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Lei Shen

Publications and source records attributed to Lei Shen.

At least 19 recordsLinked to original sources

Contrasting redox-related physiological responses associated with HaGATA23 and HaGATA36 during Orobanche cumana parasitism in sunflower (Helianthus annuus L.).

Helianthus annuus is an economically important Asteraceae species used for seed oil production and ornamental purposes, but its production is seriously affected by the root-parasitic plant Orobanche cumana. GATA transcription factors are zinc-finger DNA-binding regulators involved in plant development and stress adaptation. However, the molecular characteristics of GATA transcription factors in Helianthus annuus and their contribution to Helianthus annuus -Orobanche cumana interaction remain poorly understood. Here, 36 HaGATA members were retrieved from the Helianthus annuus genome and classified into four phylogenetic clades. Chromosomal placement, collinearity, gene structure, motif composition, and promoter elements varied among the 36 HaGATA members, indicating evolutionary conservation coupled with functional diversification. Expression analysis and RT-qPCR analyses revealed differential expression patterns among HaGATA genes under O. cumana stress, with HaGATA23 markedly downregulated and HaGATA36 strongly upregulated. Overexpression of HaGATA23 was associated with increased malondialdehyde (MDA) accumulation and unfavorable changes in antioxidant enzyme activities, whereas its silencing showed the opposite physiological tendency. In contrast, overexpression of HaGATA36 reduced malondialdehyde accumulation, increased peroxidase (POD), catalase (CAT), and superoxide dismutase (SOD) activities, while its silencing showed the reverse tendency. These results indicate that HaGATA23 and HaGATA36 are candidate genes associated with contrasting redox-related physiological responses during O. cumana stress. This work provides evidence that GATA transcription factors are associated with redox-related physiological responses in sunflower under O. cumana treatment and identifies HaGATA23 and HaGATA36 as functionally divergent candidate genes for further validation.

Helianthus↗

Arginine methylation-dependent METTL14-SMN interaction regulates RNA m6A homeostasis.

N6-methyladenosine (m6A) homeostasis is essential for development, and its dysregulation is linked to cancers and neurological disorders. However, the mechanisms regulating m6A remain unclear. Here, we identify the survival of motoneuron (SMN) protein as a novel interaction partner of METTL14, a key component of the m6A methyltransferase complex. SMN binds METTL14 via its Tudor domain in an arginine methylation-dependent manner. Mutations in the SMN Tudor domain identified in spinal muscular atrophy (SMA) disrupt its interaction with METTL14 and reduce m6A levels in patient-derived fibroblasts, linking m6A dysregulation to SMA pathology. Both SMN knockdown and SMA mutations impair m6A deposition on the mRNAs of DNA repair genes, mirroring the effects of METTL14 hypomethylation. Consequently, SMA patient fibroblasts are hypersensitive to DNA-damaging agents due to reduced levels of DNA repair gene expression. To explore the function of METTL14 arginine methylation in vivo, we generated a Mettl14 methylation-deficient mouse model (Mettl14RK). Although this model does not show SMA-like phenotypes, the mutants are partially embryonic lethal and show abnormal hematopoiesis, underscoring a role for methylated METTL14 in early development.

Methyltransferases↗

Microenvironmental genomic alterations and clinicopathological behavior in head and neck squamous cell carcinoma.

