Changes of gut microbiota and short chain fatty acids in patients with Peutz-Jeghers syndrome.

Peutz-Jeghers Syndromeis a rare autosomal dominant genetic disease characterized by gastrointestinal hamartomatous polyps and skin and mucous membrane pigmentation. The pathogenesis of PJS remains unclear; however, it may be associated with mutations in the STK11 gene, and there is currently no effective treatment available. The gut microbiota plays an important role in maintaining intestinal homeostasis in the human body, and an increasing number of studies have reported a relationship between gut microbiota and human health and disease. However, relatively few studies have been conducted on the gut microbiota characteristics of patients with PJS. In this study, we analyzed the characteristics of the gut microbiota of 79 patients with PJS using 16 S sequencing and measured the levels of short-chain fatty acids in the intestines. The results showed dysbiosis in the gut microbiota of patients with PJS, and decreased synthesis of short-chain fatty acids. Bacteroides was positively correlated with maximum polyp length, while Agathobacter was negatively correlated with age of onset. In addition, acetic acid, propionic acid, and butyric acid were positively correlated with the age of onset but negatively correlated with the number of polyps. Furthermore, the butyric acid level was negatively correlated with the frequency of endoscopic surgeries. In contrast, we compared the gut microbiota of STK11-positive and STK11-negative patients with PJS for the first time, but 16 S sequencing analysis revealed no significant differences. Finally, we established a random forest prediction model based on the gut microbiota characteristics of patients to provide a basis for the targeted diagnosis and treatment of PJS in the future.

Non-enzymatic heparanase enhances gastric tumor proliferation via TFEB-dependent autophagy.

Heparanase (HPA) is the predominant enzyme that cleaves heparan sulfate and plays a critical role in a variety of pathophysiological processes. HPA activity has been traditionally correlated with tumor metastasis due to participation in the cleavage and remodeling of the extracellular matrix (ECM). Apart from its well-characterized catalytic properties, HPA was noticed to exert biological functions not rely on its enzymatic activity. This feature is supported by studies showing induction of signaling events, such as Src and AKT, by nonenzymatic HPA mutant. We provide evidence here that active HPA and inactive HPA mutant proteins enhance gastric cancer cell growth, possibly attributed to TFEB-mediated autophagy. Similarly, HPA gene silencing resulted in decreased gastric cancer cell proliferation and autophagy. Besides, TFEB inhibition reduced cell growth and autophagy induced by nonenzymatic HPA. Notably, HPA and TFEB were significantly elevated in gastric carcinomas compared with the adjacent gastric tissue. Moreover, the elevation of HPA gene expression and upregulation of TFEB levels have been associated with advanced clinical stage and poor prognosis of gastric cancer, providing strong clinical support for a connection between TFEB and HPA. Thus, neutralizing the nonenzymatic function of HPA and the related TFEB-driven autophagy may profoundly impact gastric cancer progression.

Role of lncSLCO1C1 in gastric cancer progression and resistance to oxaliplatin therapy.

BACKGROUND: Gastric carcinoma (GC) is one of the most deadly diseases due to tumour metastasis and resistance to therapy. Understanding the molecular mechanism of tumour progression and drug resistance will improve therapeutic efficacy and develop novel intervention strategies. METHODS: Differentially expressed long non-coding RNAs (lncRNAs) in clinical specimens were identified by LncRNA microarrays and validated in different clinical cohorts by quantitative real-time polymerase chain reaction (qRT-PCR), in situ hybridisation and bioinformatics analysis. Biological functions of lncRNA were investigated by using cell proliferation assays, migration assays, xenograft tumour models and bioinformatics analysis. Effects of lncSLCO1C1 on GC cell survival were assessed by comet assays and immunofluorescence assays. Underlying molecular mechanisms were further explored by using a number of technologies including RNA pull-down, mass spectrometry analysis, RNA immunoprecipitation, co-immunoprecipitation, miRNA sequencing, luciferase reporter assays and molecular modelling. RESULTS: LncSLCO1C1 was highly upregulated in GC tissue samples and associated with GC patients' poor overall survival. Overexpression of lncSLCO1C1 promoted proliferation and migration, whereas decreased lncSLCO1C1 expression produced the opposite effects. lncSLCO1C1 also mediated tumour resistance to chemotherapy with oxaliplatin by reducing DNA damage and increasing cell proliferation. Despite sequence overlapping between lncSLCO1C1 and PDE3A, alternations of PDE3A expression had no effect on the GC cell progression, indicating that lncSLCO1C1, not PDE3A, related with the progression of GC cells. Mechanistically, lncSLCO1C1 serves as a scaffold for the structure-specific recognition protein 1 (SSRP1)/H2A/H2B complex and regulates the function of SSRP1 in reducing DNA damage. Meanwhile, lncSLCO1C1 functions as a sponge to adsorb miR-204-5p and miR-211-5p that target SSRP1 mRNA, and thus increases SSRP1 expression. Patients with high expressions of both lncSLCO1C1 and SSRP1 have poor overall survival, highlighting the role of lncSLCO1C1 in GC progression. CONCLUSIONS: LncSLCO1C1 promotes GC progression by enhancing cell growth and preventing DNA damage via interacting and scaffolding the SSRP1/H2A/H2b complex and absorbing both miR-211-5p and miR-204-5p to increase SSRP1 expression.

