• CERKL
• Celastrol
• Ferroptosis
• Gastric Cancer
• PCR Array

• Pentacyclic Triterpenes/pharmacology
• Ferroptosis/drug effects
• Ferroptosis/genetics
• Stomach Neoplasms/drug therapy
• Stomach Neoplasms/genetics
• Stomach Neoplasms/pathology
• Stomach Neoplasms/metabolism
• Humans
• Reactive Oxygen Species/metabolism
• Cell Line, Tumor
• Animals
• Cell Proliferation/drug effects
• Triterpenes/pharmacology
• Antineoplastic Agents, Phytogenic/pharmacology
• Glutathione/metabolism
• Mice, Inbred BALB C
• Iron/metabolism
• Mice, Nude
• Phospholipid Hydroperoxide Glutathione Peroxidase/metabolism
• Phospholipid Hydroperoxide Glutathione Peroxidase/genetics
• Phytotherapy
• Mice
• Cell Movement/drug effects
• Amino Acid Transport System y+

• EFTUD2
• GSPT1
• GUF1
• Gastric cancer (GC)
• prognosis

• Gastric cancer
• Human epidermal growth factor receptor 2
• Review
• Targeted therapy

• elderly patients with metastatic gastrointestinal cancer
• reminiscence therapy
• anxiety and depression
• spiritual well-being
• quality of life

• Humans
• Quality of Life
• Male
• Female
• Gastrointestinal Neoplasms/psychology
• Gastrointestinal Neoplasms/therapy
• Aged
• Anxiety/therapy
• Mental Health
• Depression/therapy
• Treatment Outcome
• Surveys and Questionnaires
• Middle Aged
• Aged, 80 and over
• Psychiatric Status Rating Scales
• Psychotherapy/methods

• FENDRR
• RNAs.
• biomarker
• cancer
• lncRNAs
• regulatory mechanism

• Male
• Humans
• RNA, Long Noncoding/genetics
• Epigenesis, Genetic
• Lung Neoplasms/genetics
• MicroRNAs/genetics
• Lung/metabolism
• Gene Expression Regulation, Neoplastic

• AQP3
• LncRNA LINC00659
• gastric cancer
• metastasis
• miR-370
• prognosis

• Aquaporin 3/genetics
• Aquaporin 3/metabolism
• Cell Line, Tumor
• Cell Movement/genetics
• Cell Proliferation/genetics
• Gene Expression Regulation, Neoplastic
• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Sp1 Transcription Factor/genetics
• Sp1 Transcription Factor/metabolism
• Stomach Neoplasms/genetics
• Stomach Neoplasms/metabolism
• Stomach Neoplasms/pathology
• Up-Regulation

The effective components contained in compound Kushen injection (CKI) and the genes and signalling pathways related to gastric cancer (GC) were analyzed through the network pharmacology method of traditional Chinese medicine, and various possible mechanisms by which CKI affects the proliferation, differentiation, survival, and metastasis of GC cells were discussed. The PI3K/AKT signalling pathway is considered to be one of the most important pathways targeted by CKI in the regulation of GC cells. The implementation of related cell experiments also confirmed the information we revealed.

Effective drug components of Kushen and Baituling in CKI were identified from the Traditional Chinese Medicine Systems Pharmacology Database (TCMSP). Genes related to GC were identified using the GENECARD and OMIM databases. The common target genes related to the effective components of the drug and GC were identified using the intersection method and visualized using software. A protein–protein interaction network (PPI) was established using STRING online software to confirm the key genes. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to predict the key pathways of CKI in GC treatment. BGC-803 and MKN-28 GC cells were used to verify the signalling pathway. Cell proliferation, apoptosis, migration ability, and invasion ability were assessed using CCK8, flow cytometry, scratch, and transwell assays. Immunofluorescence assays and western blotting were used to detect the expression of related proteins.

CKI regulated GC cells through 35 effective drug components of GC-related target genes. In total, 194 genes were common targets of CKI and GC. The most significant function of the enriched genes was DNA-binding transcription activator activity as demonstrated by GO enrichment analysis. The metabolic pathway with the highest enrichment was the PI3K/AKT signalling pathway as demonstrated by KEGG enrichment analysis. Our cell experimental evidence also shows that CKI inhibits GC cell growth and migration and induce GC cell apoptosis. In addition, CKI inhibits the EMT process in GC cells through the PI3K/AKT signalling pathway.