CONTEXT: Carcinogens associated with head and neck squamous cell carcinoma (SCC) genesis should inflict genomic alterations not only on the epithelium but also the mesenchyme of the aerodigestive tract. Therefore, the apparently nonmalignant stroma surrounding the tumor epithelium can acquire genomic alterations and contribute to cancer initiation and progression. OBJECTIVES: To determine compartment-specific loci of loss of heterozygosity or allelic imbalance (LOH/AI) and to identify which genomic alterations restricted to the stroma cell population contribute to aggressiveness of head and neck SCC disease. DESIGN, SETTING, AND PATIENTS: Tumor epithelium and surrounding stroma were isolated from 122 US patients with oral cavity and oropharyngeal or hypopharyngeal SCC and subjected to whole-genome LOH/AI analysis using 366 microsatellite markers. Samples, collected between 2001 and 2004, were pulled and transferred in batches of 10 to 30 between 2002 and 2005. Laser capture microdissection DNA extraction and technical genotyping occurred on a rolling model between 2002 and November 2005. MAIN OUTCOME MEASURES: Compartment-specific frequency and distribution of LOH/AI were determined, and hot spots of genomic alterations identified. Compartment-specific LOH/AI events were correlated with presenting clinicopathologic characteristics. RESULTS: Tumor-associated stroma of head and neck SCC from smokers were found to have a high degree of genomic alterations. A correlation between tumor aggressiveness could be found for a specific set of 5 loci. Three stroma-specific loci (D4S2417, D3S360, and D19555) were associated with tumor size (pT) and regional nodal metastases (pN). Furthermore, 2 epithelial-specific LOH/AI hot spots were positively correlated with pN status and clinical stage. CONCLUSIONS: Stroma-specific genetic alterations are associated with smoking-related head and neck SCC genesis. These findings suggest novel prognostic or diagnostic biomarkers and identify potential new molecular targets for therapeutic and preventive intervention.

Aged↗

Prostaglandin E(2) protects human lung fibroblasts from cigarette smoke extract-induced apoptosis via EP(2) receptor activation.

Prostaglandin E(2) (PGE(2)) has been shown to have a strong cytoprotective effect, inhibiting apoptosis. In the present study, we evaluated whether PGE(2) has a protective effect on cigarette smoke extract (CSE)-induced apoptosis in human lung fibroblasts. Apoptosis was assessed by various methods, including DNA content analysis. CSE (15%-20%) led to apoptosis and induced imbalance in favor of pro- over anti-apoptotic protein expression and activated caspases. PGE(2) blocked CSE-induced apoptosis and modulated the balance of pro- and anti-apoptotic proteins and decreased the activation of caspases. This anti-apoptotic effect was mediated via EP(2) receptor activation as the EP(2) agonist butaprost mimicked PGE(2) activity and siRNA for the EP(2) receptor blocked it. An adenylyl cyclase inhibitor was found to abolish the PGE(2)-mediated cytoprotective effect. Correspondingly, c-AMP analogs blocked CSE-induced apoptosis. Consistently, the protein kinase A (PKA) inhibitor KT-5720 abolished PGE(2)-mediated protection. PGE(2) and butaprost phosphorylated Bad and KT-5720 blocked phosphorylation. These results suggest that PGE(2) inhibits CSE-induced apoptosis via EP(2) receptor activation and activation of PKA, which leads to an alteration in the balance between pro- and anti-apoptotic factors. Through such a mechanism, PGE(2) may alter survival of cells in the smoke-exposed lungs, thus affecting the pathogenesis of cigarette smoke-induced disease.

Adenylyl Cyclase Inhibitors↗

Using participant event monitoring in a cohort study of unintentional injuries among children and adolescents.

OBJECTIVES: We conducted a 3-year cohort study of 407 youths aged 9 to 18 years to develop multivariable risk prediction models of agriculture-related injuries. METHODS: Data were obtained via participant event monitoring, with youths self-reporting injuries and exposures in daily diaries over a 13-week period. We evaluated data quality by comparing injury self-reports with other injury data. RESULTS: Semilogarithmic plots of rates of all unintentional injuries combined (US data from 2000) as well as of agriculture-related injuries (US and Canadian data from 19 previous studies) graphed as a function of injury severity exhibited linearity, as did plots based on the present results. Severity-specific unintentional injury rates were 1.4- to 4.3-times higher than national rates, suggesting that our methodology can significantly reduce injury underreporting. In addition, at each severity level, estimated agriculture-related injury rates were 5.8- to 9.3-times higher than rates from previous national, regional, and state-based studies. CONCLUSIONS: Our approach to participant event monitoring can be implemented with youths aged 9 to 18 years and will yield reliable daily data on unintentional injuries.

