• Perimenopause
• cancer survivors
• hormone replacement therapy
• non-gynaecological
• postmenopause

• Female
• Humans
• Cancer Survivors
• Hormone Replacement Therapy/adverse effects
• Hormone Replacement Therapy/methods
• Neoplasms/metabolism
• Neoplasms/mortality

• cachexia
• depression
• estrogen
• pain
• progesterone
• social interaction

• National Natural Science Foundation of China
• Bethune Charitable Foundation

• CD147
• cancer-associated fibroblast
• estrogen
• gastric cancer
• matrix metalloproteinase

Gastric cancer is one of the first malignant cancers in the world and a large number of people die every year due to this disease. Many genetic and epigenetic risk factors have been identified that play a major role in gastric cancer. HOTAIR is an effective epigenetic agent known as long noncoding RNA (lncRNA). HOTAIR has been described to have biological functions in biochemical and cellular processes through interactions with many factors, leading to genomic stability, proliferation, survival, invasion, migration, metastasis, and drug resistance. In the present article, we reviewed the prognostic value of the molecular mechanisms underlying the HOTAIR regulation and its function in the development of Gastric Cancer, whereas elucidation of HOTAIR–protein and HOTAIR–DNA interactions can be helpful in the identification of cancer processes, leading to the development of potential therapeutic strategies.

• Expression
• Gastric cancer
• HOTAIR regulation
• Regulatory pathways

The overall incidence of gastric cancer is higher in men than women worldwide. However, gastric signet-ring cell carcinoma (GSRC) is more frequently observed in younger female patients.

To analyze clinicopathological differences between sexes in GSRC, because of the limited evidence regarding association between sex-specific differences and survival.

We reviewed medical records for 1431 patients who received treatment for GSRC at the Cancer Hospital, Chinese Academy of Medical Sciences between January 2011 and December 2018 and surveyed reproductive factors. Clinicopathological characteristics were compared between female and male patients. Cox multivariable model was used to compare the mortality risks of GSRC among men, menstrual women, and menopausal women.

Of 1431 patients, 935 patients were male and 496 were female (181 menstrual and 315 menopausal). The 5-year overall survival in male, menstrual female and menopausal female groups was 65.6%, 76.5% and 65%, respectively (P < 0.01). Menstruation was found to be a protective factor (hazard ratio = 0.58, 95% confidence interval: 0.42–0.82).

The mortality risk of GSRC in menstrual women was lower than that in men. This study identified the protective effects of female reproductive factors in GSRC.

• Gastric carcinoma
• Signet-ring cell
• Female reproductive factor
• Menopause

• Cholesterol
• Gastric cancer
• Lipid
• Menopause

• Alternative therapies
• HRT
• cancer
• menopause

Rapid advance in oncology leads to increasing survival of oncologic patients. More and more of them live long enough to reach either the natural age of menopause or, as a side effect of their oncotherapy, experience the cessation of gonadal function, leading to premature ovarian insufficiency, with disturbing vasomotor symtoms and long-term negative cardiovascular and skeletal effects. Thus, an ever increasing number of cancer survivors search endocrinologic help in the form of hormone replacement therapy (HRT). The misinterpretation of the WHI (Women's Health Initiative) Study has lead to an irrational fear of female hormone replacement, both by the general population and medical professionals. It has seemed the logical and safe conclusion to many physicians to avoid HRT, supposing that this attitude definitely causes no harm, whereas the decision of prescribing estrogen alone or with progestins might bear oncologic and thromboembolic risks and may even lead to litigation in case of a potentially related complication. However, it was known even before the WHI results that premature menopause and hypogonadism decreases the life expectancy of women by years through its skeletal and cardiovascular effects, and this negative effect correlates with the length of the hypoestrogenaemic period. Therefore, the denial of HRT also needs to be supported by evidence and should be weighed againts the risks of HRT. Yet, the oncologic risk of HRT is extremely difficult to assess. In this work we review the latest evidence from in vitro experiments to clinical studies, regarding HRT in survivors of gynecologic and non-gynecologic cancers. Based on our literature research, we group tumours regarding the oncologic risk of properly chosen female hormone replacement therapy in cancer survivors as follows: ’HRT is advanageous’ (e.g. endometrial cancer type I, cervical adenocarcinoma, haematologic malignancies, local cutaneous malignant melanoma, colorectal cancer, hepatocellular cancer); ’HRT is neutral’ (e.g. BRCA 1/2 mutation carriers without cancer, endometrial cancer type II, uterinal carcinosarcoma and adenosarcoma, certain types of ovarian cancer, cervical, vaginal and vulvar squamous cell carcinoma, prolactinoma, kidney cancer, pancreatic cancer, thyroid cancer); ’HRT is relatively contraindicated’ for various reasons (e.g. leiomyosarcoma, certain types of ovarian tumours, brain tumours, advanced metastatic malignant melanoma, lung cancer, gastric cancer, bladder cancer); ’HRT is diasadvantageous and thus contraindicated’ (e.g. breast cancer, endometrial stroma sarcoma, meningioma, glioma, hormone receptor positive gastric and bladder cancer).

