robust anti-tumor properties, show considerable potential in TNBC treatment as they can identify and eliminate tumor cells without reliance on MHC restrictions. These cells demonstrate extensive proliferation both in vitro and in vivo, and can directly target tumors through cytotoxic effects or indirectly by promoting other immune responses. Studies suggest that expansion and adoptive transfer strategies targeting Vδ2 and Vδ1 γδT cell subtypes have shown promise in preclinical TNBC models. This review compiles and discusses the existing literature on the primary subgroups of γδT cells, their roles in cancer therapy, their contributions to tumor cell cytotoxicity and immune modulation, and proposes potential strategies for future γδT cell-based immunotherapies in TNBC.

The Inhibition of Fibrosis and Inflammation in Obstructive Kidney Injury via the miR-122-5p/SOX2 Axis Using USC-Exos.

Background: Fibrosis and inflammation due to ureteropelvic junction obstruction substantially contributes to poor renal function. Urine-derived stem-cell-derived exosomes (USC-Exos) have therapeutic effects through paracrine. Methods: In vitro, the effects of USC-Exos on the biological functions of HK-2 and human umbilical vein endothelial cells were tested. Cell inflammation and fibrosis were induced by transforming growth factor-ß1 and interleukin-1ß, and their anti-inflammatory and antifibrotic effects were observed after exogenous addition of USC-Exos. Through high-throughput sequencing of microRNA in USC-Exos, the pathways and key microRNAs were selected. Then, the antifibrotic and anti-inflammatory effects of exosomal miR-122-5p and target genes were verified. The role of the miR-122-5p/SOX2 axis in anti-inflammatory and antifibrotic effects was verified. In vivo, a rabbit model of partial unilateral ureteral obstruction (PUUO) was established. Magnetic resonance imaging recorded the volume of the renal pelvis after modeling, and renal tissue was pathologically analyzed. Results: We examined the role of USC-Exos and their miR-122-5p content in obstructive kidney injury. These Exos exhibit antifibrotic and anti-inflammatory activities. SOX2 is the hub gene in PUUO and negatively related to renal function. We confirmed the binding relationship between miR-122-5p and SOX2. The anti-inflammatory and antifibrotic effects of miR-122-5p were inhibited, indicating that miR-122-5p has anti-inflammatory and antifibrotic effects by inhibiting SOX2 expression. In vivo, the PUUO group showed typical obstructive kidney injury after modeling. After USC-Exo treatment, the shape of the renal pelvis shown a remarkable improvement, and inflammation and fibrosis decreased. Conclusions: We confirmed that miR-122-5p from USC-Exos targeting SOX2 is a new molecular target for postoperative recovery treatment of obstructive kidney injury.

A novel pyroptosis-related gene signature exhibits distinct immune cells infiltration landscape in Wilms' tumor.

BACKGROUND: Wilms' tumor (WT) is the most common renal tumor in childhood. Pyroptosis, a type of inflammation-characterized and immune-related programmed cell death, has been extensively studied in multiple tumors. In the current study, we aim to construct a pyroptosis-related gene signature for predicting the prognosis of Wilms' tumor. METHODS: We acquired RNA-seq data from TARGET kidney tumor projects for constructing a gene signature, and snRNA-seq data from GEO database for validating signature-constructing genes. Pyroptosis-related genes (PRGs) were collected from three online databases. We constructed the gene signature by Lasso Cox regression and then established a nomogram. Underlying mechanisms by which gene signature is related to overall survival states of patients were explored by immune cell infiltration analysis, differential expression analysis, and functional enrichment analysis. RESULTS: A pyroptosis-related gene signature was constructed with 14 PRGs, which has a moderate to high predicting capacity with 1-, 3-, and 5-year area under the curve (AUC) values of 0.78, 0.80, and 0.83, respectively. A prognosis-predicting nomogram was established by gender, stage, and risk score. Tumor-infiltrating immune cells were quantified by seven algorithms, and the expression of CD8( +) T cells, B cells, Th2 cells, dendritic cells, and type 2 macrophages are positively or negatively correlated with risk score. Two single nuclear RNA-seq samples of different histology were harnessed for validation. The distribution of signature genes was identified in various cell types. CONCLUSIONS: We have established a pyroptosis-related 14-gene signature in WT. Moreover, the inherent roles of immune cells (CD8( +) T cells, B cells, Th2 cells, dendritic cells, and type 2 macrophages), functions of differentially expressed genes (tissue/organ development and intercellular communication), and status of signaling pathways (proteoglycans in cancer, signaling pathways regulating pluripotent of stem cells, and Wnt signaling pathway) have been elucidated, which might be employed as therapeutic targets in the future.

