[Prevention and treatment of endometrial cancer].

Endometrial cancer is rising in incidence, especially in young women. This rise in incidence has implications for both primary prevention and screening in high-risk population. In the past several years, our understanding of the integration of clinically related genomic and pathologic data optimized the management of endometrial cancer. The updated 2023 FIGO staging includes the histological and molecular classification to better reflect the improved understanding of the heterogenous nature of endometrial carcinoma. Standard primary treatment is quite essential, however, selection of patients for adjuvant radiation or chemotherapy remains in controversy. Molecular characterization of endometrial cancer is becoming critical in directing treatment for advanced and recurrent disease, and the addition of immunotherapy to frontline chemotherapy is becoming the standard of care. More attention should be given to increase awareness of survivorship issues and improve patient quality-of-life.

Niraparib maintenance therapy in patients with platinum-sensitive recurrent ovarian cancer using an individualized starting dose (NORA): a randomized, double-blind, placebo-controlled phase III trial☆.

BACKGROUND: This study evaluated maintenance treatment with niraparib, a potent inhibitor of poly(ADP-ribose) polymerase 1/2, in patients with platinum-sensitive recurrent ovarian cancer. PATIENTS AND METHODS: In this phase III, double-blind, placebo-controlled study conducted at 30 centers in China, adults with platinum-sensitive recurrent ovarian cancer who had responded to their most recent platinum-containing chemotherapy were randomized 2 : 1 to receive oral niraparib (300 mg/day) or matched placebo until disease progression or unacceptable toxicity (NCT03705156). Following a protocol amendment, patients with a bodyweight <77 kg or a platelet count <150 × 103/µl received 200 mg/day, and all other patients 300 mg/day, as an individualized starting dose (ISD). Randomization was carried out by an interactive web response system and stratified by BRCA mutation, time to recurrence following penultimate chemotherapy, and response to most recent chemotherapy. The primary endpoint was progression-free survival (PFS) assessed by blinded independent central review. RESULTS: Between 26 September 2017 and 2 February 2019, 265 patients were randomized to receive niraparib (n = 177) or placebo (n = 88); 249 patients received an ISD (300 mg, n = 14; 200 mg, n = 235) as per protocol. In the intention-to-treat population, median PFS was significantly longer for patients receiving niraparib versus placebo: 18.3 [95% confidence interval (CI), 10.9-not evaluable] versus 5.4 (95% CI, 3.7-5.7) months [hazard ratio (HR) = 0.32; 95% CI, 0.23-0.45; P < 0.0001], and a similar PFS benefit was observed in patients receiving an ISD, regardless of BRCA mutation status. Grade ≥3 treatment-emergent adverse events occurred in 50.8% and 19.3% of patients who received niraparib and placebo, respectively; the most common events were neutrophil count decreased (20.3% versus 8.0%) and anemia (14.7% versus 2.3%). CONCLUSIONS: Niraparib maintenance treatment reduced the risk of disease progression or death by 68% and prolonged PFS compared to placebo in patients with platinum-sensitive recurrent ovarian cancer. Individualized niraparib dosing is effective and safe and should be considered standard practice in this setting.

Maternal Hypertension, Advanced Doppler Haemodynamics and Therapeutic Precision: Principles and Illustrative Cases.

PURPOSE OF REVIEW: Maternal hypertension is a common and serious condition associated with increased maternal and foetal morbidity and mortality, with early detection and management improving outcomes. RECENT FINDINGS: Blood pressure (BP) changes of pre-eclampsia are defined after 20 gestational weeks, while haemodynamic changes can be detected at 5-11 weeks using a specialised non-invasive Doppler stroke volume (SV) monitor. Thus, advanced haemodynamic monitoring allows for physiologically precise identification of circulatory abnormalities, and implementation of appropriate therapy within the first trimester. We measured the oscillometric BP and advanced haemodynamics (USCOM 1A) of 3 unselected women with singleton pregnancies, consecutively listed for therapeutic induction for maternal hypertension at 32-41 weeks gestational age. While the BP's of the patients varied, it was the haemodynamics, particularly SV, cardiac output, systemic vascular resistance, Smith Madigan Inotropy Index, and oxygen deliver, that identified differing patterns of circulatory dysfunction, therapeutic objectives, and predicted post-partum complications of the mother and child. First trimester screening of maternal haemodynamics may allow for earlier detection of circulatory derangements, selection of patient precise interventions, and improved maternal-foetal outcomes.