Demethylase ALKBH5 suppresses invasion of gastric cancer via PKMYT1 m6A modification.

BACKGROUND: Gastric cancer (GC) is one of the most pernicious tumors that seriously harm human healthcare. GC metastasis is one of the prime cause of failed cancer treatment, but correlation between N6-methyladenosine (m6A) and GC metastasis was less reported. METHODS: Methylated RNA immunoprecipitation sequencing (MeRIP-seq) of GC tissues was conducted. Quantitative real-time PCR (qRT-PCR), western blotting and immunohistochemistry (IHC) were taken to determine the expression of ALKBH5 in GC tissues and cell lines. RNA-seq together with MeRIP-qRT-PCR was used to screen the target gene of ALKBH5. RNA pulldown, mass spectrometry and RNA immunoprecipitation (RIP) were used to search the "reader" protein of target gene. The mechanism was also validated via a tail vein injection method for lung metastasis model. RESULTS: Decreased expression of ALKBH5 was detected in GC samples, and it was correlated with clinical tumor distal metastasis and lymph node metastasis. ALKBH5 interference promoted metastasis of GC cells and this effect was closely related to the demethylase activity of ALKBH5. PKMYT1, as a downstream target of ALKBH5, promoted invasion and migration in GC. Caused by ALKBH5 knockdown or its demethylase activity mutation, upregulated expression of PKMYT1 indicated that ALKBH5 modulates expression of PKMYT1 in an m6A-dependent manner. IGF2BP3 helped stabilize the mRNA stability of PKMYT1 via its m6A modification site. CONCLUSIONS: This study established an ALKBH5-PKMYT1-IGF2BP3 regulation system in metastasis, representing a new therapeutic target for GC metastasis.

Human telomerase reverse transcriptase (hTERT) synergistic with Sp1 upregulate Gli1 expression and increase gastric cancer invasion and metastasis.

Abnormal expression of human telomerase reverse transcriptase (hTERT) has been widely identified in tumors, but the relevant mechanism is not well known. This study aims to investigate the role and mechanism of hTERT in gastric cancer metastasis. Gastric cancer and adjacent non-tumor tissues were collected and the expression levels of hTERT and Gli1 were detected by immunohistochemistry. The results demonstrated that hTERT and Gli1 expression levels in gastric cancer tissue were significantly higher than adjacent non-tumor tissues. Western blot and quantitative real-time PCR were used to an identified expression of the related protein in BGC-823 and SGC-7901 cells. The interactions between hTERT and Sp1 were tested by co-immunoprecipitation experiments. Chromatin immunoprecipitation was performed to confirm that Sp1 and hTERT could bind to the Gli1 promoter. Chromatin reimmunoprecipitation assay further demonstrated that both hTERT and Sp1 bind to the Sp1 site of the Gli1 promoter. Moreover, the hTERT, Sp1, and Gli1 were upregulate was verified in human gastric cancer tissues. These results showed that the expression levels of hTERT in GC tissues were strongly closed to the depth of invasion, lymph node metastasis, TNM (tumor, node, metastasis) stage, and distant metastasis. By combining Sp1 and Gli1 promoter, hTERT upregulated Gli1 expression and promoted invasion and metastasis of GC cells. Overall, these data provide a new molecular mechanism of hTERT to promotes gastric cancer progression. Targeting the hTERT/Sp1/Gli1 axis may represent a new therapeutic strategy.

Role of heparanase 2 (Hpa2) in gastric cancer.