Accidents, Occupational↗

Endoscopic findings and pathologic characteristics of gastric eosinophilic granuloma: a report of 18 patients.

AIM: To investigate the endoscopic findings and patholo-gic characteristics of gastric eosinophilic granuloma (GEG). METHODS: A retrospective study of 18 cases of gastric eosinophilic granulomas was conducted. Gastroscopy was performed and all specimens of biopsies were stained by HE and observed under light microscopy. RESULTS: Ulcer was the most frequent endoscopic appearance. The others included deformed pylorus and/or duodenal bulb, esophagitis, mucous hyperemia and/or mucosal erosion. Eosinophilic cell infiltration and generous hyperplasia of arterioles, venules and lymph vessels were found in the lesions of the patients. Interstitium had massive eosinophilic infiltrates and was made up of collagen fibers and fibroblasts. Lymphoid follicles were revealed in some sections of biopsies. CONCLUSION: GEG is lack of specific symptoms and physical signs. It can be misdiagnosed as gastric ulcer in most cases before biopsies. Endoscopy and endoscopic multiple deep biopsies in suspected areas are indispensable for correct diagnosis of GEG.

Adult↗

Time-dependent recordkeeping fatigue among youth completing health diaries of unintentional injuries.

PROBLEM: Increasingly, investigators are asking youth to self-report daily activity patterns and health outcomes in diary studies. This study assesses recordkeeping fatigue with respect to data quality and event reporting among youth participating in a health diary study. METHOD: Unintentional injury data were collected during a 13-week longitudinal diary study of Ohio youth exposed to agricultural hazards. Two analyses were conducted using data from 2000. Analysis 1 examined trends in discernable recordkeeping errors (DREs) over the course of follow-up. Analysis 2 assessed trends in injury reporting over follow-up. RESULTS: The percentage of items containing a DRE showed a slight, non-significant decline throughout follow-up. Injury reporting declined significantly (p<0.001) over follow-up. SUMMARY: There was no compelling evidence of respondent fatigue with respect to DREs. The observed decline in injury reporting is problematic because estimates of youth injury incidence in health diary studies may vary depending upon the length of the follow-up period.

Adolescent↗

Mutation-positive and mutation-negative patients with Cowden and Bannayan-Riley-Ruvalcaba syndromes associated with distinct 10q haplotypes.

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) encodes a tumor-suppressor phosphatase frequently mutated in both sporadic and heritable forms of human cancer. Germline mutations are associated with a number of heritable cancer syndromes that are jointly referred to as the "PTEN hamartoma tumor syndrome" (PHTS) and include Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Proteus-like syndrome. Germline PTEN mutations have been identified in a significant proportion of patients with PHTS; however, there are still many individuals with classic diagnostic features for whom mutations have yet to be identified. To address this, we took a haplotype-based approach and investigated the association of specific genomic regions of the PTEN locus with PHTS. We found this locus to be characterized by three distinct haplotype blocks 33 kb, 65 kb, and 43 kb in length. Comparisons of the haplotype distributions for all three blocks differed significantly among patients with PHTS and controls (P=.0098, P<.0001, and P<.0001 for blocks 1, 2, and 3, respectively). "Rare" haplotype blocks and extended haplotypes account for two-to-threefold more PHTS chromosomes than control chromosomes. PTEN mutation-negative patients are strongly associated with a haplotype block spanning a region upstream of PTEN and the gene's first intron (P=.0027). Furthermore, allelic combinations contribute to the phenotypic complexity of this syndrome. Taken together, these data suggest that specific haplotypes and rare alleles underlie the disease etiology in these sample populations; constitute low-penetrance, modifying loci; and, specifically in the case of patients with PHTS for whom traditional mutations have yet to be identified, may harbor pathogenic variant(s) that have escaped detection by standard PTEN mutation-scanning methodologies.

