Tensin Homolog Gene Research Articles

Quantitative and qualitative characterization of two PTEN clones: SP218 and 138G6.

e23266Background: The PTEN(phosphatase and tensin homolog) gene, commonly deleted on chromosome ten, encodes for a tumor suppressing protein which regulates cellular differentiation and proliferati...

Integration and bioinformatics analysis of DNA-methylated genes associated with drug resistance in ovarian cancer.

The main obstacle to the successful treatment of ovarian cancer is the development of drug resistance to combined chemotherapy. Among all the factors associated with drug resistance, DNA methylation apparently plays a critical role. In this study, we performed an integrative analysis of the 26 DNA-methylated genes associated with drug resistance in ovarian cancer, and the genes were further evaluated by comprehensive bioinformatics analysis including gene/protein interaction, biological process enrichment and annotation. The results from the protein interaction analyses revealed that at least 20 of these 26 methylated genes are present in the protein interaction network, indicating that they interact with each other, have a correlation in function, and may participate as a whole in the regulation of ovarian cancer drug resistance. There is a direct interaction between the phosphatase and tensin homolog (PTEN) gene and at least half of the other genes, indicating that PTEN may possess core regulatory functions among these genes. Biological process enrichment and annotation demonstrated that most of these methylated genes were significantly associated with apoptosis, which is possibly an essential way for these genes to be involved in the regulation of multidrug resistance in ovarian cancer. In addition, a comprehensive analysis of clinical factors revealed that the methylation level of genes that are associated with the regulation of drug resistance in ovarian cancer was significantly correlated with the prognosis of ovarian cancer. Overall, this study preliminarily explains the potential correlation between the genes with DNA methylation and drug resistance in ovarian cancer. This finding has significance for our understanding of the regulation of resistant ovarian cancer by methylated genes, the treatment of ovarian cancer, and improvement of the prognosis of ovarian cancer.

Early Behavioral Abnormalities and Perinatal Alterations of PTEN/AKT Pathway in Valproic Acid Autism Model Mice.

Exposure to valproic acid (VPA) during pregnancy has been linked with increased incidence of autism, and has repeatedly been demonstrated as a useful autism mouse model. We examined the early behavioral and anatomical changes as well as molecular changes in mice prenatally exposed to VPA (VPA mice). In this study, we first showed that VPA mice showed developmental delays as assessed with self-righting, eye opening tests and impaired social recognition. In addition, we provide the first evidence that primary cultured neurons from VPA-treated embryos present an increase in dendritic spines, compared with those from control mice. Mutations in phosphatase and tensin homolog (PTEN) gene are also known to be associated with autism, and mice with PTEN knockout show autistic characteristics. Protein expression of PTEN was decreased and the ratio of p-AKT/AKT was increased in the cerebral cortex and the hippocampus, and a distinctive anatomical change in the CA1 region of the hippocampus was observed. Taken together, our study suggests that prenatal exposure to VPA induces developmental delays and neuroanatomical changes via the reduction of PTEN level and these changes were detectable in the early days of life.

Genodermatosis Affecting the Skin and Mucosa of the Head and Neck: Clinicopathologic, Genetic, and Molecular Aspect--PTEN-Hamartoma Tumor Syndrome/Cowden Syndrome.

PTEN hamartoma tumor syndrome refers to a spectrum of disorders caused by mutations in the phosphatase and tensin homolog (PTEN) gene. Cowden syndrome, the principal PTEN-related disorder is characterized by multiple neoplasms and hamartomas, mucosal papillomatosis, and skin lesions, trichilemmomas. Trichilemmomas and mucocutaneous papillomatous papules are one of the first signs of the disease. Early recognition of these skin lesions may help on diagnosing an underlying malignancy and early cancer screening.

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells.

Brain damage caused by perinatal asphyxia is dangerous for neonatal infants, but the mechanism by which it occurs remains elusive. In this study, microRNA-152 (miR-152) expression was induced by low oxygen levels in rat models of hypoxia brain damage, as well as in human brain microvascular endothelial cells (HBMECs) cultured in vitro. Analysis of the sequence of miR-152 revealed that the phosphatase and tensin homolog gene (PTEN) is probably the target of miR-152 both in humans and rats. When HBMECs were transfected with miR-152 mimics, PTEN expression was inhibited at both the mRNA and protein levels. Moreover, transfection with the miR-152 mimic also inhibited apoptosis induced by hypoxia. Furthermore, expression of the pro-apoptotic gene Bax was downregulated while the anti-apoptotic gene Bcl2 was upregulated after miR-152 mimic transfection. Taken together, these results indicate that miR-152 induced by hypoxia suppresses cell apoptosis and acts as a protective factor during hypoxia by repressing PTEN.