Heparanase is highly implicated in tumor metastasis due to its capacity to cleave heparan sulfate and, consequently, remodel the extracellular matrix underlying epithelial and endothelial cells. In striking contrast, only little attention was given to its close homolog, heparanase 2 (Hpa2), possibly because it lacks heparan sulfate-degrading activity typical of heparanase. We subjected sections of gastric carcinoma to immunostaining and correlated Hpa2 immunoreactivity with clinical records, including tumor grade, stage and patients' status. We over-expressed Hpa2 in gastric carcinoma cell lines and examined their tumorigenic properties in vitro and in vivo. We also evaluated the expression of Hpa2 by gastric carcinoma cells following inhibition of the proteasome, leading to proteotoxic stress, and the resulting signaling responsible for Hpa2 gene regulation. Here, we report that gastric cancer patients exhibiting high levels of Hpa2 survive longer. Similarly, mice administrated with gastric carcinoma cells engineered to over-express Hpa2 produced smaller tumors and survived longer than mice administrated with control cells. This was associated with increased phosphorylation of AMP-activated protein kinase (AMPK), a kinase that is situated at the center of a tumor suppressor network. We also found that MG132, an inhibitor of the proteasome that results in proteotoxic stress, prominently enhances Hpa2 expression. Notably, Hpa2 induction by MG132 appeared to be mediated by AMPK, and AMPK was found to induce the expression of Hpa2, thus establishing a loop that feeds itself where Hpa2 enhances AMPK phosphorylation that, in turn, induces Hpa2 expression, leading to attenuation of gastric tumorigenesis. These results indicate that high levels of Hpa2 in some tumors are due to stress conditions that tumors often experience due to their high rates of cell proliferation and high metabolic demands. This increase in Hpa2 levels by the stressed tumors appears critically important for patient outcomes.

Helicobacter pylori-Induced Heparanase Promotes H. pylori Colonization and Gastritis.

Chronic gastritis caused by Helicobacter pylori (H. pylori) infection has been widely recognized as the most important risk factor for gastric cancer. Analysis of the interaction between the key participants in gastric mucosal immunity and H. pylori infection is expected to provide important insights for the treatment of chronic gastritis and the prevention of gastric cancer. Heparanase is an endoglycosidase that degrades heparan sulfate, resulting in remodeling of the extracellular matrix thereby facilitating the extravasation and migration of immune cells towards sites of inflammation. Heparanase also releases heparan sulfate-bound cytokines and chemokines that further promote directed motility and recruitment of immune cells. Heparanase is highly expressed in a variety of inflammatory conditions and diseases, but its role in chronic gastritis has not been sufficiently explored. In this study, we report that H. pylori infection promotes up-regulation of heparanase in gastritis, which in turn facilitates the colonization of H. pylori in the gastric mucosa, thereby aggravating gastritis. By sustaining continuous activation, polarization and recruitment of macrophages that supply pro-inflammatory and pro-tumorigenic cytokines (i.e., IL-1, IL-6, IL-1ß, TNF-α, MIP-2, iNOS), heparanase participates in the generation of a vicious circle, driven by enhanced NFκB and p38-MAPK signaling, that supports the development and progression of gastric cancer. These results suggest that inhibition of heparanase may block this self-sustaining cycle, and thereby reduce the risk of gastritis and gastric cancer.

Using psychological interventions in the nursing care of rectal cancer patients.

PURPOSE: To explore the significance of psychological interventions in the nursing care of rectal cancer patients undergoing ostomy surgery. METHODS: We recruited 120 rectal cancer patients undergoing ostomy surgery in our hospital from March 2017 to March 2018 as the study cohort, and they were equally and randomly divided into a control group and an observation group. The control group was administered routine nursing, and the observation group was administered routine nursing combined with psychological nursing. The patients' conditions were evaluated using the self-rating anxiety scale (SAS), the self-rating depression scale (SDS), the MOS item short form health survey (SF-36), and their defecation. The two groups' satisfaction levels with the nursing were also compared. RESULTS: The SAS, SDS, HAMA, and HAMD scores in the two groups after the treatment were lower than they were before the treatment, and the observation group was much lower. The SF-36 scores, the patients' defecation, the nursing satisfaction levels, and the sleep durations in the observation group were higher than they were in the control group, and there were fewer incidences of postoperative complications in the observation group than there were in the control group (P < 0.05). CONCLUSION: The effects of psychological interventions in the nursing of rectal cancer patients undergoing ostomy surgery are significant. The interventions can relieve the patients' bad moods, stabilize the patients' conditions, and improve the patients' defecation, so it is superior to routine nursing.

hTERT Promotes CRC Proliferation and Migration by Recruiting YBX1 to Increase NRF2 Expression.