TRMT13 inhibits the growth of papillary thyroid cancer by targeting ANAPC4.

The recently discovered gene TRMT13 encodes a type of RNA methylase and is a member of the CCDC family (also called CCDC76). Here, we delineate its role in papillary thyroid cancer (PTC). Bioinformatics analysis shows significant TRMT13 and ANAPC4 downregulation in PTC and reveals that the expression levels of both genes are linearly correlated. Subsequent analyses confirm that both TRMT13 and ANAPC4 expressions are downregulated in PTC tissues and that this change in expression has a significant impact on cancer diagnosis. We conduct assays on PTC cells subjected to TRMT13 and ANAPC4 silencing or overexpression to assess the biological effects of these genes. We also perform rescue experiments to validate the regulatory effects of TRMT13 on ANAPC4. A nude mouse tumor model is used to evaluate the effects of TRMT13 and ANAPC4 on PTC tumorigenesis. TRMT13 expression is decreased in PTC tissues and cell lines and is positively correlated with that of ANAPC4. Cell assays reveal that TRMT13/ANAPC4 attenuates the malignancy of PTC cells by restraining cell proliferation, migration and invasion, while rescue experiments corroborate that ANAPC4 is a downstream target of TRMT13. In the nude mouse xenograft model, both TRMT13 and ANAPC4 inhibit tumor growth, and TRMT13 and ANAPC4 expression levels are significantly associated with survival. Taken together, these findings lead to the conclusion that TRMT13 inhibits PTC growth via ANAPC4, indicating a new role of TRMT13 and providing insights into the tRNA methyltransferase and coiled-coil domain-containing protein families.

FRAX486, a PAK inhibitor, overcomes ABCB1-mediated multidrug resistance in breast cancer cells

The overexpression of P-glycoprotein (P-gp/ABCB1) is a leading cause of multidrug resistance (MDR). Hence, it is crucial to discover effective pharmaceuticals that counteract ABCB1-mediated multidrug resistance. FRAX486 is a p21-activated kinase (PAK) inhibitor. The objective of this study was to investigate whether FRAX486 can reverse ABCB1-mediated multidrug resistance, while also exploring its mechanism of action. The CCK8 assay demonstrated that FRAX486 significantly reversed ABCB1-mediated multidrug resistance. Furthermore, western blotting and immunofluorescence experiments revealed that FRAX486 had no impact on expression level and intracellular localization of ABCB1. Notably, FRAX486 was found to enhance intracellular drug accumulation and reduce efflux, resulting in the reversal of multidrug resistance. Docking analysis also indicated a strong affinity between FRAX486 and ABCB1. This study highlights the ability of FRAX486 to reverse ABCB1-mediated multidrug resistance and provides valuable insights for its clinical application.

A systematic review of qualitative research on the self-management experience of breast cancer patients.

OBJECTIVE: To integrate the qualitative research on the self-management experience of breast cancer patients and conduct a systematic review of their self-management experience. METHODS: Using a computer to search a series of databases such as CNKI, Wanfang, VIP, and China Biomedical Database, systematically collect and integrate qualitative research on the self-management experience of breast cancer patients, and the search time is limited to January 2010 to December 2022. The qualitative research quality evaluation standard of the Joanna Briggs Institute Centre for Evidence-Based Health Care in Australia was used as the evaluation standard of this project to complete the accurate evaluation of the literature; Meta-analysis was used to complete the effective integration of the results. RESULTS: 17 pieces of literature were included in this project, and 37 research results with strong integrity were extracted accordingly. On this basis, 7 different categories were summarised, and three integrated results were obtained: the experience of maintaining self-management, symptom recognition, and self-management. CONCLUSION: In the different stages of self-management of breast cancer patients, medical staff should give targeted guidance to help patients obtain a good prognosis.