• Breast cancer
• Cancer survivor
• Estrogen replacement
• Estrogen-progestin replacement
• Gynecologic cancer
• HRT
• Hormone replacement therapy
• MHT
• Menopausal hormone therapy
• Non-gynecologic cancer
• Oncologic patient
• Recurrence risk

• Breast Neoplasms/etiology
• Cancer Survivors
• Estrogens/adverse effects
• Estrogens/metabolism
• Estrogens/therapeutic use
• Female
• Genital Neoplasms, Female/etiology
• Hormone Replacement Therapy/adverse effects
• Humans
• Neoplasms/etiology
• Neoplasms, Second Primary/etiology
• Progesterone/adverse effects
• Progesterone/metabolism
• Progesterone/therapeutic use

• Estrogen receptor alpha
• Estrogen receptor beta
• Meta-Analysis
• Stomach neoplasms
• TCGA

To evaluate sex differences and the effects of oestrogen administration in rat gastric mucosal defence.

Sex differences in gastric mucus thickness and accumulation rate, absolute gastric mucosal blood flow using microspheres, the integrity of the gastric mucosal epithelium in response to a chemical irritant and the effects of oestrogen administration on relative gastric mucosal blood flow in an acute setting was assessed in an in vivo rat experimental model. Subsequently, sex differences in the distribution of oestrogen receptors and calcitonin gene related peptide in the gastric mucosa of animals exposed to oestrogen in the above experiments was evaluated using immunohistochemistry.

The absolute blood flow in the GI-tract was generally higher in males, but only significantly different in the corpus part of the stomach (1.12 ± 0.12 mL/min•g in males and 0.51 ± 0.03 mL/min•g in females) (P = 0.002). After removal of the loosely adherent mucus layer the thickness of the firmly adherent mucus layer in males and females was 79 ± 1 µm and 80 ± 3 µm respectively. After 60 min the mucus thickness increased to 113 ± 3 µm in males and 121 ± 3 µm in females with no statistically significant difference seen between the sexes. Following oestrogen administration (0.1 followed by 1 µg/kg•min), mean blood flow in the gastric mucosa decreased by 31% [68 ± 13 perfusion units (PFU)] in males which was significantly different compared to baseline (P = 0.02). In females however, mean blood flow remained largely unchanged with a 4% (5 ± 33 PFU) reduction. The permeability of the gastric mucosa increased to a higher level in females than in males (P = 0.01) after taurocholate challenge. However, the calculated mean clearance increase did not significantly differ between the sexes [0.1 ± 0.04 to 1.1 ± 0.1 mL/min•100 g in males and 0.4 ± 0.3 to 2.1 ± 0.3 mL/min•100 g in females (P = 0.065)]. There were no significant differences between 17β-Estradiol treated males (mean ratio of positive staining ± SEM) (0.06 ± 0.07) and females (0.11 ± 0.11) in the staining of ERα (P = 0.24). Also, there were no significant differences between 17β-Estradiol treated males (0.18 ± 0.21) and females (0.06 ± 0.12) in the staining of ERβ (P = 0.11). Finally, there were no significant differences between 17β-Estradiol treated males (0.04 ± 0.05) and females (0.11 ± 0.10) in the staining of CGRP (P = 0.14).