AKT1 is a key gene for CKI treatment of GC. CKI inhibited GC cell growth and migration and induced GC cell apoptosis. In addition, CKI regulated the EMT process in GC cells through the PI3K/AKT signalling pathway.

• CKI
• EMT
• Gastric cancer
• PI3K/AKT

• MYC regulated genes
• Sapaju sapella treatment.
• gastric cancer
• menadione
• new CDC25B therapy

• oncology
• tumours

• Cost-effectiveness
• Greece
• metastatic gastric cancer
• third line treatment
• trifluridine/tipiracil

• HER2
• PDL1
• T cell killing
• c-MET
• gastric cancer
• prognostic

• gastric cancer
• serum extracellular vesicle mir-215-5p
• early tumor recurrence
• prognosis
• diagnosis

• Biomarkers, Tumor
• Extracellular Vesicles
• Humans
• MicroRNAs
• Neoplasm Recurrence, Local
• Prognosis
• Stomach Neoplasms/genetics

• Diagnosis
• Prognosis
• Therapeutic target
• lncRNA DDX11-ASA

Despite the progress during the last decade, patients with advanced gastric and esophageal cancers still have poor prognosis. Finding optimal therapeutic strategies represents an unmet need in this field. Several prognostic and predictive factors have been evaluated and may guide clinicians in choosing a tailored treatment. Data from large studies investigating the role of immunotherapy in gastrointestinal cancers are promising but further investigations are necessary to better select those patients who can mostly benefit from these novel therapies. This review will focus on the treatment of metastatic esophageal and gastric cancer. We will review the standard of care and the role of novel therapies such as immunotherapies and CAR-T. Moreover, we will focus on the analysis of potential predictive biomarkers such as Modify as: Microsatellite Instability (MSI) and PD-L1, which may lead to treatment personalization and improved treatment outcomes. A multidisciplinary point of view is mandatory to generate an integrated approach to properly exploit these novel antiproliferative agents.

• esophageal cancer
• gastric cancer
• genetics
• immunotherapy
• multidisciplinary

• TJP1
• circRNA
• circSMC3
• gastric cancer
• miR-4720-3p

Gastric cancer (GC) remains the third leading cause of cancer-related death despite several improvements in targeted therapy. There is therefore an urgent need to investigate new treatment strategies, including the identification of novel biomarkers for patient stratification. In this study, we evaluated the effect of FDA-approved kinase inhibitors on GC. Through a combination of cell growth, migration and invasion assays, we identified dasatinib as an efficient inhibitor of GC proliferation. Mass-spectrometry-based selectivity profiling and subsequent knockdown experiments identified members of the SRC family of kinases including SRC, FRK, LYN and YES, as well as other kinases such as DDR1, ABL2, SIK2, RIPK2, EPHA2, and EPHB2 as dasatinib targets. The expression levels of the identified kinases were investigated on RNA and protein level in 200 classified tumor samples from patients, who had undergone gastrectomy, but had received no treatment. Levels of FRK, DDR1 and SRC expression on both mRNA and protein level were significantly higher in metastatic patient samples regardless of the tumor stage, while expression levels of SIK2 correlated with tumor size. Collectively, our data suggest dasatinib for treatment of GC based on its unique property, inhibiting a small number of key kinases (SRC, FRK, DDR1 and SIK2), highly expressed in GC patients.

• SIK2
• SRC-kinases
• biomarker
• dasatinib
• gastric cancer

• compound kushen injection
• efficacy
• gastric cancer
• meta–analysis
• safety
• systematic review

• Drugs, Chinese Herbal/administration & dosage
• Drugs, Chinese Herbal/adverse effects
• Humans
• Injections
• Meta-Analysis as Topic
• Stomach Neoplasms/drug therapy
• Systematic Reviews as Topic
• Treatment Outcome