High human telomerase reverse transcriptase (hTERT) expression is related to severe Colorectal Cancer (CRC) progression and negatively related to CRC patient survival. Previous studies have revealed that hTERT can reduce cancer cellular reactive oxygen species (ROS) levels and accelerate cancer progression; however, the mechanism remains poorly understood. NFE2-related factor 2 (NRF2) is a molecule that plays a significant role in regulating cellular ROS homeostasis, but whether there is a correlation between hTERT and NRF2 remains unclear. Here, we showed that hTERT increases CRC proliferation and migration by inducing NRF2 upregulation. We further found that hTERT increases NRF2 expression at both the mRNA and protein levels. Our data also revealed that hTERT primarily upregulates NRF2 by increasing NRF2 promoter activity rather than by regulating NRF2 mRNA or protein stability. Using DNA pull-down/MS analysis, we found that hTERT can recruit YBX1 to upregulate NRF2 promoter activity. We also found that hTERT/YBX1 may localize to the P2 region of the NRF2 promoter. Taken together, our results demonstrate that hTERT facilitates CRC proliferation and migration by upregulating NRF2 expression through the recruitment of the transcription factor YBX1 to activate the NRF2 promoter. These results provide a new theoretical basis for CRC treatment.

Function of Non-coding RNA in Helicobacter pylori-Infected Gastric Cancer.

Gastric cancer is a common malignant tumor of the digestive system. Its occurrence and development are the result of a combination of genetic, environmental, and microbial factors. Helicobacter pylori infection is a chronic infection that is closely related to the occurrence of gastric tumorigenesis. Non-coding RNA has been demonstrated to play a very important role in the organism, exerting a prominent role in the carcinogenesis, proliferation, apoptosis, invasion, metastasis, and chemoresistance of tumor progression. H. pylori infection affects the expression of non-coding RNA at multiple levels such as genetic polymorphisms and signaling pathways, thereby promoting or inhibiting tumor progression or chemoresistance. This paper mainly introduces the relationship between H. pylori-infected gastric cancer and non-coding RNA, providing a new perspective for gastric cancer treatment.

The role of m6A modification in physiology and disease.

Similar to DNA epigenetic modifications, multiple reversible chemical modifications on RNAs have been uncovered in a new layer of epigenetic modification. N6-methyladenosine (m6A), a modification that occurs in ~30% transcripts, is dynamically regulated by writer complex (methylase) and eraser (RNA demethylase) proteins, and is recognized by reader (m6A-binding) proteins. The effects of m6A modification are reflected in the functional modulation of mRNA splicing, export, localization, translation, and stability by regulating RNA structure and interactions between RNA and RNA-binding proteins. This modulation is involved in a variety of physiological behaviors, including neurodevelopment, immunoregulation, and cellular differentiation. The disruption of m6A modulations impairs gene expression and cellular function and ultimately leads to diseases such as cancer, psychiatric disorders, and metabolic disease. This review focuses on the mechanisms and functions of m6A modification in a variety of physiological behaviors and diseases.

Microplastic abundance, distribution and composition in the mid-west Pacific Ocean.

Microplastic pollution is widespread across most ocean basins around the world. Microplastics (MPs) are small plastic particles that have a significant impact on the marine environment. Various research on plastic pollution have been conducted in several regions. However, currently, there is limited data on the distribution and concentration of MPs in the mid-west Pacific Ocean. Therefore, this study we investigated the abundance, distribution, characteristics, and compositions of MPs in this region. Sea surface water samples collected from 18 stations showed a microplastic concentration range of 6028-95,335 pieces/km2 and a mean concentration of 34,039 ± 25,101 pieces/km2. Highest microplastic concentrations were observed in the seamount region of western Pacific. We observed a significant positive correlation between microplastic abundance and latitude across the study region. It was observed that microplastic concentrations decreased with increasing offshore distance at sites located on a 154° W transect. Fibres/filaments were the dominant microparticles observed in this study (57.4%), followed by fragments (18.3%). The dominant particle size range was 1-2.5 mm (35.1%), followed by 0.5-1 mm (28.5%), and the dominant particle colour was white (33.8%), followed by transparent (31.0%) and green (24.6%). The most common polymer identified by µ-Raman was polypropylene (39.1%), followed by polymethyl methacrylate (16.2%), polyethylene (14.1%) and polyethylene terephthalate (14.2%). The possible sources and pathways of microplastics in the study area were proposed based on the morphological and compositional characteristics of particles, their spatial distribution patterns, and shipboard current profiling (ADCP). Our study contributes to the further understanding of MPs in remote ocean areas.