Lhermitte-Duclos disease with neurofibrillary tangles in heterotopic cerebral grey matter

Lhermitte-Duclos disease (LDD), a disorder first described by French physicians Lhermitte and Duclos in 1920 [25], is a benign, slow growing dysplastic gangliocytoma of the cerebellum, characterized by replacement of the granule cell layer by abnormal granule and Purkinje like cells. The most frequent presenting signs and symptoms are megalocephaly, increased intracranial pressure, nausea, hydrocephalus, ataxia, gait abnormalities, and intermittent headaches, all of which are attributed to the mass effect [6,11,25]. Many cases are associated with a mutation in the phosphatase and tensin homolog or PTEN gene which is also involved in numerous otherwise unrelated central nervous system abnormalities, namely Cowden syndrome [1,6,11], autism spectrum disorder [18], cerebral cortical dysplasia [11,30] and Bannayan-Riley-Ruvalcaba syndrome [30]. The presence of cortical heterotopia has been reported in a small number of LDD cases [3,5,17,32]. We describe a unique case of LDD with cerebral cortical heterotopic grey matter containing neurofibrillary tangles.

PTEN and p16 genes as epigenetic biomarkers in oral squamous cell carcinoma (OSCC): a study on south Indian population.

Phosphatase and tensin homolog (PTEN) and p16INK4a (p16) genes are tumor suppressor genes, associated with epigenetic alterations. PTEN and p16 promoter hypermethylation is a major epigenetic silencing mechanism leading to cancer. The cooperation between PTEN and p16 in pathogenesis of cancers suggest that their combination might be considered as potential molecular marker for specific subgroups of patients. Hence, the present study aimed to investigate whether PTEN and p16 promoter methylations were involved in oral squamous cell carcinoma (OSCC) in south Indian subjects. DNA methylation quantitative analyses of the two candidate tumor suppressor genes PTEN and p16 were performed by methylation-specific polymerase chain reaction (MSP). Fifty OSCC biopsy samples and their corresponding non-malignant portions as controls were studied comparatively. The methylation status was correlated with the clinical manifestations. Twelve out of 50 patients (24%) were found to be methylated for PTEN gene, whereas methylation of the p16 gene occurred in 19 out of 50 cases (38%). A statistically significant result was obtained (P = <0.0001 and 0.017) for both PTEN and p16 genes. PTEN and p16 promoter methylation may be the main mechanism leading to the low expression of PTEN and p16 genes indicating the progress of tumor development. Our data suggest that a low PTEN and p16 expression due to methylation may contribute to the cancer progression and could be useful for prognosis of OSCC. Therefore, analysis of promoter methylation in such genes may provide a biomarker valuable for early detection of oral cancer.

The PTEN tumor suppressor gene and its role in lymphoma pathogenesis.

The phosphatase and tensin homolog gene PTEN is one of the most frequently mutated tumor suppressor genes in human cancer. Loss of PTEN function occurs in a variety of human cancers via its mutation, deletion, transcriptional silencing, or protein instability. PTEN deficiency in cancer has been associated with advanced disease, chemotherapy resistance, and poor survival. Impaired PTEN function, which antagonizes phosphoinositide 3-kinase (PI3K) signaling, causes the accumulation of phosphatidylinositol (3,4,5)-triphosphate and thereby the suppression of downstream components of the PI3K pathway, including the protein kinase B and mammalian target of rapamycin kinases. In addition to having lipid phosphorylation activity, PTEN has critical roles in the regulation of genomic instability, DNA repair, stem cell self-renewal, cellular senescence, and cell migration. Although PTEN deficiency in solid tumors has been studied extensively, rare studies have investigated PTEN alteration in lymphoid malignancies. However, genomic or epigenomic aberrations of PTEN and dysregulated signaling are likely critical in lymphoma pathogenesis and progression. This review provides updated summary on the role of PTEN deficiency in human cancers, specifically in lymphoid malignancies; the molecular mechanisms of PTEN regulation; and the distinct functions of nuclear PTEN. Therapeutic strategies for rescuing PTEN deficiency in human cancers are proposed.