Ion channels play important roles in regulating various cellular processes and malignant transformation. Expressions of some chloride channels have been suggested to be associated with patient survival in gastric cancer (GC). However, little is known about the expression and function of TTYH3, a gene encoding a chloride ion channel, in cancer progression. Here, we comprehensively analyzed the expression of TTYH3 and its clinical outcome in GC using publicly available cancer gene expression and patient survival data through various databases. We examined the differences of TTYH3 expression between cancers and their normal tissues using the Oncomine, UALCAN, and GEO (Gene Expression Omnibus) databases. TTYH3 expression was investigated from immunohistochemistry images using the Human Protein Atlas database. Copy number alterations and mutations of TTYH3 were analyzed using cBioPortal. The co-expression profile of TTYH3 in GC was revealed using Oncomine. The gene ontology and pathway analyses were done using those co-expressed genes via the Enrichr tool to explore the predicted signaling pathways in GC. TTYH3 mRNA and protein levels in GC were significantly greater than those in normal tissue. Kaplan–Meier analysis revealed the upregulation of TTYH3 expression, which was significantly correlated with worse patient survival. Collectively, our data suggest that TTYH3 might be a potential prognostic marker for GC patients.

• TTYH3
• cancer progression
• clinical outcomes
• gastric cancer
• multiomics analysis
• patient survival

• Apoptosis
• Gastric cancer
• JNK
• ROS
• Schisantherin A

• apoptosis
• gastric cancer
• invasion
• lncRNA CCAT1
• miR-219-1
• proliferation

1,4-Naphthoquinone derivatives have superior anticancer effects, but their use has been severely limited in clinical practice due to adverse side effects. To reduce the side effects and extend the anticancer effects of 1,4-naphthoquinone derivatives, 2-(butane-1-sulfinyl)-1,4-naphthoquinone (BQ) and 2-(octane-1-sulfinyl)-1,4-naphthoquinone (OQ) were synthesized, and their anticancer activities were investigated. The anti-proliferation effects, determined by MTT assays, showed that BQ and OQ significantly inhibited the viability of gastric cancer cells and had no significant cytotoxic effect on normal cell lines. The apoptotic effect was determined by flow cytometry, and the results showed that BQ and OQ induced cell apoptosis by regulating the mitochondrial pathway and cell cycle arrest at the G2/M phase via inhibition of the Akt signaling pathway in AGS cells. Furthermore, BQ and OQ significantly increased the levels of reactive oxygen species (ROS) and this effect was blocked by the ROS scavenger NAC in AGS cells. BQ and OQ induced apoptosis by upregulating the protein expression of p38 and JNK and downregulating the levels of ERK and STAT3. Furthermore, expression levels of these proteins were also blocked after NAC treatment. These results demonstrated that BQ and OQ induced apoptosis and cell cycle arrest at the G2/M phase in AGS cells by stimulating ROS generation, which caused subsequent activation of MAPK, Akt and STAT3 signaling pathways. Thus, BQ and OQ may serve as potential therapeutic agents for the treatment of human gastric cancer.

• Cancer stem cell
• Gastric cancer
• Lauren classification
• Mucin phenotype expression

• Biomarkers, Tumor/genetics
• Disease Progression
• Gene Expression Regulation, Neoplastic
• Humans
• Mucins/genetics
• Neoplastic Stem Cells/pathology
• Phenotype
• Prognosis
• Stomach Neoplasms/classification
• Stomach Neoplasms/genetics
• Stomach Neoplasms/pathology

• PD-L1
• avelumab
• gastric cancer

• Antibodies, Monoclonal/administration & dosage
• Antibodies, Monoclonal/adverse effects
• Antibodies, Monoclonal/therapeutic use
• Antibodies, Monoclonal, Humanized
• Antineoplastic Agents/administration & dosage
• Antineoplastic Agents/adverse effects
• Antineoplastic Agents/therapeutic use
• Biomarkers, Tumor
• Humans
• Maintenance Chemotherapy
• Molecular Targeted Therapy
• Neoplasm Staging
• Stomach Neoplasms/drug therapy
• Stomach Neoplasms/pathology
• Treatment Outcome

• FENDRR
• RASSF1A
• TET2
• gastric cancer
• methylation
• miR-214-3p
• proliferation

• Apoptosis
• GC
• Proliferation
• TIA1
• miR-487a

• Diagnosis
• HOXA-AS2
• Prognosis
• Therapeutic target
• lncRNA

• Gastric cancer
• P53
• biologic behavior
• saRNA

• NADPH oxidases
• drug target
• online database
• prognosis
• stomach cancer

• Gastric
• Gastroesophageal junction
• Immune checkpoint inhibitors
• Immunotherapy
• PD-1/PD-L1

• Humans
• Immunotherapy/methods
• Neoplasm Metastasis
• Stomach Neoplasms/drug therapy
• Stomach Neoplasms/pathology

Myosin phosphatase target subunit 1 (MYPT1) serves as a subgroup of myosin phosphatases, and is frequently low-expressed in human cancers. However, little is known about the effects of MYPT1 in gastric cancer (GC).