Inhibition of MGMT-mediated autophagy suppression decreases cisplatin chemosensitivity in gastric cancer.

Cisplatin (DDP) is the first-line drug for the treatment of gastric cancer (GC). However, DDP resistance is common. Autophagy, which is closely related to chemoresistance, is a process of resolving and recycling proteins and damaged cellular organs. Additionally, O-6-methylguanine-DNA methyltransferase (MGMT) is responsible for alkylating drug resistance. However, the relationship between autophagy and MGMT in response to DDP in GC is still unknown. In the present study, we determined that autophagy induced by DDP decreases chemosensitivity in GC cell lines. DDP may have induced autophagy in GC by inhibiting MGMT to increase autophagy-related gene (ATG) 4B. Inhibition of MGMT-mediated ATG4B suppression resulted in autophagy induction and DDP resistance. In vivo, combined DDP and autophagy inhibitor chloroquine (CQ) enhanced the anti-tumor effect of DDP; additionally, the negative correlation of MGMT and ATG4B was confirmed. High expression of MGMT and low expression of ATG4B were significantly correlated with favorable five-year survival rate (P < 0.05) in 66 clinicopathologically characterized GC cases. Our study demonstrate that DDP inhibits MGMT-mediated autophagy suppression to decrease chemosensitivity in GC, which provides a novel therapeutic strategy to promote DDP chemosensitivity in GC.

New sights in cancer: Component and function of N6-methyladenosine modification.

M6A is the most prevalent modification among epigenetics. M6A occurs on different sites of RNA and exerts important functions in specific circumstances, such as mRNA splicing, stability, nuclear export, translation or damage response. Different aspects of the concrete machinery of m6A modification have been studied, including its writing, erasing and reading capabilities. The molecular and biological functions of the m6A modification and enzymes, as well as their functions in different cancers have been substantially published. The present review summarizes these findings and provides clear description of the problems involved. The probable roles of m6A modification may acts on other cancers, suggesting that it may be a treatment target for these cancers.

Emodin-induced autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes.

BACKGROUND: Emodin, a major component of Polygonum multiflorum (PM), has been reported to exert both protective and toxic effects in several cell types. However, the effects and underlying mechanisms of action of emodin in hepatic cells are still obscure. METHODS: The present study used the normal human liver cell line L02 to investigate the effects and mechanisms of emodin in hepatic cells. After treatment with emodin, L02 cells were examined for viability, apoptosis and autophagy with the Cell Counting Kit-8 (CCK-8), annexin V/PerCP staining and GFP-LC3 plasmid transfection. The expression of proteins including cleaved caspase-3, LC3B-I/II, p-PI3K, PI3K, p-AKT, AKT, p-mTOR, mTOR and actin was examined by using Western blot. RESULTS: Emodin significantly inhibited the viability of and induced apoptosis in L02 cells in a dose- and time-dependent manner. In addition, emodin increased the number of GFP-LC3 puncta in L02 cells and upregulated the expression of LC3B-II compared to those in control cells. Furthermore, emodin significantly decreased the expression of p-PI3K, p-AKT and p-mTOR in a dose-dependent manner compared to that in control cells without altering the expression of PI3K, AKT and mTOR. Notably, cotreatment with emodin and 3-methyladenine (3-MA) or rapamycin significantly increased and decreased the apoptosis rate of L02 cells, respectively, compared to that of cells treated with emodin alone. CONCLUSION:  In conclusion, emodin exhibited cytotoxicity in the L02 human hepatic cell line by promoting apoptosis, and it also induced autophagy through the suppression of the PI3K/AKT/mTOR signalling pathway. The autophagy could play a protective role following emodin treatment.

Prevalence of microplastic pollution in the Northwestern Pacific Ocean.