Gastric mucosal blood flow is higher in male than in female rats and is reduced in male rats by oestrogen administration.

• Sex differences
• Gastric mucosal defence
• Blood flow
• Oestrogen
• Gastric physiology
• Mucus

• Animals
• Anti-Inflammatory Agents, Non-Steroidal/administration & dosage
• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Calcitonin Gene-Related Peptide/metabolism
• Calcitonin Gene-Related Peptide/physiology
• Diclofenac/administration & dosage
• Diclofenac/adverse effects
• Epithelium/blood supply
• Epithelium/drug effects
• Estradiol/administration & dosage
• Estradiol/pharmacology
• Estrogens/administration & dosage
• Estrogens/pharmacology
• Female
• Gastric Mucosa/blood supply
• Gastric Mucosa/drug effects
• Gastric Mucosa/metabolism
• Male
• Models, Animal
• Permeability
• Rats
• Rats, Sprague-Dawley
• Receptors, Estrogen/metabolism
• Receptors, Estrogen/physiology
• Sex Factors
• Taurocholic Acid/administration & dosage
• Taurocholic Acid/adverse effects

• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Belgium/epidemiology
• Databases, Factual/trends
• Europe/epidemiology
• Female
• France/epidemiology
• Humans
• Italy/epidemiology
• Male
• Middle Aged
• Population Surveillance/methods
• Portugal/epidemiology
• Registries
• Spain/epidemiology
• Stomach Neoplasms/diagnosis
• Stomach Neoplasms/mortality
• Survival Rate/trends
• Switzerland/epidemiology
• Young Adult

Worldwide, gastric cancer is one of the most common malignancies with high mortality. Various aspects of the development and progression of gastric cancer continue to be extensively investigated in order to further our understanding and provide more effective means for the prevention, diagnosis, and treatment of the disease. Estrogen receptors (ERs) are steroid hormone receptors that regulate cellular activities in many physiological and pathological processes in different tissues. There are two distinct forms of ERs, namely ERα and ERβ, with several alternative-splicing isoforms for each. They show distinct tissue distribution patterns and exert different biological functions. Dysregulation of ERs has been found to be associated closely with many diseases, including cancer. A number of studies have been conducted to investigate the role of ERs in gastric cancer, the possible mechanisms underlying these roles, and the clinical relevance of deregulated ERs in gastric cancer patients. To date, inconsistent associations of different ERs with gastric cancer have been reported. These inconsistencies may be caused by variations in in vitro cell models and clinical samples, including assay conditions and protocols with regard to different forms of ERs. Given the potential of the deregulated ERs as diagnostic/prognostic markers or therapeutic targets for gastric cancer, it will be important to identify/confirm the association of each ER isoform with gastric cancer, to determine the specific roles and interactions that these individual ER isoforms play under specific conditions in the development and/or progression of gastric cancer, and to elucidate precisely these mechanisms. In this review, we summarize the achievements from early ER studies in gastric cancer to the most up-to-date discoveries, with an effort to provide a comprehensive understanding of the role of ERs roles in gastric cancer and its possible mechanisms. Furthermore, we propose directions for future investigations.

• Gastric cancer
• Estrogen receptor
• Isoform
• Carcinogenesis
• Mechanism
• Genomic pathway
• Non-genomic pathway

• Animals
• Antineoplastic Agents, Hormonal/therapeutic use
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Estrogen Antagonists/therapeutic use
• Humans
• Receptors, Estrogen/antagonists & inhibitors
• Receptors, Estrogen/genetics
• Receptors, Estrogen/metabolism
• Signal Transduction
• Stomach Neoplasms/drug therapy
• Stomach Neoplasms/genetics
• Stomach Neoplasms/metabolism
• Stomach Neoplasms/pathology

The presence of estrogen receptor alpha has been reported in the cell and tissue levels in gastric cancer; however, its impact on patients’ survival remains unclear. The aim of this study was to investigate the expression of estrogen receptor in gastric carcinoma as well as its relationship with the clinicopathologic findings of the patients.