Correction to: Maternal Hypertension, Advanced Doppler Haemodynamics and Therapeutic Precision: Principles and Illustrative Cases.

The original publication of this article, unfortunately, contains the following errors.

[Effects of Prrx2 gene silencing on the proliferation of breast cancer and its molecular mechanisms].

Objective: The aim of this study was to investigate the effects of silencing Paired related homoeobox 2 (Prrx2) expression on the proliferation of breast cancer and its molecular mechanisms. Methods: Short hairpin RNA knockdown of Prrx2 was used to examine cellular effects of Prrx2. The level of Prrx2 was verified by Western blot. MTT assay was used to analyze the proliferation of breast cancer cells in vitro. To investigate the effect of Prrx2 depletion on tumor growth in vivo, a nude mouse xenograft model was performed. Results: The expression of Prrx2 decreased 91.2% in MDA-MB-231 cells and 88.7% in MCF-7 cells after transfection with interfering vectors (P<0.05). MTT assay showed that the proliferation of cells in silenced Prrx2 expression group was significantly inhibited compared with the control group (P<0.05). Nude mice transplanted tumors showed that the growth of transplanted tumors was slow after silencing Prrx2 expression, and the weight of the tumors of silenced Prrx2 expression group were smaller than those of the control group ((160.2±26.3)mg vs (365.4±19.7)mg, P<0.05). Western blot showed that silencing Prrx2 expression inhibited the expression of ß-catenin in breast cancer cell nucleus and down-regulated the activity of Wnt/ß-catenin signaling pathway. Conclusions: Silencing Prrx2 expression can effectively inhibit the proliferation and growth of breast cancer, suggesting that Prrx2 may become a new target for the treatment of breast cancer.

Cloning, overexpression, purification, and modeling of a lectin (Rhinocelectin) with antiproliferative activity from Tiger Milk Mushroom, Lignosus rhinocerus.

A lectin gene from the Tiger Milk Mushroom Lignosus rhinocerus TM02® was successfully cloned and expressed via vector pET28a in Escherichia coli BL21(DE3). The recombinant lectin, Rhinocelectin, with a predicted molecular mass of 22.8 kDa, was overexpressed in water-soluble form without signal peptide and purified via native affinity chromatography Ni-NTA agarose. Blast protein analysis indicated the lectin to be homologous to jacalin-related plant lectin. In its native form, Rhinocelectin exists as a homo-tetramer predicted with four chains of identical proteins consisting of 11 beta-sheet structures with only one alpha-helix structure. The antiproliferative activity of the Rhinocelectin against human cancer cell lines was concentration dependent and selective. The IC50 values against triple negative breast cancer cell lines MDA-MB-231 and breast cancer MCF-7 are 36.52 ± 13.55 µg mL-1 and 53.11 ± 22.30 µg mL-1 , respectively. Rhinocelectin is only mildly cytotoxic against the corresponding human nontumorigenic breast cell line 184B5 with IC50 value at 142.19 ± 36.34 µg mL-1 . The IC50 against human lung cancer cell line A549 cells is 46.14 ± 7.42 µg mL-1 while against nontumorigenic lung cell line NL20 is 41.33 ± 7.43 µg mL-1 . The standard anticancer drug, Doxorubicin exhibited IC50 values mostly below 1 µg mL-1 for the cell lines tested. Flow cytometry analysis showed the treated breast cancer cells were arrested at G0/G1 phase and apoptosis induced. Rhinocelectin agglutinated rat and rabbit erythrocytes at a minimal concentration of 3.125 µg mL-1 and 6.250 µg mL-1 , respectively.

Comparing monovalent and combination hepatitis B vaccine outcomes in children delivered by mothers with chronic hepatitis B.