People are increasingly aware of ubiquitous microplastic (MP) pollution in the world's ocean due to its far-reaching harmful impacts on marine ecosystem and potential hazards to human health, yet surprisingly comparatively limited studies about the abundance, source, transport, and fate of MPs in the Northwestern Pacific Ocean are available. We conducted the field survey of MPs pollution at the surface of the Northwestern Pacific Ocean between August 25 and September 26, 2017. MPs were collected from 18 sampling stations in the Northwestern Pacific Ocean using a manta trawl net with a mesh size of ∼330 µm and a rectangular net opening of 0.45 × 1 m. The abundance, shape, color, size, chemical composition, and surface morphology were characterized using light microscopy, µ-Raman spectroscopy, and scanning electron microscopy (SEM). The results show surface MPs at concentrations ranging over two orders of magnitude (6.4 × 102 to 4.2 × 104 particles km-2) and a mean abundance of 1.0 × 104 particles km-2. The most concentrated MPs were found at XTJ3-9, which may be associated with the convergence of surface currents collectively affected by the Kuroshio and its extension, adjacent eddies, and flow regimes. Polyethylene accounts for 57.8% of enumerated MPs, followed by polypropylene (36.0%) and nylon (3.4%). Pellets, sheets, lines, and films are major forms which may be linked to the breakdown of larger particles, aging processes, and movement over long distances by prevailing currents. Four possible MPs migration pathways were proposed based on the source-specific distribution, chemical fingerprints, size distribution patterns, and the observed physical oceanographic parameters.

Microplastics in the Northwestern Pacific: Abundance, distribution, and characteristics.

Prevalence of microplastics (MPs) throughout the world's oceans has raised growing concerns due to its detrimental effects on the environment and living organisms. Most recent studies of MPs, however, have focused on the estuaries and coastal regions. There is a lack of study of MPs pollution in the open ocean. In the present study, we conducted field observations to investigate the abundance, spatial distribution, and characteristics (composite, size, color, shape and surface morphology) of MPs at the surface of the Northwestern Pacific Ocean. Samples of MPs were collected at 18 field stations in the Northwestern Pacific Ocean using a surface manta trawl with a mesh size of ~330 µm and width of 1 m from August 25 to September 26, 2017. The MPs were characterized using light microscopy, Micro-Raman spectroscopy, and scanning electron microscopy (SEM). Our field survey results indicate the ubiquity of MPs at all stations with an abundance from 6.4 × 102 items km-2 to 4.2 × 104 items km-2 and an average abundance of 1.0 × 104 items km-2. The Micro-Raman spectroscopic analysis of the MPs samples collected during our field survey indicates that the dominant MPs is polyethylene (57.8%), followed by polypropylene (36.0%) and nylon (3.4%). The individual chemical compositions of MPs from the stations within the latitude range 123-146°E are comparable with each other, with PE being the dominating composition. Similar chemical fingerprints were observed at these field stations, suggesting that the MPs originated from similar sources. In contrast, the major MPs at the field stations adjacent to Japan is polypropylene, which may originate from the nearby land along the coast of Japan. Physical oceanography parameters were also collected at these stations. The spatial distribution of MPs is largely attributed to the combined effects of flow pattern, adjacent ocean circulation eddies, the Kuroshio and Kuroshio Extension system.

Proportion of Uterine Malignant Tumors in Patients with Laparoscopic Myomectomy: A National Multicenter Study in China.

BACKGROUND: The Food and Drug Administration recently announced that the use of morcellation may cause fibroids or pelvic dissemination and metastasis of uterine sarcoma; therefore, the use of morcellation is limited in the USA. A large sample study is necessary to assess the proportion of uterine malignant tumors found in patients with laparoscopic myomectomy. METHODS: A national multicenter study was performed in China. From 2002 to 2014, 33,723 cases were retrospectively selected. We calculated the prevalence and recorded the clinical characteristics of the patients with malignancy after morcellation application. A total of 62 cases were finally pathologically confirmed as malignant postoperatively. Additionally, the medical records of the 62 patients were analyzed in details. RESULTS: The proportion of postoperative malignancy after morcellation application was 0.18% (62/33,723) for patients who underwent laparoscopic myomectomy. Nearly 62.9% (39/62) of patients had demonstrated blood flow signals in the uterine fibroids before surgery. And, 23 (37.1%) patients showed rapid growth at the final preoperative ultrasound. With respect to the pathological types, 38 (61.3%) patients had detectable endometrial stromal sarcoma, 13 (21.0%) had detectable uterine leiomyosarcoma, only 3 (3.2%) had detectable carcinosarcoma, and 5 (8.1%) patients with leiomyoma had an undetermined malignant potential. CONCLUSIONS: The proportion of malignancy is low after using morcellation in patients who undergo laparoscopic myomectomy. Patients with fast-growing uterine fibroids and abnormal ultrasonic tumor blood flow should be considered for malignant potential, and morcellation should be avoided.