Alleles↗

Distinct expression profiles for PTEN transcript and its splice variants in Cowden syndrome and Bannayan-Riley-Ruvalcaba syndrome.

Cowden syndrome (CS) and Bannayan-Riley-Ruvalcaba syndrome (BRRS) are autosomal dominant hamartoma syndromes. Germline PTEN mutations have been associated with 85% of CS cases and 65% of BRRS cases and also with other disorders, which are collectively referred to as the "PTEN hamartoma tumor syndrome." The human PTEN gene has been previously found to express two naturally occurring splice variants (SVs). Recently, we identified eight novel naturally occurring PTEN SVs that result in different downstream signaling effects: SV3a, SV3b, SV3c (inclusion of various lengths of intron 3 3' of exon 3), SV5a, SV5b, SV5c, SV5d (inclusion of various lengths of intron 5 3' of exon 5), and SV Delta Ex6 (deletion of exon 6). We therefore sought to characterize the relative expression of 5', middle, and 3' full-length PTEN mRNA (FL-PTEN) and also of these eight PTEN SVs in 85 (65 female and 20 male) patients with CS/BRRS (with or without PTEN mutations) compared with 27 controls, using a SYBR green quantitative polymerase chain reaction method. Significantly reduced FL-PTEN levels were found in the probands, compared with those of controls (P < .01). Apart from FL-PTEN, SV3a is the most consistently relatively underexpressed in patients compared with controls. The patients showed relative underexpression of SV3a and SV3b and overexpression of SV5b (P = .005, P = .02, and P = .04, respectively). Indeed, there appears to be an SV expressional genotype-phenotype correlation in which the SV expressional profiles are distinct among CS, CS-like, and BRRS. The reduced FL-PTEN transcript expression, associated with differential expression of PTEN SVs, regardless of PTEN mutation status, supports the concept that modulation of PTEN inactivation may also occur at the transcription level influencing the specific phenotypes seen in these syndromes.

Base Sequence↗

Photoelectron imaging of propanal by resonant multiphoton ionization via the 3s Rydberg state.

We report the conformationally- and vibrationally-selected photoelectron spectroscopy of propanal obtained by resonance-enhanced multiphoton ionization (REMPI) using photoelectron imaging. These photoelectron spectra, employing (2 + 1) ionization via the (n, 3s) Rydberg transitions in the range from 365 to 371 nm, confirm that there are two stable conformer origins in the lowest ionic state, the cis conformer with a co-planar CCCO geometry and a gauche conformer with a approximately 119 degrees CCCO dihedral angle. From ab initio calculations at the B3LYP/6-311++G** level, we find the gauche conformer is slightly more stable, with the energy difference between two conformers determined to be only 65 cm(-1). In our photoelectron spectra, the vertical ionization potential (IP) for the cis conformer of propanal was then determined to be 9.999 (+/-0.003) eV, while that of the gauche conformer of propanal was estimated to be 9.944 eV. A long vibrational progression in the in-plane CCCO deformation vibrational mode, v, for the cis conformer is systematically observed in all photoelectron spectra in which this mode is excited, suggesting that the geometry of the ground ionic state is significantly different from that of the 3s Rydberg state, particularly along the v(15) coordinates.

Aldehydes↗

Total-genome analysis of BRCA1/2-related invasive carcinomas of the breast identifies tumor stroma as potential landscaper for neoplastic initiation.