The study was performed on 100 endoscopic biopsies of gastric adenocarcinoma for estrogen receptor expression using an immunohistochemical method, and their relationship with the clinicopathologic findings of the patients, such as age, gender, tumor site, size, grade, depth of tumor invasion (T), and lymphatic status (N), were analyzed using independent sample t-test and Pearson Chi-square test. A P < 0.05 was considered significant in all analyses.

Using an immunohistochemical method on endoscopic biopsies of 74 males and 26 females with the mean age of 63 years, estrogen receptor was found to be positive in 41% of patients. No significant difference was found between estrogen receptor expression and other clinicopathologic findings (P = 0.75). There was a significant difference between estrogen receptor (+) and estrogen receptor (−) groups in nodal involvement (P = 0.001). The estrogen receptor (+) patients had more number of lymph nodes involved.

This study showed that lymph node involvement has a significant relationship with estrogen receptor expression. However, no significant relationship was found between estrogen receptor expression and other clinicopathologic findings such as age, gender, tumor site in stomach, tumor size, tumor grade, and T-stage.

• Clinicopathologic findings
• estrogen receptor
• gastric cancer
• immunohistochemical technique

• ANLN
• Anillin
• Gastric cancer
• Proliferative tumor
• Single sample prediction

• Adult
• Aged
• Aged, 80 and over
• Asian People/genetics
• China
• Female
• Gastrectomy
• Genome-Wide Association Study
• Humans
• MAP Kinase Kinase Kinase 1/genetics
• Male
• Middle Aged
• Polymorphism, Single Nucleotide
• Prognosis
• Risk Factors
• Stomach Neoplasms/genetics
• Stomach Neoplasms/mortality
• Stomach Neoplasms/surgery
• Survival Analysis

• mnng, n-methyl-n′-nitro-n-nitrosoguanidine
• er, estrogen receptor
• pcna, proliferating cell nuclear antigen

• Animals
• Blotting, Western
• Estrogen Receptor beta/metabolism
• Female
• Male
• Methylnitronitrosoguanidine/toxicity
• Proliferating Cell Nuclear Antigen/metabolism
• Rats
• Rats, Wistar
• Real-Time Polymerase Chain Reaction
• Reverse Transcriptase Polymerase Chain Reaction
• Sex Factors
• Stomach Neoplasms/chemically induced
• Stomach Neoplasms/metabolism

• age
• ethnicity
• gastric cancer
• gender
• survival

• P30 CA014089 NCI NIH HHS

• gastric cancer
• er-α36
• lymph node metastasis

• Adenocarcinoma/genetics
• Adenocarcinoma/metabolism
• Adenocarcinoma/pathology
• Adult
• Aged
• Case-Control Studies
• Cell Line, Tumor
• Estrogen Receptor alpha/genetics
• Estrogen Receptor alpha/metabolism
• Female
• Gene Expression Regulation, Neoplastic
• Humans
• Lymph Nodes/metabolism
• Lymph Nodes/pathology
• Lymphatic Metastasis
• Male
• Middle Aged
• Protein Isoforms/genetics
• Protein Isoforms/metabolism
• Stomach Neoplasms/genetics
• Stomach Neoplasms/metabolism
• Stomach Neoplasms/pathology

• R01 DK070016 NIDDK NIH HHS
• DK070016 NIDDK NIH HHS

• Colonic Neoplasms/metabolism
• Esophageal Neoplasms/metabolism
• Estrogens/metabolism
• Gallbladder Neoplasms/metabolism
• Gastrointestinal Neoplasms/metabolism
• Humans
• Stomach Neoplasms/metabolism

AIM: To investigate the relationship between the expression of checkpoint with fork head associated and ring finger (CHFR) and P53 protein in gastric cancer (GC) and the clinicopathologic characteristics, and to explore the correlated molecular mechanism of CHFR and p53 genes in gastric carcinogenesis.