AIM: We compared the vaccine effectiveness of monovalent and combination hepatitis B vaccine regimens in infants born to chronic hepatitis B carrier mothers. METHODS: An observational cohort of neonates was recruited over 78 months from two public hospital maternity units in Singapore. We enrolled term infants, born to chronic hepatitis B surface antigen-positive mothers regardless of their hepatitis Be antigen status, who completed the hepatitis B virus (HBV) vaccination programme in Singapore. Infants born to mothers on antiviral therapy, or with concurrent hepatitis C or human immunodeficiency virus infection were excluded. All infants received hepatitis B immunoglobulin at birth. One group received three doses of monovalent hepatitis B vaccine (0, 1, 6 months) (regimen A). The other group received two doses of monovalent vaccine, followed by one dose combination vaccine DTaP-IPV-Hib-HBV (0, 1, 6 months) (regimen B). Vaccine effectiveness was determined by immunoprophylaxis failure leading to HBV vertical transmission. Immunogenicity was assessed by hepatitis B surface antibody (anti-HBs) levels at 9 months of age. RESULTS: Total of 177 term neonates received regimen A and 115 received regimen B. Immunoprophylaxis failure rate was low, 2.3 and 2.6% (P = 1.00) in regimen A and B, respectively. Mean anti-HBs titres were similar at 643 ± 374 and 561 ± 396 IU/L (P = 0.08) for regimen A and B, respectively. CONCLUSION: Hepatitis B vaccine regimens using monovalent or combination vaccine for the third dose showed similarly high vaccine effectiveness and low immunoprophylaxis failure rate in term infants born to chronic hepatitis B carrier mothers.

KrasG12D-LOH promotes malignant biological behavior and energy metabolism of pancreatic ductal adenocarcinoma cells through the mTOR signaling pathway.

Oncogenic Kras with loss of heterozygosity (LOH) is frequently detected in various tumours. However, the exact function and mechanism by which KrasG12D-LOH operates remain unclear. Therefore, the current study investigated the effect of KrasG12D-LOH on the malignant phenotype of pancreatic ductal adenocarcinoma (PDAC) cells. Our investigation revealed that KrasG12D-LOH is associated with increased proliferation, invasion and reduced apoptosis in PDAC cells. The results also exhibited enhanced glycolytic phenotype of KrasG12D-LOH PDAC cells. Hyperactive mTOR plays a significant role in the initiation and maintenance of tumors. To investigate the correlation between KrasG12D-LOH and mTOR, the mTOR signaling pathway was detected by western blot analysis. We found that KrasG12D-LOH up-regulated Akt, AMPK, REDD1 and mTOR in PDAC cells. In summary, our results demonstrated that KrasG12D-LOH promotes oncogenic Kras-induced PDAC by regulating energy metabolism and mTOR signaling pathway. These data may provide novel therapeutic perspectives for PDAC.

Left atrial appendage mass.

Left atrial (LA) masses are known to be associated with peripheral embolization. Accurate identification of etiology is crucial because treatment strategies may differ. We present the case of a young woman, who was initially diagnosed with a LA thrombus and anticoagulated. The diagnosis was revised to a primary cardiac tumor after review of the echocardiographic findings. Surgical excision revealed an atrial myxoma in an unusual location.

Genome re-sequencing to identify single nucleotide polymorphism markers for muscle color traits in broiler chickens.

OBJECTIVE: Meat quality including muscle color in chickens is an important trait and continuous selective pressures for fast growth and high yield have negatively impacted this trait. This study was conducted to investigate genetic variations responsible for regulating muscle color. METHODS: Whole genome re-sequencing analysis using Illumina HiSeq paired end read method was performed with pooled DNA samples isolated from two broiler chicken lines divergently selected for muscle color (high muscle color [HMC] and low muscle color [LMC]) along with their random bred control line (RAN). Sequencing read data was aligned to the chicken reference genome sequence for Red Jungle Fowl (Galgal4) using reference based genome alignment with NGen program of the Lasergene software package. The potential causal single nucleotide polymorphisms (SNPs) showing non-synonymous changes in coding DNA sequence regions were chosen in each line. Bioinformatic analyses to interpret functions of genes retaining SNPs were performed using the ingenuity pathways analysis (IPA). RESULTS: Millions of SNPs were identified and totally 2,884 SNPs (1,307 for HMC and 1,577 for LMC) showing >75% SNP rates could induce non-synonymous mutations in amino acid sequences. Of those, SNPs showing over 10 read depths yielded 15 more reliable SNPs including 1 for HMC and 14 for LMC. The IPA analyses suggested that meat color in chickens appeared to be associated with chromosomal DNA stability, the functions of ubiquitylation (UBC) and quality and quantity of various subtypes of collagens. CONCLUSION: In this study, various potential genetic markers showing amino acid changes were identified in differential meat color lines, that can be used for further animal selection strategy.