We have shown that the tumor microenvironment of sporadic breast cancer is diverse in genetic alterations and contributes to the cancer phenotype. The dynamic morphology of the mammary gland might be of special interest in hereditary breast/ovarian cancer syndrome (HBOC). We hypothesized that hotspots of loss of heterozygosity or allelic imbalance (LOH/AI) within the tumor stroma of BRCA1/2-related breast cancers provide an impaired mammary stroma that could facilitate later malignant transformation of the breast epithelium. We conducted a total genome LOH/AI scan of DNA derived from the epithelium and stroma of 51 BRCA1/2-related breast cancers, using 372 microsatellite markers. We compared these data with those from a set of 134 sporadic breast cancers. HBOC-related breast cancers accumulated significantly more genetic alterations than did sporadic breast cancers. BRCA1/2-related breast cancer stroma showed LOH/AI at 59.7% of all loci analyzed, similar to the average frequency of LOH/AI observed in the epithelium (66.2%). This is remarkably different from sporadic breast cancers, for which the average epithelial LOH/AI frequency (36.7%) far exceeds the average stromal LOH/AI frequency (28.4%) (P=.03). We identified 11 hotspot loci of LOH/AI in the BRCA1/2 stroma, encompassing genes such as POLD1, which functions in DNA replication, and SDHB. In a subset of samples, enriched for BRCA1 cases, we found 45.0% overall LOH/AI in the stroma, which was significantly higher than the 41.8% LOH/AI observed in corresponding epithelium (P=.04). Together, our data indicate that, in HBOC-related breast cancers, the accumulation of genomic instability in the cancer stroma coincides with that in the neoplastic epithelium, and we postulate that such a genetically unstable stroma might facilitate a microenvironment that functions as a landscaper that promotes genomic instability in the epithelium and, subsequently, neoplastic transformation.

Adult↗

Correlation between ultrasonographic and pathologic diagnosis of liver fibrosis due to chronic virus hepatitis.

AIM: To evaluate the validity of ultrasonographic and pathologic diagnosis of liver fibrosis in patients with chronic viral hepatitis. METHODS: The liver fibrosis status in 324 patients was evaluated by both needle biopsy and ultrasonography. Liver fibrosis was divided into S0-S4 stages. S4 stage was designated as definite cirrhosis. The ultrasonographic examination included qualitative variables, description of liver surface and parenchyma, and quantitative parameters, such as diameter of vessels, blood flow velocity and spleen size. RESULTS: Ultrasonographic qualitative description of liver surface and parenchyma was related with the severity of fibrosis. Among the quantitative ultrasonographic parameters, cut-off value of spleen length (12.1 cm) had a sensitivity of 0.600 and a specificity of 0.753 for diagnosis of liver cirrhosis. The diameters of spleen (8 mm) and portal vein (12 mm) had a diagnostic sensitivity of 0.600 and 0.767, and a diagnostic specificity of 0.781 and 0.446, respectively. The diagnostic accuracy for liver cirrhosis was moderately satisfactory, and the negative predictive values of these parameters reached near 0.95. CONCLUSION: Ultrasonography can predict the degree of liver fibrosis or cirrhosis. A single ultrasonographic parameter is limited in sensitivity and specificity for the diagnosis of early cirrhosis. The presence or absence of liver cirrhosis in patients with chronic virus hepatitis can be detected using 2 or 3 quantitative and qualitative parameters, especially the length of spleen, the diameter of spleen vein and echo pattern of liver surface.

Adolescent↗

Reactive nitrogen species augment fibroblast-mediated collagen gel contraction, mediator production, and chemotaxis.