METHODS: Five paraffin blocks of tissue microarray were constructed using a Tissue Array Machine (Steve Leighton Beecher Instruments, USA), including 151 cases of primary GC (101 cases with matched normal mucosa, intestinal metaplasia or dysplasia). Envision immunohistochemical method was employed to detect the protein expression of CHFR and mutant p53 in GC and precancerous tissues mentioned above.

RESULTS: The positive rate of CHFR protein expression in GC (49.67%, 75/151) was significantly lower than that in normal gastric mucosa (85.25%, 52/61)(P < 0.05). The down-regulation or absence of mitotic checkpoint CHFR protein expression was correlated with the sex of GC patients. The absent rate of CHFR protein expression in the female GC patients was significantly higher than that in the male GC ones (64% vs 43.56%, P < 0.05). The absent rates was also significantly different between GC patients of Borrmann Ⅲ + Ⅳ and Ⅰ + Ⅱ types (57.14% vs 34.78%, P < 0.05). In the present study, though CHFR protein expression showed no significant difference among various histological types of GC, the absent rate of CHFR protein expression was the highest (71.43%) in signet ring cell carcinoma. The absent expression of CHFR protein was not related to the depth of invasion and lymph node metastasis of GC. In addition, no correlation was found between the expression of CHFR and P53 protein expression in GC (P > 0.05).

CONCLUSION: Down-regulation or absence of mitotic checkpoint CHFR protein expression is frequent events in GC and may take a part in gastric carcinogenesis. Abnormal expression of CHFR may be of more importance in the development of female patients and diffuse-type GC.

• Checkpoint with fork head associated and ring finger
• Mutant p53
• Gastric Cancer
• Immunohistochemistry

AIM: To investigate the effect of cimetidine on the proliferation and apoptosis of human gastric cancer cell line SGC-7901 and its related mechanism.

METHODS: Human gastric cancer cell SGC-7901 was cultivated by routine method, then treated with different concentrations of cimetidine. The proliferation of SGC-7901 cells was examined by MTT assay, and the cell cycle and apoptosis were detected by flow cytometry. After Hoechst33258 staining, the morphologic changes of SGC-7901 cells were observed under fluorescence microscope, and the ultrastructure of the cells was investigated by transmission electron microscopy. The levels of Bcl-2 and Bax protein expression were detected by Western blot analysis.

RESULTS: After dealing with cimetidine (0.5, 1, 2.5, 5, 10 mmol/L) for 24 and 48 hours, we found that cimetidine significantly inhibited the proliferation of SGC-7901 cells in a time- and concentration-dependent manner (24 h: 0.705 ± 0.018, 0.560 ± 0.038, 0.408 ± 0.029, 0.276 ± 0.042, 0.205 ± 0.031 vs 0.803 ± 0.012, P < 0.05; 48 h: 0.902 ± 0.024, 0.671 ± 0.015, 0.420 ± 0.030, 0.180 ± 0.037, 0.117 ± 0.021 vs 1.079 ± 0.040, P < 0.05), whereas there was no significant cytotoxic effect as the concentration was below 0.25 mmol/L. cimetidine at the concentrations of 0.5, 1, 2.5, 5, and 10 mmol/L induced typical apoptosis of SGC-7901 cells, and flow cytometry showed an apoptosis peak. The percentage of G0/G1-phase cells was significantly increased (60.83% ± 2.27%, 67.21% ± 1.18%, 75.15% ± 4.01%, 81.88% ± 3.10%, 86.99% ± 1.43% vs 50.28% ± 1.97%, P < 0.05). The expression of Bcl-2 protein was decreased while that of Bax protein was increased following cimetidine treatment.

CONCLUSION: Cimetidine may inhibit the proliferation of SGC-7901 cells through inducing cell apoptosis and cell cycle arrest.