A systems approach identifies time-dependent associations of multimorbidities with pancreatic cancer risk.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is usually diagnosed in late adulthood; therefore, many patients suffer or have suffered from other diseases. Identifying disease patterns associated with PDAC risk may enable a better characterization of high-risk patients. METHODS: Multimorbidity patterns (MPs) were assessed from 17 self-reported conditions using hierarchical clustering, principal component, and factor analyses in 1705 PDAC cases and 1084 controls from a European population. Their association with PDAC was evaluated using adjusted logistic regression models. Time since diagnosis of morbidities to PDAC diagnosis/recruitment was stratified into recent (<3 years) and long term (≥3 years). The MPs and PDAC genetic networks were explored with DisGeNET bioinformatics-tool which focuses on gene-diseases associations available in curated databases. RESULTS: Three MPs were observed: gastric (heartburn, acid regurgitation, Helicobacter pylori infection, and ulcer), metabolic syndrome (obesity, type-2 diabetes, hypercholesterolemia, and hypertension), and atopic (nasal allergies, skin allergies, and asthma). Strong associations with PDAC were observed for ≥2 recently diagnosed gastric conditions [odds ratio (OR), 6.13; 95% confidence interval CI 3.01-12.5)] and for ≥3 recently diagnosed metabolic syndrome conditions (OR, 1.61; 95% CI 1.11-2.35). Atopic conditions were negatively associated with PDAC (high adherence score OR for tertile III, 0.45; 95% CI, 0.36-0.55). Combining type-2 diabetes with gastric MP resulted in higher PDAC risk for recent (OR, 7.89; 95% CI 3.9-16.1) and long-term diagnosed conditions (OR, 1.86; 95% CI 1.29-2.67). A common genetic basis between MPs and PDAC was observed in the bioinformatics analysis. CONCLUSIONS: Specific multimorbidities aggregate and associate with PDAC in a time-dependent manner. A better characterization of a high-risk population for PDAC may help in the early diagnosis of this cancer. The common genetic basis between MP and PDAC points to a mechanistic link between these conditions.

The effect of fibroblast growth factor 15 deficiency on the development of high fat diet induced non-alcoholic steatohepatitis.

Non-alcoholic steatohepatitis (NASH) is a form of non-alcoholic fatty liver disease (NAFLD) characterized by steatosis, inflammation, and fibrosis often associated with metabolic syndrome. Fibroblast growth factor 15 (FGF15), an endocrine factor mainly produced in the distal part of small intestine, has emerged to be a critical factor in regulating bile acid homeostasis, energy metabolism, and liver regeneration. We hypothesized that FGF15 alters the development of each of the listed features of NASH. To test this hypothesis, four-week old male Fgf15-/- and their corresponding wild-type (WT) mice were fed either a high fat diet (HFD) or a control chow diet for six months. The results confirmed that HFD feeding for six months in WT mice recapitulated human NASH phenotype, including macrovesicular steatosis, inflammation, and fibrosis. Whereas FGF15 deficiency had no effect on the severity of liver steatosis or inflammation, it was associated with decreased liver fibrosis. Furthermore, FGF15 deficiency resulted in abnormal bile acid homeostasis, increased insulin resistance, increased HFD-induced serum triglycerides, decreased inductions of hepatic cholesterol content by HFD, and altered gene expression of lipid metabolic enzymes. These data suggest that FGF15 improves lipid homeostasis and reduces bile acid synthesis, but promotes fibrosis during the development of NASH.

[DNA methylation modification of BRMS1 in triple-negative breast cancer and its correlation with tumor metastasis].

Objective: To investigate the effect of methylation status of breast cancer metastasis suppressor gene 1 (BRMS1) on the expression of breast cancer and the biological behavior of cancer cells in triple-negative breast cancer (TNBC). Methods: The expression of BRMS1 in TNBC tissues and corresponding non-malignant tissues and its relationship with clinicopathological parameters were detected by immunohistochemistry. The mRNA and protein expression of BRMS1 in normal breast epithelial cells and TNBC cells were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. The methylation specific polymerase chain reaction (MSP) was used to detect the methylation status of BRMS1 in each cell. These cells were treated with demethylated preparations (5-Aza-dC) to re-activate BRMS1 expression. Using tumor cell invasion assay to detect influence of BRMS1 demethylation on the invasion capacity of cancer cells. The data were statistically analyzed. Results: The positive expression rate of BRMS1 protein in TNBC tissues was significantly lower than that in corresponding non-malignant tissues (χ(2)= 6.635, P<0.05). The mRNA expression level of BRMS1 in patients with lymph node metastasis was significantly lower than those with no lymph node metastasis (P=0.018). The down-regulation of BRMS1 expression was related to the methylation of DNA promoter, which was statistically significant (χ(2)=14.68, P<0.05). The mRNA and protein expression of BRMS1 was also correlated with tumor size and TNM staging (P=0.000-0.003). After using 5-Aza-dC, the number of cells with invasive capacity was significantly lower than those of the control group (t=3.262-10.72, P<0.05). Conclusions: The decrease of BRMS1 expression in TNBC cells is related to the methylation of DNA. Demethylation can inhibit the invasion of breast cancer cells.