Reactive nitrogen species (RNS) such as peroxynitrite cause cellular injury and tissue inflammation. Excessive production of nitrotyrosine, which is a footprint of RNS, has been observed in the airways of patients with asthma and chronic obstructive pulmonary disease, disorders characterized by tissue remodeling. The aim of this study was to evaluate whether RNS can affect tissue remodeling through direct effects on fibroblasts, and to determine if these effects depend on production of transforming growth factor-beta (TGF-beta). To accomplish this, human fetal lung fibroblasts (HFL-1) were used to assess fibroblast-mediated contraction of floating gels and chemotaxis toward fibronectin. In addition, the ability of fibroblasts to release TGF-beta1, fibronectin, and vascular endothelial growth factor (VEGF) was assessed by enzyme-linked immunosorbent assay. Authentic peroxynitrite significantly augmented gel contraction (P < 0.01) and chemotaxis (P < 0.01) compared with control in a concentration-dependent manner. Similarly, the peroxynitrite donor 3-morpholynosidenonimine hydrochloride (SIN-1) also augmented gel contraction (P < 0.01). RNS also significantly increased TGF-beta1 (P < 0.01), fibronectin (P < 0.01), and VEGF (P < 0.01) release into the media in both 3D gel and monolayer culture. Anti-TGF-beta antibody reversed RNS-augmented gel contraction (P < 0.01) and mediator production (P < 0.01). Anti-TGF-beta antibody also partially, but significantly, reversed RNS-augmented chemotaxis toward fibronectin (P < 0.01). Finally, peroxynitrite enhanced expression of alpha5beta1 integrin, which is a receptor for fibronectin (P < 0.01), and neutralizing anti-TGF-beta antibody suppressed peroxynitrite-augmented alpha5beta1 expression (P < 0.01). These results suggest that RNS can affect the tissue repair process by modulating TGF-beta1.

Animals↗

Pro- and antiinflammatory cytokine signaling: reciprocal antagonism regulates interferon-gamma production by human natural killer cells.

Activated monocytes produce proinflammatory cytokines (monokines) such as interleukin (IL)-12, IL-15, and IL-18 for induction of interferon-gamma (IFN-gamma) by natural killer (NK) cells. NK cells provide the antiinflammatory cytokine transforming growth factor (TGF)-beta, an autocrine/negative regulator of IFN-gamma. The ability of one signaling pathway to prevail over the other is likely important in controlling IFN-gamma for the purposes of infection and autoimmunity, but the molecular mechanism(s) of how this counterregulation occurs is unknown. Here we show that in isolated human NK cells, proinflammatory monokines antagonize antiinflammatory TGF-beta signaling by downregulating the expression of the TGF-beta type II receptor, and its signaling intermediates SMAD2 and SMAD3. In contrast, TGF-beta utilizes SMAD2, SMAD3, and SMAD4 to suppress IFN-gamma and T-BET, a positive regulator of IFN-gamma. Indeed, activated NK cells from Smad3(-/-) mice produce more IFN-gamma in vivo than NK cells from wild-type mice. Collectively, our data suggest that pro- and antiinflammatory cytokine signaling reciprocally antagonize each other in an effort to prevail in the regulation of NK cell IFN-gamma production.

Animals↗

[Peripheral plasma Big endothelin 1 levels in patients with gastric carcinoma undergoing radical gastrectomy and its relationship with tumor recurrence].

OBJECTIVE: To investigate the plasma Big endothelin-1 levels in patients with gastric carcinoma before and after radical gastrectomy, and explore its clinical significance. METHODS: One hundred and six patients with gastric carcinoma and 20 controls were enrolled. The Big ET-1 plasma levels were examined by enzyme-linked immuno absorbent assay before and on the 1st, 3rd, and 10th day after curative surgery, and then were tested every 3 months in the patients with advanced gastric cancer. RESULTS: All patients, except those with stage I gastric cancer, had significantly higher mean plasma Big ET-1 levels compared with normal controls (P=0.000). Higher plasma Big ET-1 levels were associated with lymph node metastasis (P=0.020) and serosal infiltration (P=0.035). The plasma Big Endothelin-1 levels were markedly increased on the first post-operative day (1st POD) in all patients,but decreased on the 3rd POD with no significant difference compared to the preoperative levels. On the 10th POD, the patients with stage I and II gastric cancer showed marked reduction in plasma Big ET-1 levels (P=0.010 and P=0.000, respectively), whereas no significant difference was observed in stage III and IV patients. During the follow-up, the plasma Big ET-1 levels just before recurrence in stage II patients were significantly higher compared with the levels on the 10th POD (P=0.011). CONCLUSIONS: Plasma Big ET-1 might be a reliable marker to determine the severity of gastric carcinoma. Monitoring plasma Big ET-1 levels after curative resection in stage II gastric cancer patients is valuable to predict recurrence.