FSH Regulates mRNA Translation in Mouse Oocytes and Promotes Developmental Competence.

A major challenge in assisted reproductive technology is to develop conditions for in vitro oocyte maturation yielding high-quality eggs. Efforts are underway to assess whether known hormonal and local factors play a role in oocyte developmental competence and to identify the molecular mechanism involved. Here we have tested the hypothesis that FSH improves oocyte developmental competence by regulating the translational program in the oocyte. Accumulation of oocyte proteins (targeting protein for the Xenopus kinesin xklp2 and IL-7) associated with improved oocyte quality is increased when cumulus-oocyte complexes are incubated with FSH. This increase is due to enhanced translation of the corresponding mRNAs, as indicated by microinjection of constructs in which the 3' untranslated region of the Tpx2 or Il7 transcripts is fused to the luciferase reporter. A transient activation of the phosphatidyl-inositol 3-phosphate/AKT cascade in the oocyte preceded the increase in translation. When the epidermal growth factor (EGF) receptor is down-regulated in follicular cells, the FSH-induced rate of maternal mRNA translation and AKT activation were lost, demonstrating that the effects of FSH are indirect and require EGF receptor signaling in the somatic compartment. Using Pten(fl/fl):Zp3cre oocytes in which the AKT is constitutively activated, translation of reporters was increased and was no longer sensitive to FSH stimulation. More importantly, the oocytes lacking the phosphate and tensin homolog gene showed increased developmental competence, even when cultured in the absence of FSH or growth factors. Thus, we demonstrate that FSH intersects with the follicular EGF network to activate the phosphatidyl-inositol 3-phosphate/AKT cascade in the oocyte to control translation and developmental competence. These findings provide a molecular rationale for the use of FSH to improve egg quality.

Association of genetic polymorphisms in PTEN and additional gene-gene interaction with risk of esophageal squamous cell carcinoma in Chinese Han population.

This study aims to investigate the association of five single nucleotide polymorphisms (SNPs) in the phosphatase and tensin homologue (PTEN) gene and additional role of gene-gene interaction with esophageal squamous cell carcinoma (ESCC), based on a Chinese case-control study. A total of 871 subjects (420 males and 451 females) were selected, including 425 ESCC cases and 446 controls. Five SNPs were selected for genotyping in the case-control study: rs2735343, rs555895, rs2299939, rs17431184 and rs701848. Logistic regression model was used to examine the association between five SNP and ESCC, and additional interaction among five SNP, odds ratio (OR) and 95% confident interval (95%CI) were calculated. All genotypes were distributed according to Hardy-Weinberg equilibrium in controls. The carriers of homozygous mutant of rs2735343 and rs701848 polymorphism revealed increased ESCC risk than those with wild-type homozygotes, and OR (95%CI) were 1.27 (1.09-2.08) and 1.45 (1.17-1.98), respectively. We also found a potential gene-gene interaction between rs2735343 and rs701848 (P = 0.0010), and a potential gene-gene interaction among all five SNP (P = 0.0107) after covariates adjustment. Subjects with TC or CC of rs2735343 and TC or CC of rs701848 genotype have highest ESCC risk, compared to subjects with TT of rs2735343 and TT of rs701848 genotype, OR (95% CI) was 2.76 (1.37-3.45) after covariates adjustment. The carriers of homozygous mutant of rs2735343 and rs701848 polymorphism revealed increased ESCC risk. We also found a potential gene-gene interaction between rs2735343 and rs701848 and a potential gene-gene interaction among all five SNPs.

