Biomedical subjects

Y Z Wang

Publications and source records attributed to Y Z Wang.

At least 19 recordsLinked to original sources

PubMed2001

Differential gene expression of adenosine A1, A2a, A2b, and A3 receptors in the human enteric nervous system.

Adenosine receptors (ADORs) in the enteric nervous system may be of importance in the control of motor and secretomotor functions. Gene expression and distribution of neural adenosine A1, A2a, A2b, or A3 receptors (Rs) in the human intestine was investigated using immunochemical, Western blotting, RT-PCR, and short-circuit current (I(sc)) studies. Adenosine A1R, A2aR, A2bR, or A3R mRNAs were differentially expressed in neural and nonneural layers of the jejunum, ileum, colon, and cecum and in HT-29, T-84, T98G, and Bon cell lines. A1R, A2aR, A2bR, and A3R immunoreactivities (IRs) were differentially expressed in PGP 9.5-immunoreactive neurons. A2bR IR occurs exclusively in 50% of submucosal vasoactive intestinal peptide (VIP) neurons (interneurons, secretomotor or motor neurons) in jejunum, but not colon; A2aR is also found in other neurons. A3R IR occurs in 57% of substance P-positive jejunal submucosal neurons (putative intrinsic primary afferent neurons) and less than 10% of VIP neurons. Western blots revealed bands for A3R at 44 kDa, 52 kDa, and 66 kDa. A2aR and A2bR are coexpressed in enteric neurons and epithelial cells. 5'-N-methylcarboxamidoadenosine or carbachol evoked an increase in I(sc). A2bR IR is more prominent than A2aR IR in myenteric neurons, nerve fibers, or glia. A1R is expressed in jejunal myenteric neurons and colonic submucosal neurons. Regional differences also exist in smooth muscle expression of ADOR IR(s). It is concluded that neural and nonneural A1, A2a, A2b, and A3Rs may participate in the regulation of neural reflexes in the human gut. Clear cell and regional differences exist in ADOR gene expression, distribution, localization, and coexpression.

Blotting, Western↗

PubMed2001

Fragmented condensate ground state of trapped weakly interacting bosons in two dimensions.

The ground state and its structure for a rotating, harmonically trapped N-boson system with a weak repulsive contact interaction are studied as the angular momentum L increases up to 3N. We show that the ground state is generally a fragmented condensate due to angular momentum conservation. In response to an (arbitrarily weak) asymmetric perturbation of the trap, however, the fragmented ground state can be transformed into a single condensate state. We manifest this intrinsic instability by calculating the conditional probability distributions, which show patterns analogous to the boson density distributions predicted by mean-field theory.

Journal Article↗

PubMed2001

Evidence that epithelial and mesenchymal estrogen receptor-alpha mediates effects of estrogen on prostatic epithelium.

In combination with androgens, estrogens can induce aberrant growth and malignancy of the prostate gland. Estrogen action is mediated through two receptor subtypes: estrogen receptors alpha (ERalpha) and beta (ERbeta). Wild-type (wt) and transgenic mice lacking a functional ERalpha (alphaERKO) or ERbeta (betaERKO) were treated with the synthetic estrogen diethylstilbestrol (DES). DES induced prostatic squamous metaplasia (SQM) in wt and betaERKO but not in alphaERKO mice, indicating an essential role for ERalpha, but not ERbeta, in the induction of SQM of prostatic epithelium. In order to determine the respective roles of epithelial and stromal ERalpha in this response, the following tissue recombinants were constructed with prostatic epithelia (E) and stroma (S) from wt and ERKO mice: wt-S+wt-E, alphaERKO-S+alphaERKO-E, wt-S+alphaERKO-E, and alphaERKO-S+wt-E. A metaplastic response to DES was observed in wt-S+wt-E tissue recombinants. This response to DES involved multilayering of basal epithelial cells, expression of cytokeratin 10, and up-regulation of the progesterone receptor. Tissue recombinants containing alphaERKO-E and/or -S (alphaERKO-S+alphaERKO-E, wt-S+alphaERKO-E, and alphaERKO-S+wt-E) failed to respond to DES. Therefore, full and uniform epithelial SQM requires ERalpha in the epithelium and stroma. These results provide a novel insight into the cell-cell interactions mediating estrogen action in the prostate via ERalpha.

Animals↗

PubMed2001

Paracrine regulation of apoptosis by steroid hormones in the male and female reproductive system.