PIWIL1 Promotes Malignant Progression of Papillary Thyroid Carcinoma by Inducing EVA1A Expression.

INTRODUCTION: Papillary thyroid carcinoma (PTC) is the most common subtype of thyroid cancer. Previous studies have reported on the ectopic expression of P-element-induced wimpy testis ligand 1 (PIWIL1) in various human cancers, but its role in PTC progression has not been investigated. METHODS: In this study, we measured the expression levels of PIWIL1 and Eva-1 homolog A (EVA1A) in PTC using qPCR and WB. We performed a viability assay to evaluate PTC cell proliferation and used flow cytometry to investigate apoptosis. Moreover, we conducted a Transwell invasion assay to quantify cell invasion and assessed PTC growth in vivo using xenograft tumor models. RESULTS: Our findings showed PIWIL1 to be highly expressed in PTC and promote cell proliferation, cell cycle activity, and cell invasion, while suppressing apoptosis. Additionally, PIWIL1 accelerated tumor growth in PTC xenografts by modulating the EVA1A expression. CONCLUSION: Our study suggests that PIWIL1 contributes to the progression of PTC through EVA1A signaling, indicating its potential role as a therapeutic target for PTC. These results provide valuable insights into PIWIL1 function and may lead to more effective treatments for PTC.

Small extracellular vesicles derived from tendon stem cells promote the healing of injured Achilles tendons by regulating miR-145-3p.

The therapeutic role of tendon stem cells (TSCs) in tendon-related injuries has been well documented. Small extracellular vesicles (sEVs) are being increasingly used as new biotherapeutic agents for various diseases. Therefore, the potential function of TSC-sEVs in tendon injury repair warrants further investigation. In this study, we explored the effects of TSC-sEVs on TSC proliferation, migration, and differentiation in vitro in an autocrine manner. We further used a novel exosomal topical treatment with TSC-sEVs loaded with gelatin methacryloyl (GelMA) hydrogel in vivo; we mixed sufficient amounts of TSC-sEVs with GelMA hydrogel to cover the damaged molded Achilles tendon tissue and then exposed them to UV irradiation for coagulation. GelMA loading ensured that TSC-sEVs were slowly released at the injury site over a long period, thereby achieving their full local therapeutic effects. Treatment with TSC-sEVs loaded with GelMA significantly improved the histological score of the regenerated tendon by increasing the tendon expression while inhibiting the formation of excessive ossification and improving the mechanical properties of the tissue. Moreover, miRNA sequencing in TSC-sEVs, TSCs, and TSCs receiving sEVs revealed that TSC-sEVs altered the miRNA expression profile of TSCs, with increased expression of miR-145-3p. In conclusion, our study demonstrates that TSC-sEVs can play a key role in treating tendon injuries and that loading them with GelMA can enhance their effect in vivo. Moreover, miR-145-3p has a major functional role in the effect of TSC-sEVs. This study offers new therapeutic ideas for the local treatment of Achilles tendon injuries using sEVs. STATEMENT OF SIGNIFICANCE: In this study, we demonstrated that TSC-sEVs play a key role in treating tendon injuries and that loading them with GelMA hydrogel can act as a fixation and slow release in vivo. Moreover, it identifies the major functional role of miR-145-3p in the effect of TSCs that were identified and validated by miRNA sequencing. Our study provides a basis for further research on GelMA slow-release assays that have potential clinical applications. It offers new therapeutic ideas for the local treatment of Achilles tendon injuries using TSC-sEVs.

Role of Caveolae family-related proteins in the development of breast cancer.