ATPS-88TEMOZOLOMIDE AND EVEROLIMUS IN THE TREATMENT OF PAPILLARY TUMOR OF THE PINEAL REGION

Papillary tumor of the pineal region (PTPR) is a rare neuroepithelial tumor thought to arise from the ependymal cells of the subcommissural organ which was first described in 2003 and subsequently classified as a Grade II-III tumor in the WHO registry in 2007. They tend to be well-circumscribed, occasionally cystic tumors that, histologically, consist of sheets of epithelioid cells and perivascular pseudorosettes with papillary structures consisting of cuboidal cells. These tumors have a high rate of local recurrence but infrequent CSF dissemination. Because fewer than 100 cases have been reported, a consensus on treatment has not been reached, though maximal surgical resection correlates with a better prognosis and radiotherapy may confer a benefit, as well. The role of chemotherapy remains unclear and regimens including procarbazine, lomustine, and vincristine as well at temozolomide have been reported. Recently, chromosome 10 deletions and mutations in the PTEN (phosphatase and tensin homolog) gene located on chromosome 10 are common in PTPR. Because PTEN is involved in the PI3K/Akt/mTOR signaling pathway, mTOR inhibitors, such as everolimus may be effective against this tumor type. We present a patient with PTPR who underwent complete resection followed by local radiotherapy. He later developed leptomeningeal disease and underwent whole brain radiation therapy. He was also treated with metronomic temozolomide and subsequently by everolimus after he developed a temozolomide-resistant durally-based metastatic lesion.

The Interaction Between Androgen Receptor and PDGF-D in the Radiation Response of a Human Prostate Cancer Cell Line

The Interaction Between Androgen Receptor and PDGF-D in the Radiation Response of a Human Prostate Cancer Cell Line

Small Bowel Polyposis Without Diagnosis

A 19 year old male presents with nausea and vomiting. He is treated for gastroenteritis but returns with intussusception and small bowel obstruction that is managed conservatively. Two months later the intussusception recurs with 30 pound weight loss and hematochezia. An exploratory laparotomy is performed and a segment of jejunum with carpeting polyps is resected. He denies a history of cognitive delay and mucocutaneous freckling. On physical exam he is well-developed with a head circumference of 62cm. He has normal abdominal, skin, genital and neurologic exams. Upper endoscopy shows H. pylori gastritis and a stricture at the surgical anastomosis which is dilated. A colonoscopy and capsule endoscopy reveal only lymphoid follicles in the terminal ileum. Pathology from the jejunal resection is significant for hamartomatous polyps containing gastric type tissue. The patient's clinical condition is most consistent with Cowden Syndrome/PTEN Hamartoma Syndrome. He undergoes genetic testing that reveals a variant of uncertain significance (VUS) in the phosphatase and tensin homolog (PTEN) gene. Cowden syndrome is a rare genetic condition that carries an increased risk for multiple cancers. Our patient had two major clinical criteria, macrocephaly (>97th percentile) and hamartomatous intestinal polyps. Approximately 85% of individuals with an operational diagnosis of Cowden syndrome have autosomal dominant mutations identified in the PTEN gene on chromosome 10, which acts as a negative regulator of cell cycle pathways including mTOR and PI3K-AKT. Mutations can be deleterious or a VUS. Our case is unique in that the polyps architecturally resembled Peutz-Jeghers Syndrome (PJS) with an arborizing lamina propria and a lack of significant inflammation or dysplasia. However, the polyps were almost entirely composed of gastric foveolar and pyloric type mucosa, which is highly atypical in small bowel PJS. Furthermore, there have been few reports of small bowel hamartomas associated with Cowden syndrome, and none involving the jejunum to our knowledge. The patient also did not have any classic mucocutaneous findings or family members with a similar phenotype. Up to 44% of CS/PTHS cases arise from de novo PTEN mutations. It is not yet known if his VUS impacts protein function and/or predisposes to increased cancer risk. It is also unclear if the H. pylori infection contributed to his polyposis, however polyp regression after antibiotic therapy is reported.Figure 1Figure 2Figure 3

Frequency of PTEN alterations, TMPRSS2-ERG fusion and their association in prostate cancer