• Stomach neoplasms
• cimetidine
• Apoptosis
• Cell cycle

• Adenocarcinoma/genetics
• Adenocarcinoma/metabolism
• Adenocarcinoma/pathology
• Adult
• Aged
• Aged, 80 and over
• Biomarkers, Tumor/biosynthesis
• Biomarkers, Tumor/genetics
• Cell Differentiation
• Estrogen Receptor alpha/biosynthesis
• Estrogen Receptor alpha/genetics
• Estrogen Receptor beta/biosynthesis
• Estrogen Receptor beta/genetics
• Female
• Gene Expression Regulation, Neoplastic
• Humans
• Immunohistochemistry
• Male
• Middle Aged
• Neoplasm Staging
• Prognosis
• Protein Precursors/biosynthesis
• Protein Precursors/genetics
• RNA, Neoplasm/genetics
• Reverse Transcriptase Polymerase Chain Reaction
• Severity of Illness Index
• Stomach Neoplasms/genetics
• Stomach Neoplasms/metabolism
• Stomach Neoplasms/pathology
• Thymosin/analogs & derivatives
• Thymosin/biosynthesis
• Thymosin/genetics

AIM: To study the expression of trefoil factor 1 (TFF1) and TFF2 in precancerous condition and gastric cancer and to explore the relationship between TFFs and tumorigenesis, precancerous condition and gastric cancer.

METHODS: The expression of TFF1 and TFF2 was immunohistochemically analyzed in paraffin-embedded samples from 140 patients including 35 cases of chronic superficial gastritis (CSG), 35 cases of gastric ulcer (GU), 35 cases of chronic atrophic gastritis (CAG) and 35 cases of gastric cancer (GC).

RESULTS: TFF1 and TFF2 were located in cytoplasm of gastric mucous cells. In CSG, GU, CAG and GC, the level of TFF1 expression had a decreased tendency (P < 0.05). The expression of TFF2 was higher in GU than in CSG, but the difference was not significant. The expression of TFF2 also had a decreased tendency in GU, CAG, and GC (P < 0.05).

CONCLUSION: The reduced expression of TFF1 and TFF2 in precancerous conditions and gastric cancer may be associated with the proliferation and malignant transformation of gastric mucosa. More investigations are needed to explore the mechanism of TFFs and the relationship between TFFs and gastric cancer.

• Trefoil factor
• Gastric cancer
• Immunohis-tochemistry

• Case-Control Studies
• Cell Proliferation
• Cell Transformation, Neoplastic/pathology
• Disease Progression
• Female
• Gastric Mucosa/chemistry
• Gastric Mucosa/pathology
• Gastritis/pathology
• Gastritis/physiopathology
• Gene Expression Regulation, Neoplastic
• Humans
• Immunohistochemistry
• Male
• Middle Aged
• Peptides/genetics
• Peptides/physiology
• Precancerous Conditions/chemistry
• Precancerous Conditions/genetics
• Precancerous Conditions/pathology
• Stomach Neoplasms/chemistry
• Stomach Neoplasms/genetics
• Stomach Neoplasms/pathology
• Trefoil Factor-1
• Trefoil Factor-2
• Tumor Suppressor Proteins/genetics
• Tumor Suppressor Proteins/physiology

• Adenocarcinoma/diagnosis
• Adenocarcinoma/metabolism
• Adenocarcinoma/secondary
• Breast Neoplasms/metabolism
• Breast Neoplasms/pathology
• Cadherins/analysis
• Estrogen Receptor alpha/biosynthesis
• Female
• Humans
• Immunohistochemistry
• Receptors, Progesterone/analysis
• Stomach Neoplasms/diagnosis
• Stomach Neoplasms/metabolism
• Stomach Neoplasms/secondary

• Breast Neoplasms/drug therapy
• Colonic Neoplasms/drug therapy
• Endometrial Neoplasms/drug therapy
• Female
• Hormone Replacement Therapy
• Humans
• Kidney Neoplasms/drug therapy
• Liver Neoplasms/drug therapy
• Lung Neoplasms/drug therapy
• Melanoma/drug therapy
• Meningioma/drug therapy
• Menopause/drug effects
• Menopause/metabolism
• Neoplasms/drug therapy
• Ovarian Neoplasms/drug therapy
• Risk Factors
• Survivors
• Thyroid Neoplasms/drug therapy
• Urinary Bladder Neoplasms/drug therapy
• Uterine Cervical Neoplasms/drug therapy
• Vulvar Neoplasms/drug therapy

AIM: To explore the expression of fragile histidine triad (FHIT) and non-metastasis 23-H₁ (nm23-H₁) and to investigate their relations with clinicopathological behaviors of gastric cancer.