Breast cancer has become the most significant malignant tumor threatening women's lives. Caveolae are concave pits formed by invagination of the plasma membrane that participate in many biological functions of the cell membrane, such as endocytosis, cell membrane assembly, and signal transduction. In recent years, Caveolae family-related proteins have been found to be closely related to the occurrence and development of breast cancer. The proteins associated with the Caveolae family-related include Caveolin (Cav) and Cavins. The Cav proteins include Cav-1, Cav-2 and Cav-3, among which Cav-1 has attracted the most attention as a tumor suppressor and promoting factor affecting the proliferation, apoptosis, migration, invasion and metastasis of breast cancer cells. Cav-2 also has dual functions of inhibiting and promoting cancer and can be expressed in combination with Cav-1 or play a regulatory role alone. Cav-3 has been less studied in breast cancer, and the loss of its expression can form an antitumor microenvironment. Cavins include Cavin-1, Cavin-2, Cavin-3 and Cavin-4. Cavin-1 inhibits Cav-1-induced cell membrane tubule formation, and its specific role in breast cancer remains controversial. Cavin-2 acts as a breast cancer suppressor, inhibiting breast cancer progression by blocking the transforming growth factor (TGF-ß) signaling pathway. Cavin-3 plays an anticancer role in breast cancer, but its specific mechanism of action is still unclear. The relationship between Cavin-4 and breast cancer is unclear. In this paper, the role of Caveolae family-related proteins in the occurrence and development of breast cancer and their related mechanisms are discussed in detail to provide evidence supporting the further study of Caveolae family-related proteins as potential targets for the diagnosis and treatment of breast cancer.

Mast cell activation may contribute to adverse health transitions in COVID-19 patients with frailty.

A prominent aspect of the post-coronavirus disease-2019 (post-COVID-19) era is long-COVID. Therefore, precise patient classification and exploration of the corresponding factors affecting long-COVID are crucial for tailored treatment strategies. Frailty is a common age-related clinical syndrome characterized by deteriorated physiological functions of multiple organ systems, which increases susceptibility to stressors. Herein, we performed an inclusion and exclusion analysis (definite COVID-19 infection diagnosis, clear underlying disease information, ≥60 years old, and repeated sampling of clinical cases) of 10,613 blood samples and identified frailty cases for further investigation. RNA-Seq data were used for differential gene expression and functional and pathway analyses. The results revealed that patients with frailty were more prone to poor health conversions and more sequelae, and the blood transcriptome had obvious disturbances in pathways associated with immune regulation, metabolism, and stress response. These adverse health transitions were significantly associated with mast cell activation. Additionally, NCAPG, MCM10, and CDC25C were identified as hub genes in the peripheral blood differential gene cluster, which could be used as diagnostic markers of poor health conversion. Our results indicate that healthcare measures should be prioritized to mitigate adverse health outcomes in this vulnerable patient group, COVID-19 patients with frailty, in post-COVID era.

PIWIL2 restrains the progression of thyroid cancer via interaction with miR-146a-3p.

OBJECTIVE: The classical role of PIWIL2 is to regulate reproduction by binding to piRNA, but its tumor-related function has received increasing attention in recent years. This study aims to explore its role in the progression of thyroid cancer (TC). METHODS: First, we measured and analyzed the levels of PIWIL2 and miR-146a-3p in TC tissue and adjacent tissues as well as several TC cell lines. We demonstrated the clinical significance of PIWIL2 and miR-146a-3p through the survival rate. Based on these results, we selected TPC-1 and KTC-3 cell lines for our cell experiments. We treated these cell lines with PIWIL2 lentivirus, PIWIL2 siRNA, miR-146a-3p mimic, or miR-146a-3p inhibitor and measured cell proliferation, cell cycle, apoptosis, migration, and invasion. We used PCR and Western blot to quantify the mRNA and protein levels of PIWIL2, while we used luciferase reporter assay and RNA binding protein immunoprecipitation to explore the relationship between miR-146a-3p and PIWIL2. Finally, we developed a xenograft tumor model to confirm the effects of the miR-146a-3p/PIWIL2 axis on TC progression in vivo. RESULTS: We identified that PIWIL2 and miR-146a-3p exhibit opposite expression alterations in TC tissues and that PIWIL2 serves as a 'sponge' by adsorbing miR-146a-3p. Up-regulating PIWIL2 decelerated the proliferation, metastasis, and cell cycle progression of TPC-1 and KTC-3 cells, but accelerated the apoptosis of TC cells, while miR-146a-3p exhibited opposite effects. Finally, overexpressing PIWIL2 restrained the progression of TC in nude mice, which can be reversed by increasing miR-146a-3p expression. Inhibiting PIWIL2, on the other hand, promoted the progression of TC in vivo, which can be reversed by inhibiting miR-146a-3p. CONCLUSION: PIWIL2 may inhibit the progression of TC by sponging miR-146a-3p, providing new insights into the early treatment, recrudescence treatment, and metastasis treatment of TC.