In our study, MYPT1 expression was detected by quantitative real-time reverse transcription PCR (qRT-PCR) in GC tissues, different advanced pathological stages of GC tissues, and preoperative and postoperative patients. Kaplan-Meier analysis was used to measure the overall survival of GC patients. MYPT1 expression was analyzed by qRT-PCR and Western blot assays in GES-1 cells and GC cells. Cell proliferation, cycle, and migration and invasion abilities were detected by CCK-8, flow cytometry, and Transwell assays. E-cadherin, TIMP-2, MMP-2, MMP-9 RhoA, and p-RhoA expressions were assessed by qRT-PCR and Western blot assays in treated SNU-5 cells.

Our results indicated that MYPT1 was down-regulated in GC tissues and cells, and is related to clinical stages and overall survival of GC. Functional research demonstrated that overexpression of MYPT1 can inhibit cell proliferation, cell cycle progression, and migration and invasion of GC cells. Many studies on mechanisms reported that overexpression of MYPT1 dramatically improved the expression levels of cell cycle-related genes (Cyclin D1 and c-myc), significantly increased epithelial marker (E-cadherin) expression, and decreased invasion-associated genes (TIMP-2 and MMP-2) expressions in SNU-5 cells. In addition, we found that MYPT1 suppressed RhoA phosphorylation.

We verified that MYPT1 inhibits GC cell proliferation and metastasis by regulating RhoA phosphorylation.

Factors affecting trastuzumab efficacy in advanced gastric cancer (GC) are largely unknown. Heterogeneity is a notable feature of HER2 in GC. Whether the heterogeneity influences trastuzumab efficacy is still unknown.

The HER2^homogeneous group and HER2^{heterogeneous} group showed no statistical difference in RR (46.4% vs 55.0%, P = 0.558), PFS (5.80 vs 6.30 months, P = 0.804) and OS (16.00 vs 16.00 months, P = 0.787). The Lauren^intestinal group and Lauren^{non-intestinal} group demonstrated no discrepancy in PFS (6.00 vs 6.00 months, P = 0.912) and OS (16.50 vs 14.00 months, P = 0.227). However, by combining HER2 heterogeneity and Lauren classification, PFS and OS of HER2^homogeneous/Lauren^{non-intestinal} subgroup was the shortest among the 4 subgroups (P = 0.012 and P = 0.037), which was much shorter than the other patients (PFS:3.00 vs 6.30 months, P = 0.003; OS: 4.50 vs 16.50 months, P = 0.004). Univariate and multivariate analysis showed that HER2 heterogeneity combined with Lauren classification was an independent prognostic factor in both PFS (P = 0.031 and P = 0.002) and OS (P = 0.039 and P = 0.013).

48 patients with HER2 positive advanced GCs accepting trastuzumab treatment were retrospectively analyzed. Based on HER2 heterogeneity, the patients were divided into a HER2^homogeneous group and a HER2^{heterogeneous} group. Response rate (RR), progression free survival (PFS), and overall survival (OS) were compared. Main clinicopathological factors including Lauren classification were subjected to subgroup analysis.

HER2 heterogeneity alone may not correlate with trastuzumab efficacy in HER2 positive advanced GCs. HER2 heterogeneity combined with Lauren classification may help to identify a subgroup with poor response to trastuzumab which is homogeneous HER2 positive and non-intestinal type.