BackgroundPhosphatase and tensin homolog (PTEN) gene aberration and trans membrane protease, serine 2 (TMPRSS2)–v-ets avian erythroblastosis virus E26 oncogene homolog (ERG) fusion are the most prevalent genomic events in prostate cancer. In this study we aimed to evaluate the frequency of PTEN alteration and TMPRSS2-ERG fusion and possible link between these two biomarkers in Iranian men. MethodsWe assessed 42 fresh frozen tissue samples of prostate cancer (PCA) obtained by radical prostatectomy, interrogating the TMPRSS2-ERG fusion gene along with PTEN gene status using Real Time PCR and FISH methods. ResultsUsing Real Time PCR we identified the TMPRSS2-ERG fusion in 64% (27/42) of tumor samples, which was confirmed by FISH technique, giving 21 positive samples with deletion, suggesting the presence of TMPRSS2-ERG fusion gene. By contrast, PTEN deletion was detected in 52% (11/21) of PCA samples, which all showed low expression in Real Time. Concomitance of PTEN deletion or low expression and TMPRSS2-ERG fusion was present in PCA samples (P=0.005). All of the PTEN deletion samples showed TMPRSS2-ERG fusion, (11/11, 100%) while not all of the TMPRSS2-ERG fusion positive samples showed PTEN deletion. None of 29 cases of BPH and 8 cases of normal zone of tumor tissue showed TMPRSS2-ERG fusion. ConclusionsThese results indicate that PTEN loss occurs in cooperation with TMPRSS2-ERG fusion in PCA. While the majority of PCA samples harbor TMPRSS2-ERG fusion as well as PTEN gene deletion, normal tissues do not show these molecular aberrations.

Effects of PTEN gene alteration in patients with gallbladder cancer

Gallbladder cancer (GBC) is an aggressive malignancy usually diagnosed in an advanced stage. We investigated the effects of alterations of the phosphatase and tensin homologue (PTEN) gene on the occurrence and development of GBC, which has not been previously reported. A total 141 cases of GBC were analyzed for mutation, expression, and methylation across the nine exons of the PTEN gene. DNA sequencing methods were applied for mutation detection, whereas protein expression and methylation status were evaluated by immunohistochemical and methylation-specific PCR analysis, respectively. Novel PTEN mutations were observed in 6.3% of cases (9/141), and they included two silent mutations. In mutant cases, according to changes in codons, the respective amino acid sequences were also changed, which caused of proteins. A high percentage (72%) of loss of protein expression was observed more often in cases than in control samples. Interestingly, all nine cases with mutations showed loss of PTEN expression, whereas four of these nine cases showed positive promoter methylation. Hypermethylation was significantly more common in older patients than in younger ones (P<0.02). These findings suggest that PTEN mutations and inactivation may play an important role in the development and progression of gallbladder carcinoma.

Abstract 2289: A novel mouse model of endometrial cancer: epithelial specific Pten deletion with lactoferrin-iCre

Abstract Endometrial cancer is a common gynecological malignancy, causing approximately 8,000 deaths each year in the United States. Underlying causes of endometrial cancer are not clearly understood, and treatment options for patients with advanced stages are limited. Animal models that spontaneously develop cancer are powerful tools for studying the mechanism of cancer initiation and progression and for developing treatment strategies. We previously created a mouse model of endometrial cancer in which the floxed phosphatase and tensin homologue (Pten) gene was deleted by Cre expression under the control of a progesterone receptor (PR) promoter. Pten is a tumor suppressor with the highest frequency of mutation in human endometrial cancer. In the PtenloxP/loxP/PR-Cre mouse model, uterine deletion of Pten resulted in complex atypical hyperplasia of the uterine epithelium by three weeks of age with cancer occurring by one month. As PR is expressed in the epithelium, stroma, and myometrium compartments, the question remains whether Pten deletion in the uterine epithelium alone contributes to endometrial cancer since human endometrial cancer is derived from epithelial cells. To address this question, we used lactoferrin-iCre (Ltf-Cre) mice to specifically delete Pten in the uterine epithelium, since lactoferrin is restricted to the epithelium of adult mice. We found that PtenloxP/loxP/Ltf-Cre mice develop complex atypical hyperplasia in uterine epithelium by three months of age, whereas uteri from immature mice are normal. These results demonstrate that Pten deletion specifically in the uterine epithelium can contribute to toward endometrial cancer in mice. This mouse model will help us to study in detail the initiation and progression of endometrial cancer. This study was supported in parts by grants from NIH-P01-CA-77839 (S. K. D). Citation Format: Takiko Daikoku, Jumpei Terakawa, Sudhansu K. Dey. A novel mouse model of endometrial cancer: epithelial specific Pten deletion with lactoferrin-iCre. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2289. doi:10.1158/1538-7445.AM2015-2289