Bi0·5Na0·5TiO3/ZnO Z-scheme heterojunction for piezo-photocatalytic water remediation: Mechanical energy harvesting and energy band configuration.

The decaying photocatalytic rate caused by carrier recombination is a thorny problem that has not been properly solved. Improvement of photocatalysis can be achieved through structural innovation, diversification of catalytic modes, or a combination of both. Herein, effective separation of photo-generated carriers in Bi0·5Na0·5TiO3/ZnO composites was achieved by heterojunction construction for energy band regulation and synchronously mechanical energy harvesting from piezoelectric effect. The formation of heterojunctions between Bi0·5Na0·5TiO3 and ZnO was confirmed by electron microscopy and analysis of X-ray photoelectron spectroscopy spectra. The degradation performance of Rhodamine B, a representative industrial dye contaminant, was optimized through the formation of Bi0·5Na0·5TiO3/ZnO heterojunctions and ultrasonic vibration harvesting. Their band structures were described in detail and electrochemical tests were performed to substantiate a novel Z-scheme heterostructure that can explain the carrier separation and transfer processes in catalysis. The piezoelectric polarization field generated by the piezoelectric effect of both Bi0·5Na0·5TiO3 and ZnO coordinates perfectly with the photocatalysis, enabling the piezo-photocatalysis. Our research opens a promising avenue in alleviating charge carrier complexation through heterojunction construction and mechanical strain for future pollutants degradation via catalysis.

The relationship between the Hippo signaling pathway and bone metastasis of breast cancer.

Bone is the most common site of metastasis from breast cancer, which is the most prevalent cancer affecting women globally. Bone metastasis from breast cancer severely affects the quality of life of patients and increases mortality. The molecular mechanisms of metastasis, colonization, and proliferation of breast cancer cells in bone are complex and involve the interaction between breast cancer cells and the bone microenvironment. However, the precise mechanism is not clear at present. In recent years, the Hippo signaling pathway has attracted much attention due to its important role in regulating the expression of major effector molecules during tumor development. In particular, studies have found that the mutation and aberrant expression of the core components of the Hippo signaling pathway affect breast cancer cell migration and invasion, indicating that this pathway plays a role in bone metastasis, although the molecular mechanism of this pathway in breast cancer metastasis has not been fully elucidated. In this review, we discuss the function of the Hippo signaling pathway, introducing its role in breast cancer metastasis, especially bone metastasis of breast cancer, so as to lay a solid theoretical foundation for further research and for the development of effective targeted therapeutic agents.

Collective and Individual Assessment of the Risk of Death from COVID-19 for the Elderly, 2020-2022.

Introduction: Coronavirus disease 2019 (COVID-19) has had profound disruptions worldwide. For a population or individual, it is critical to assess the risk of death for making preventative decisions. Methods: In this study, clinical data from approximately 100 million cases were statistically analyzed. A software and an online assessment tool were developed in Python to evaluate the risk of mortality. Results: Our analysis revealed that 76.51% of COVID-19-related fatalities occurred among individuals aged over 65 years, with frailty-associated deaths accounting for more than 80% of these cases. Furthermore, over 80% of the reported deaths involved unvaccinated individuals. A notable overlap was observed between aging and frailty-associated deaths, both of which were connected to underlying health conditions. For those with at least two comorbidities, the proportion of frailty and the proportion of COVID-19-related death were both close to 75 percent. Subsequently, we established a formula to calculate the number of deaths, which was validated using data from twenty countries and regions. Using this formula, we developed and verified an intelligent software designed to predict the death risk for a given population. To facilitate rapid risk screening on an individual level, we also introduced a six-question online assessment tool. Conclusions: This study examined the impact of underlying diseases, frailty, age, and vaccination history on COVID-19-related mortality, resulting in a sophisticated software and a user-friendly online scale to assess mortality risk. These tools offer valuable assistance in informed decision-making.