• HER2
• efficacy
• gastric cancer
• heterogeneity
• trastuzumab

This study aims to observe the expression of microRNA (miR)‐634 in different gastric cancer cell lines and tissues, and to study the effects of miR‐634 on the proliferation, migration, and invasion of the gastric cancer cells. The miR‐634 mimics and miR‐634 inhibitors were transfected by lentivirus into human gastric cancer SGC‐7901 and MGC‐803 cells, and the miR‐634 cells without transfection were used as the control group (NC group). The expression of miR‐634 in the transfected cells was detected by qRT‐PCR. Cell viability was measured by the CCK8 assay. The migration and invasion ability of the cells were detected by scratch assays and Transwell^® chamber assays, respectively, and the luciferase assay verified the binding of miR‐634 to the target gene JAG1. The expression level of miR‐634 in gastric cancer tissues and cell lines was significantly lower than that in normal adjacent tissues and control cells. The survival of cells was significantly decreased, and number of cells migrating and invading was decreased in the miR‐634 mimics group. However, in the miR‐634 inhibitor group, the opposite results were observed. Over‐expression of miR‐634 inhibited the proliferation, migration, and invasion of gastric cancer cell lines, and the miR‐634 target gene was JAG1.

• JAG1
• Gastric cancer
• MGC-803
• SGC-7901
• miR-634

• RAB1A
• gastric cancer
• human epidermal growth factor receptor 2
• prognostic factors

• gastric cancer
• kinases
• monoclonal antibodies
• precision medicine
• small-molecule kinase inhibitors
• targeted therapy

• gastrointestinal cancer
• hypermutation
• immune checkpoint inhibitor
• microsatellite instability
• precision medicine

• R01 CA160688 NCI NIH HHS

• Colorectal carcinoma
• Galectin-1
• Gastric cancer
• Hepatocellular carcinoma
• Pancreatic cancer
• β1,6-N-acetylglucosaminyltransferase V

• Cell Adhesion
• Disease Progression
• Drug Resistance, Neoplasm
• Epithelial-Mesenchymal Transition
• Galectin 1/genetics
• Galectin 1/metabolism
• Gastrointestinal Neoplasms/drug therapy
• Gastrointestinal Neoplasms/genetics
• Gastrointestinal Neoplasms/pathology
• Gene Expression Regulation, Neoplastic
• Glycosylation
• Humans
• Immune Tolerance
• Neoplasm Invasiveness/genetics
• Neoplasm Invasiveness/pathology
• Neovascularization, Pathologic/genetics
• Neovascularization, Pathologic/pathology
• Signal Transduction
• Up-Regulation

Gastric cancer exhibits a poor prognosis and is the third most common cause of cancer death worldwide. Chemotherapy of metastatic gastric cancer is based on combinations of platinum drugs and fluoropyrimidines, with added agents. Oxoplatin is a stable oral platinum(IV) prodrug which is converted to a highly active tetrachlorido(IV) complex under acidic conditions. In the present work, we studied the cytotoxic effects of oxoplatin against a panel of four gastric cancer cell lines in vitro. Furthermore, the role of HSP90 in chemoresistance of these lines was investigated using the specific inhibitor ganetespib. The KATO-III, MKN-1, MKN-28, MKN-45 lines were used in MTT chemosensitivity, cell cycle and apoptosis assays. KATO-III is a signet ring diffuse cell type, MKN-1 an adenosquamous primary, MKN-28 a well-differentiated intestinal type and the MKN-45 a poorly differentiated, diffuse type gastric carcinoma line. Cytotoxicity was tested in MTT assays and intracellular signal transduction with proteome profiler Western blot arrays. Interactions of platinum drugs and ganetespib were calculated with help of the Chou-Talalay method. The prodrug oxoplatin revealed low activity against the four gastric cancer cell lines, whereas the platinum tetrachlorido(IV) complex and cisplatin gave IC₅₀ values of 1-3 µg/ml with increasing chemoresistance observed in the order of MKN-1, KATO-III, MKN-28 to MKN-45. With exception of KATO-III and MKN-28/oxoplatin, all other cell lines featured marked synergistic toxicity with clinically achievable concentrations of ganetespib. Oral administration of a platinum agent such as oxoplatin would be of great value for patients and care providers alike. These results suggest that the oncogene-stabilizing HSP90 chaperone represents an important mediator of chemoresistance in gastric cancer. Ganetespib reduced the phosphorylation of p53, Akt1/2/3 and PRAS40, as well as of WNK1, a kinase which regulates intracellular chloride concentrations. Intracellular chloride was reported to control proliferation of gastric cancer cell lines. Expression of MUC1 was not downregulated in contrast to the expression of CAIX, a prognostic marker in gastric cancer. In conclusion, the HSP90 inhibitor ganetespib synergizes with platinum anticancer drugs and modulates intracellular signal transduction in direction of a less proliferative and aggressive phenotype.