Abstract 49: Mir-21 Contributes to Cardiac Aging by Targeting Pten

Background— Aging is among predominant risk factors for cardiovascular diseases and it also contributes to a significantly worse outcome in patients with acute myocardial infarction. MicroRNAs (miRNAs, miRs) have been indicated in aging. However, the regulatory mechanisms of miRNAs which govern the aging progress are poorly understood. Objective— To identify miRNAs responsible for cardiac aging besides miR-34 family members. Methods and Results— miRNA arrays were used to determine the dysregulated miRNAs in cardiac aging using cardiac ventricles from mice at 8 weeks and 15months of age. Besides miR-34 family members, miR-21 was also found to be elevated 3-fold in ventricles from mice aged 15 months compared to mice aged 8 weeks. Over-expression of miR-21 in the neonatal rat cardiomyocytes (NRCM) shortened the telomere length, attenuated and strengthened the activity of telomerase and senescence-related beta[[Unable to Display Character: &amp;#8211;]]galactosidase, respectively, which was similar to the aging caused by doxorubicin (DOX). Using the quantitative PCRs and Western blotting, phosphatase and tensin homologue (PTEN) gene was found to be negatively regulated by miR-21 in NRCM. Moreover, knockdown of PTEN using siRNA mimics the effects of miR-21 in pro-aging in NRCM. Interestingly, knockdown of miR-21, as well as up-regulation of PTEN, repressed NRCM aging induced by DOX. Conclusions— These findings suggest that ectopic up- or down-modulation of miR-21 may be an important regulatory mechanism governing cardiac aging by targeting PTEN. Inhibition of miR-21 represent a novel therapy for cardiac aging.

Letter regarding Xiao WZ et al. entitled "Relationships between PTEN gene mutations and prognosis in glioma: a meta-analysis".

With great interest, we read the article "Relationships between PTEN gene mutations and prognosis in glioma: a meta-analysis" (by Xiao et al. Tumor Biol 35(7):6687-6693, 2014), which has reached important conclusions that the phosphatase and tensin homolog (PTEN) gene mutations were closely related to poor prognosis of glioma patients. Through quantitative analysis, the investigators (Xiao WZ et al.) showed that glioma patients with PTEN gene mutations exhibited a significantly shorter overall survival (OS) than those without PTEN gene mutations (HR = 3.66, 95 % CI = 2.02∼5.30, P < 0.001). Ethnicity-stratified subgroup analysis demonstrated that PTEN gene mutations were closely linked to poor prognosis in glioma among Americans (HR = 3.72, 95 % CI = 1.72∼5.73, P < 0.001), while similar correlations were not observed among populations in Sweden, Italy, and Malaysia (all P > 0.05). The meta-analysis results are encouraging. Nevertheless, some deficiencies still existed that we would like to raise.

Alteration of major vault protein in human glioblastoma and its relation with EGFR and PTEN status

Glioblastoma (GBM) is the most frequent and malignant primary brain tumor. Conventional therapy of surgical removal, radiation and chemotherapy is largely palliative. Major vault protein (MVP), the main component of the vault organelle has been associated with multidrug resistance by reducing cellular accumulation of chemotherapeutic agents. With regard to cancer, MVP has been shown to be overexpressed in drug resistance development and malignant progression.The aim of the present study was to evaluate the MVP gene dosage levels in 113 archival samples from GBM and its correlation with patients’ survival and epidermal growth factor receptor (EGFR) and phosphatase and tensin homolog (PTEN) gene dosages. Fluorescent in situ hybridization revealed polysomy of chromosome 7 in 76.1% of the GBMs and EGFR amplification in a 64.6% of the tumors. Genetic status of EGFR, PTEN and MVP copies was determined by multiplex ligation-dependent probe amplification (MLPA) technique. 31% of the tumors showed the EGFR is variant III mutation (EGFRvIII) mutation and 74.3% of them presented amplification of MVP gene. Amplification of EGFR and MVP was found in a 63.7% and 56.6% of the GBM, respectively. An inverse correlation between MVP and PTEN dosage values was observed. Besides, an inverse relationship between the survival of the patients treated with chemotherapy and the levels of MVP copies was determined. In conclusion, our study reveals an important role of MVP, together with EGFRvIII and PTEN, in the progression of GBM and proposes it as a novel and interesting target for new treatment approaches.

Expression of Phosphatase and Tensin Homolog (PTEN) gene at mRNA level in equine endometrium

Expression of Phosphatase and Tensin Homolog (PTEN) gene at mRNA level in equine endometrium