Signally enhanced piezo-photocatalysis of Bi0.5Na0.5TiO3/MWCNTs composite for degradation of rhodamine B.

Recently, the lead-free piezoelectric material Bi0.5Na0.5TiO3 (BNT) has been adopted for piezo-catalysis and synergistic catalysis, such as piezo-photocatalysis. Nonetheless, the catalytic effect of single BNT is too weak to degrade multifarious contaminants. Here, BNT and multi-walled carbon nanotubes (MWCNTs) composite were prepared and the catalytic performance of BNT was prominently boosted by introducing MWCNTs as the electron capturer. Particularly, the degradation rate of Rhodamine B (RhB, a typical contaminant) could reach 90% within 30 min, with a high rate constant of 0.0805 min-1. The specific degradation pathway of RhB was analyzed. The formation of oxygen vacancies was confirmed by XPS analysis, and the vital role of oxygen vacancies in the separation of photo-generated carriers was elucidated. Meanwhile, the BNT/MWCNTs composites manifested stronger transient current response compared to single BNT under the action of light irradiation and ultrasonic vibration, respectively. According to impedance analysis, the composites exhibited lower carrier transport resistance. Eventually, the mechanism of enhanced piezo-photocatalysis was explained in detail. This study provides an effective route to break the shackle of carrier recombination and speed up the carrier transport in piezo-photocatalytic materials.

Enhanced piezo-photocatalysis in Bi0.5Na0.5TiO3@Ag composite to efficiently degrade multiple organic pollutants.

The synergistic piezo-photocatalysis with enhanced efficiency for degrading obstinate pollutants in wastewater is considered as an advanced way to ameliorate the global water contamination. In this work, we report a facile route to construct the Bi0.5Na0.5TiO3@Ag composite by photoreduction of AgNO3 to obtain Ag on Bi0.5Na0.5TiO3 nanoparticles. And the composite was used to degrade three representative pollutants, i.e. ciprofloxacin, methyl orange and mitoxantrone hydrochloride. Remarkably, for methyl orange solution with the initial concentration of 10 mg/L, the degradation rate constant of the composite reached 0.051 min-1. H+ and •O2- play a major role in this degradation process, verified by the radical quenching experiments. The absorption platform of Bi0.5Na0.5TiO3 was located in the UV region, after introducing Ag in the composite, the absorption region broadened to both UV and visible light, greatly promoting the response to light. Simultaneously, the induced piezo-potential by mechanical energy in Bi0.5Na0.5TiO3 hindered the carrier recombination, resulting in high-efficiency synergistic piezo-photocatalytic process. This work provides a paradigm to innovate both material and catalytic way for degrading multiple organic pollutants.

Correlation of placental thickness and placenta percreta in patients with placenta previa: findings from MRI.

INTRODUCTION: This study aimed to identify if placental thickness measured from MRI images correlated with placenta percreta in patients with placenta previa. METHODS: Placental thickness was retrospectively measured in 161 patients from July 2018 to August 2020. The measurements were performed at the thickest part of the placenta in the lower uterine segment on the mid-sagittal plane MR images by two independent radiologists. Intraoperative and pathologic findings were the standard of reference. Univariate and multivariate analyses were performed to identify the relationship between clinical features, placental thickness, and placenta percreta. The predictive ability of placental thickness was demonstrated using receiver operating characteristic curve analysis. RESULTS: Placental thickness in patients with placenta percreta was significantly higher than in patients with placenta increta, placenta accreta, and normal placentas (p < 0.05). Multivariate analysis revealed that placental thickness was the only independent risk factor for placenta percreta. The cutoff value of placental thickness was 4.35 cm for differentiating placenta percreta in patients with placenta previa. DISCUSSION: Patients with placenta percreta had the highest placental thickness. Placental thickness was correlated with placenta percreta.