Adult↗

[Molecular cloning of a novel low-molecular-weight glutenin subunit gene from wheat variety "Chuanmai 42"].

Using PCR-amplification method, the coding sequences of a novel low-molecular-weight glutenin (LMW-GS) gene, LMWCM42-1, was isolated from the genomic DNA of wheat (Triticum aestivum L.) variety 'Chuanmai 42'. The full coding region of this gene consisted of 846 nucleotides, and encoded a protein with 281 amino acids. LMWCM42-1 is a typical low-molecular-weight glutenin subunit (LMW-GS) gene. In spite of high similarity with the known LMW-GSs, LMWCM42-1 was quite different from the known LMW-GS in the N-terminal, central repetitive domain and C-terminal domain. It was found that LMWCM42-1 was located within the Glu-D3 locus by phylogenetic analysis.

Amino Acid Sequence↗

[Endometrial adenocarcinoma in women 40 years old or younger by treatment with progestins: report of 6 cases and review of the literatures].

OBJECTIVE: To evaluate the effectiveness and safety of fertility-sparing treatment with progestins in patients with well-differentiated endometrial adenocarcinoma in women 40 years old or younger. METHODS: Six patients before the age of 40 diagnosed with grade I endometrial adenocarcinoma, who had undergone primary progestin treatment, were retrospectively studied. The clinical records and pathologic slides and the follow-up information were reviewed. Relevant articles describing patients with endometrial adenocarcinoma who were treated with hormonal therapy were searched. A total of 56 cases were found and used in integrated analysis. RESULTS: Four of six cases responded to treatment with normal pathology on follow-up endometrial samplings. Two patients had a recurrence within a period between 10 and 12 months. No response was noted in the other two cases, who were offered surgery. Therefore, a total of 4 patients ultimately underwent hysterectomy. None of these four patients had extrauterine metastasis on postoperation pathologic examination. All these six patients were alive without evidence of disease at last follow-up. According to literatures, 46 of 56 cases responded to hormonal treatment and 11 cases had a recurrence. Seven of the 11 patients who recurred were re-treated with progesterone. Five patients had a second complete response. Sixteen of the 56 patients underwent hysterectomy. One of the patients had a pelvic recurrence after operation. The others remained without evidence of disease. Six patients in author's group had neither pregnancy nor delivery. Among 56 patients described in literatures, there were 41 person-times pregnancies and 40 infants were delivered, including 4 twins and 2 triples. CONCLUSIONS: Progestin treatment is proved a safe and feasible therapy in well-differentiated endometrial adenocarcinoma in women 40 years old or younger. This approach may provide the possibility of conceiving and carrying a pregnancy with the aid of assisted reproduction technology.

Adenocarcinoma↗

[Influence of LY294002 on protein kinase B expression in salivary adenoid cystic carcinoma (SACC)-83 and SACC-LM cells].

OBJECTIVE: To investigate the influence of LY294002 on protein kinase B expression in salivary adenoid cystic carcinoma cells (SACC). METHODS: Using Western-blot and RT-PCR detected the protein and mRNA level of protein kinase B (PKB) both in cell line, absent and present LY294002. The data were analysed by t-test. RESULTS: The expression and transcription level of PKB (Ser(473)) in SACC-83 was lower than in SACC-LM (P < 0.05). The expression of PKB (Ser(473)) in SACC cell lines with LY294002 was lower than in SACC cell lines without LY294002 (P < 0.01). The transcription level of PKB showed no difference in SACC cell lines with and without LY294002 (P > 0.05). CONCLUSIONS: In vitro, the protein expression and transcription level of PKB (Ser(473)) is higher in SACC-LM cell line than in SACC-83 cell line. In vitro, LY294002 can inhibit protein expression of PKB (Ser(473)) in SACC-83 cells and SACC-LM cells.

Carcinoma, Adenoid Cystic↗