• Gastric cancer
• HSP90
• chloride channel
• ganetespib
• platinum cytostatics

Gastric cancer is a leading cause of cancer death worldwide. Diet, obesity, smoking and chronic infections, especially with Helicobacter pylori, contribute to stomach cancer development. H. pylori possesses a variety of virulence factors including encoded factors from the cytotoxin-associated gene pathogenicity island (cagPAI) or vacuolating cytotoxin A (VacA). Most of the cagPAI-encoded products form a type 4 secretion system (T4SS), a pilus-like macromolecular transporter, which translocates CagA into the cytoplasm of the host cell. Only H. pylori strains carrying the cagPAI induce the transcription factor NF-κB, but CagA and VacA are dispensable for direct NF-κB activation. NF-κB-driven gene products include cytokines/chemokines, growth factors, anti-apoptotic factors, angiogenesis regulators and metalloproteinases. Many of the genes transcribed by NF-κB promote gastric carcinogenesis. Since it has been shown that chemotherapy-caused cellular stress could elicit activation of the survival factor NF-κB, which leads to acquisition of chemoresistance, the NF-κB system is recommended for therapeutic targeting. Research is motivated for further search of predisposing conditions, diagnostic markers and efficient drugs to improve significantly the overall survival of patients. In this review, we provide an overview about mechanisms and consequences of NF-κB activation in gastric mucosa in order to understand the role of NF-κB in gastric carcinogenesis.

• Helicobacter pylori
• NF‐κB
• Type 4 secretion system
• VacA toxin
• chemoresistance
• gastric cancer
• inflammation
• tumor microenvironment

• Animals
• Humans
• Infections/complications
• Infections/metabolism
• Inflammation Mediators/metabolism
• NF-kappa B/metabolism
• Polymorphism, Genetic
• Stomach Neoplasms/etiology
• Stomach Neoplasms/metabolism
• Tumor Suppressor Proteins/metabolism

Gastric cancer (GC) is a common disease with few effective treatment choices and poor prognosis, and has the second-highest mortality rates among all cancers worldwide. Dysregulation and/or malfunction of ion channels or aquaporins (AQPs) are common in various human cancers. Furthermore, ion channels are involved in numerous important aspects of the tumor aggressive phonotype, such as proliferation, cell cycle, apoptosis, motility, migration, and invasion. Indeed, by localizing in the plasma membrane, ion channels or AQPs can sense and respond to extracellular environment changes; thus, they play a crucial role in cell signaling and cancer progression. These findings have expanded a new area of pharmaceutical exploration for various types of cancer, including GC. The involvement of multiple ion channels, such as voltage-gated potassium and sodium channels, intracellular chloride channels, ‘transient receptor potential’ channels, and AQPs, which have been shown to facilitate the pathogenesis of other tumors, also plays a role in GC. In this review, an overview of ion channel and aquaporin expression and function in carcinogenesis of GC is presented. Studies of ion channels or AQPs will advance our understanding of the molecular genesis of GC and may identify novel and effective targets for the clinical application of GC.

• Aquaporin
• Calcium
• Chloride
• Gastric cancer
• Ion channels
• Potassium
• Sodium
• Therapeutic target

A 48-year-old woman presented with bilateral enlarged ovaries, ascites, bilateral pleural effusion, and advanced gastric cancer. Pleural fluid cytology did not reveal malignant cells. Oophorectomy, performed as a palliative procedure, was followed by rapid resolution of the pleural effusion and ascites. The patient was diagnosed with pseudo-Meigs’ syndrome, and underwent chemotherapy followed by partial gastrectomy. At the last follow-up, 84 mo following oophorectomy, she was alive, and free of disease recurrence, despite not receiving any further treatment. Pseudo-Meigs’ syndrome should be considered in patients with bilateral ovarian tumors, ascites and pleural effusion, and treatment such as oophorectomy may result in symptomatic improvement and better prognosis in similar patients.

• Pseudo-Meigs’ syndrome
• Ovarian tumor
• Gastric cancer
• Pleural effusion
• Ascites