Efficacy and toxicity of treatment with the anti-CTLA-4 antibody ipilimumab in patients with metastatic melanoma after prior anti-PD-1 therapy.

BACKGROUND: Recent phase III clinical trials have established the superiority of the anti-PD-1 antibodies pembrolizumab and nivolumab over the anti-CTLA-4 antibody ipilimumab in the first-line treatment of patients with advanced melanoma. Ipilimumab will be considered for second-line treatment after the failure of anti-PD-1 therapy. METHODS: We retrospectively identified a cohort of 40 patients with metastatic melanoma who received single-agent anti-PD-1 therapy with pembrolizumab or nivolumab and were treated on progression with ipilimumab at a dose of 3 mg kg(-1) for a maximum of four doses. RESULTS: Ten percent of patients achieved an objective response to ipilimumab, and an additional 8% experienced prolonged (>6 months) stable disease. Thirty-five percent of patients developed grade 3-5 immune-related toxicity associated with ipilimumab therapy. The most common high-grade immune-related toxicity was diarrhoea. Three patients (7%) developed grade 3-5 pneumonitis leading to death in one patient. CONCLUSIONS: Ipilimumab therapy can induce responses in patients who fail the anti-PD-1 therapy with response rates comparable to previous reports. There appears to be an increased frequency of high-grade immune-related adverse events including pneumonitis that warrants close surveillance.

Strategies to improve the outcome in locally advanced pancreatic cancer.

Pancreatic cancer is associated with the worst prognosis of all gastrointestinal malignancies. The major reasons for the dismal outcome are late diagnosis due to unspecific symptoms and aggressive tumor biology. Although highly effective chemotherapeutic options have emerged within the last decade, radical resection offers the only chance of cure. Only 10-20% of patients are resectable at presentation, and 30-40% present with borderline resectable or locally advanced/unresectable tumors. Even if resectable, the 5-year-survival rate after complete resections remains unsatisfactory, with less than 25%. This article gives an overview on current therapy standards as well as on new approaches especially for locally advanced tumors and outlines the importance of ongoing research to improve prognosis.

Maternally-derived zinc transporters ZIP6 and ZIP10 drive the mammalian oocyte-to-egg transition.

Rapid cellular zinc influx regulates early mammalian development during the oocyte-to-egg transition through modulation of the meiotic cell cycle. Despite the physiological necessity of this zinc influx, the molecular mechanisms that govern such accumulation are unknown. Here we show that the fully grown mammalian oocyte does not employ a transcriptionally based mechanism of zinc regulation involving metal response element-binding transcription factor-1 (MTF-1), as demonstrated by a lack of MTF-1 responsiveness to environmental zinc manipulation. Instead, the mammalian oocyte controls zinc uptake through two maternally derived and cortically distributed zinc transporters, ZIP6 and ZIP10. Targeted disruption of these transporters using several approaches during meiotic maturation perturbs the intracellular zinc quota and results in a cell cycle arrest at a telophase I-like state. This arrest phenocopies established models of zinc insufficiency during the oocyte-to-egg transition, indicating the essential function of these maternally expressed transporters. Labile zinc localizes to punctate cytoplasmic structures in the human oocyte, and ZIP6 and ZIP10 are enriched in the cortex. Altogether, we demonstrate a mechanism of metal regulation required for female gamete development that may be evolutionarily conserved.

Enhancing multimodality functional and molecular imaging using glucose-coated gold nanoparticles.