METHODS: PV9000 two-step immunohistochemical method was employed to detect the expression of FHIT and nm23-H₁ in 98 cases of gastric cancer.

RESULTS: The positive rates of FHIT and nm23-H₁ expression were 38.8% (38/98) and 33% (28/87) respectively. The FHIT expression related to the histological classification, Lauren classification and lymph node metastasis of gastric cancer (P < 0.05). The positive rate of FHIT protein expression became higher with the development of gastric cancer, but there was no significance (P > 0.05). The nm23-H₁ expression was negatively related to clinical staging and lymph node metastasis (P < 0.05).

CONCLUSION: FHIT may be an important candidate of tumor suppressor gene in gastric cancer. The expression of FHIT and nm23-H₁ protein has close relations with lymph node metastasis in gastric cancer, and they may work synergistically and can be important markers for predicting metastasis and evaluating prognosis of gastric cancer.

• N/A

N/A

• N/A

AIM: To investigate the relationship between the expression of VEGF, Flt1, bFGF and P⁵³, the clinicopathological characteristics and outcome in patients with gastric carcinoma.

METHODS: The relationship between VEGF, Flt1, bFGF, P⁵³ expression and clinicopathological characteristics and outcome in the patient was assessed by streptoavidin-biotin method of immunohistochemistry with polyclonal antibodies against VEGF, Flt1, bFGF, and P⁵³ protein. The survival curves were formulated using Kaplan-Meier method and analyzed by the log-rank test, and the influence of each variable on suvival was assessed by the Cox' s proportional hazard model.

RESULTS: VEGF expression was closely correlated with serosal invasion (Se, Sei invasion vs Pm, SS and M, SM invasion, P < 0.01). Expression of P⁵³ was obviously higher in the patients with lymph node metastasis than those without (lymph node metastasis vs non-lymph node metastasis, P < 0.05). There was a positive correlation between VEGF and Flt1 expression (VEGF expression in Flt1 positive group vs Flt1 negative group, P < 0.01). The factors that affected the prognosis in patients with gastric carcinoma were PTNM stage, VEGF expression, serosal invasion, and surgical curability. Flt1, bFGF, and P⁵³ expression had no influence on the prognosis of patients with gastric carcinoma (P > 0.05).

CONCLUSION: P⁵³ expression has significant relationship with lymph node metastasis in gastric carcinoma. VEGF expression is correlated with serosal invasion and the prognosis and may be a good prognostic indicator in gastric carcinoma.

• N/A

AIM: To explore the relationship between mitochondrial DNA (mtDNA) and gastric cancer by comparing the difference of mtDNA copy number in gastric cancers and paracancerous tissues.

METHODS: Hypervariable reigon (HV)₁ and HV₂ of mitochondrial D-loop region from 20 cases of gastric cancer and 20 paracancerous tissues were amplified by PCR; meantime b-actin was served as a quantitative standard marker, followed by polyacrylamide gel electrophoresis (PAGE) and silver staining, in which the difference of mtDNA copy number was compared between gastric cancers and paracancerous tissues.

RESULTS: There existed significantly quantitative difference in HV₁, HV₂ (standardized with b-actin) between gastric cancers and paracancerous tissues (P < 0.01). mtDNA copy number was associated with important enzymes in nucleus such as AKP, cAMP-PDE and cGMP-PDE (P < 0.05), although not with tumor histological type and invasive depth (P > 0.05).

CONCLUSION: The occurrence of gastric cancer is closely associated with decreased mtDNA copy number, which may be a new tumor marker.

• N/A