AIM: To describe how pegylated glucose-coated gold nanoparticles (PEG-Glu-GNPs) can help improve computed tomography (CT) imaging. MATERIALS AND METHODS: PEG-Glu-GNPs were designed for use as an imaging nanoprobe to act an effective contrast agent for both CT and PET scans. Twelve BALB/c mice were divided into two groups: mice with injected with PEG-Glu-GNPs and control mice. The mice were examined using high-resolution micro-CT at different time intervals (24 h, 7 days, and 15 days) after the injection of the particles. Greyscale density and CT attenuation values were determined to trace the excretion of the particles over time. RESULTS: Tumour contours were easily distinguished from surrounding tissue in mice injected with PEG-Glu-GNPs but not controls. This distinction was still visible at 7 days, but not at 15 days post-injection. CONCLUSION: Molecular imaging technology has enabled the development of a new generation of imaging probes. These sophisticated probes can visualize biological processes or enable early diagnosis of diseases in vivo. Compared to conventional CT images and PET scans, PEG-Glu-GNPs significantly improved image quality at the cellular and molecular level, which can significantly aid the early detection of cancer or cancer metastases.

Cell bioenergetics in Leghorn male hepatoma cells and immortalized chicken liver cells in response to 4-hydroxy 2-nonenal-induced oxidative stress.

The major objectives of this study were to compare cell bioenergetics in 2 avian liver cell lines under control conditions and in response to oxidative stress imposed by 4-hydroxy 2-nonenal (4-HNE). Cells in this study were from a chemically immortalized Leghorn male hepatoma (LMH) cell line and a spontaneously immortalized chicken liver (CELi) cell line. Oxygen consumption rate (OCR) was monitored in specialized microtiter plates using an XF24 Flux Analyzer (Seahorse Bioscience, Billerica, MA). Cell bioenergetics was assessed by sequential additions of oligomycin, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP), and antimycin-A that enables the determination of a) OCR linked to adenosine triphosphate (ATP) synthase activity, b) mitochondrial oxygen reserve capacity, c) proton leak, and d) nonmitochondrial cytochrome c oxidase activity. Under control (unchallenged) conditions, LMH cells exhibited higher basal OCR and higher OCR attributed to each of the bioenergetic components listed above compared with CELi cells. When expressed as a percentage of maximal OCR (following uncoupling with FCCP), LMH cells exhibited higher OCR due to ATP synthase and proton leak activity, but lower mitochondrial oxygen reserve capacity compared with CELi cells; there were no differences in OCR associated with nonmitochondrial cytochrome c oxidase activity. Whereas the LMH cells exhibited robust ATP synthase activity up to 50 µM 4-HNE, CELi cells exhibited a progressive decline in ATP synthase activity with 10, 20, and 30 µM 4-HNE. The CELi cells exhibited higher mitochondrial oxygen reserve capacity compared with LMH cells with 0 and 20 µM 4-HNE but not with 30 µM 4-HNE. Both cell lines exhibited inducible proton leak in response to increasing levels of 4-HNE that was evident with 30 µM 4-HNE for CELi cells and with 40 and 50 µM 4-HNE in LMH cells. The results of these studies demonstrate fundamental differences in cell bioenergetics in 2 avian liver-derived cell lines under control conditions and in response to oxidative challenge due to 4-HNE.

Preparation and characterization of W/O microemulsion for removal of oily make-up cosmetics.

OBJECTIVE: In the present study, W/O microemulsions (MEs) were prepared for efficient removal of oily make-up cosmetics and the detergency characteristics were studied. METHODS: The W/O MEs were prepared by mixing of a spontaneous emulsifier, cosurfactant and oil, and solubilizing the mixture during addition of water. The wettability and emulsifying activity were, respectively, evaluated by measuring contact angle and absorbance after preparing a total of 20 samples using three emulsifying systems and seven oils. RESULTS: Based on the results, a lower viscosity of the oil component is favourable for higher wettability, and the lower the viscosity of the emulsifying systems, the higher the wettability of the ME. Except in the case of oleic acid (OA), oils having high polarity showed significant emulsifying activity. The equation describing [detergency(ΔE)=98.1wettability(cosθ)+120.5EAI(emulsifyingactivityindex)-77.1] was derived from the detergency measurement results, and it was verified that the wettability contributed more significantly to the detergency than the emulsifying activity. CONCLUSION: These results suggest that the prepared W/O microemulsions can be utilized as cleaning agents for efficient removal of oily make-up cosmetics.