In males, androgens are essential in maintaining the integrity of the prostate. Androgen-ablation induces apoptosis of the prostatic epithelium. In females, ovariectomy induces apoptosis in uterine epithelium while progesterone inhibits this process. The objective of this study was to determine whether androgen and progesterone inhibit apoptosis, respectively, in mouse prostatic and uterine epithelia via steroid receptors in the epithelium or in the stroma. To address this question, prostatic tissue recombinants were prepared with rat urogenital sinus mesenchyme plus bladder epithelium from wild-type or testicular feminization mutant (Tfm) mice. Thus, prostatic tissue was generated having androgen receptor (AR) in both epithelium and stroma or in the stroma only. Castration of hosts induced apoptosis in the AR-negative Tfm prostatic epithelium with an epithelial apoptotic index virtually identical to prostatic tissue recombinants containing wild-type epithelium. Moreover, this castration-induced prostatic epithelial apoptosis was blocked by testosterone and dihydrotestosterone in both wild-type and Tfm prostatic tissue recombinants. Likewise, uterine tissue recombinants were prepared in which epithelium and/or stroma was devoid of progesterone receptor (PR) by using uterine epithelium and stroma of wild-type and PR knockout mice. Progesterone inhibited uterine epithelial apoptosis only in tissue recombinants prepared with PR-positive stroma. The PR status of the epithelium did not affect epithelial apoptotic index. Therefore, the apoptosis in prostatic and uterine epithelia is regulated by androgen and progesterone via stromal AR and PR, respectively. In both cases, epithelial AR or PR is not required for hormonal regulation of epithelial apoptosis in prostatic and uterine epithelium.

Androgens↗

PubMed2001

Clustering of cardiovascular risk factors with diabetes in Chinese patients: the effects of sex and hyperinsulinaemia.

OBJECTIVE: This study was designed to investigate factors which affect the clustering of cardiovascular risk factors with diabetes in Chinese patients. RESEARCH DESIGN AND METHODS: Six hundred and fifty-four patients with diabetes were assessed comprehensively for diabetes complications and cardiovascular risk factors in a metropolitan hospital in Beijing, China. Insulin resistance and secretion were also evaluated by measurement of glucose and insulin levels before and after a meal tolerance test. Results were analysed according to patient groups stratified by the number of cardiovascular risk factors coexisting with diabetes. RESULTS: Cardiovascular risk factors were common in Chinese diabetic patients. The clustering of three or more of these factors with diabetes occurred more often than by chance alone and was associated with postprandial hyperinsulinaemia. Patients with a high number of risk factors were more prone to macrovascular events but did not have higher albuminuria. Using the commonly adopted lower threshold for diagnosing obesity and central obesity in women, there were more women with multiple risk factors. However, this disappeared if the same criteria were used for men and women. Even in the presence of diabetes, cardiovascular risk factors were inadequately controlled in most patients. CONCLUSIONS: The concurrence of diabetes and other cardiovascular risk factors which constitute the metabolic syndrome is a common phenomenon in urban Chinese diabetic patients. It is associated with hyperinsulinaemia and possibly the female sex. This study emphasises the importance of public health measures to control cardiovascular risk factors in patients with diabetes.

Aged↗

PubMed2001

Accuracy of administrative and trauma registry databases.

OBJECTIVE: Accurate data are needed to evaluate clinical outcomes, therapeutic modalities, and quality of care in trauma. Administrative data, usually used for billing, and trauma registries, have been used to perform these functions. This study compares data for trauma patients from administrative and trauma registry databases at a Level I trauma center. METHODS: Data from patients injured in 1998 were obtained from both the trauma registry and administrative database. These International Classification of Diseases, Ninth Revision, Clinical Modification codes signify an admitting diagnosis of trauma. Patients from each database were "matched" by admission date, medical record number, age, and name. The two matched data sets were compared for accuracy in recording data. Chi-square analysis was used to compare groups. RESULTS: There were 2,702 patients found in both databases. One hundred eighteen patients with significant trauma were recorded in the trauma registry, but not in the administrative database. Comparison of recorded data for "matched" patients is as follows. The underreporting of mechanism of injury, diagnoses, diagnostic interventions, surgical procedures, and complications was rampant throughout the administrative database. Statistical significance was seen in the comparison between the trauma registry and the administrative database with motor vehicle collisions (458 vs. 391), abdominal injuries (346 vs. 293), orthopedic injuries (1,243 vs. 1,101), and thoracic injuries (486 vs. 397). Diagnostic interventions such as diagnostic peritoneal lavage, head computed tomographic scans, and abdominal computed tomographic scans were all grossly underrecorded, with only 40%, 12%, and 9% captured by the administrative database, respectively. Analysis of surgical procedures revealed these same trends, with statistical significance seen in abdominal and orthopedic procedures. Complications such as acute respiratory distress syndrome and deep venous thrombosis showed statistically significant differences. Mortality was underreported in the administrative database, with 14 deaths omitted. CONCLUSION: This study shows that administrative data have copious omissions of specific injuries, diagnostic and therapeutic interventions, as well as complications. The trauma registry recorded more of the diagnoses, diagnostics, procedures, and outcomes in the care of trauma patients. Trauma registries may be more useful than administrative databases in assessing quality of care and diagnostic and therapeutic interventions.

Adult↗

PubMed2001

Effects of aging on shape discrimination.

A large number of senior patients manifest eye diseases in addition to normal aging changes in their visual system. Visual tests not affected by age would be very useful in early detection of age-related eye diseases. The purpose of this study was to determine the effects of aging on the detection of contour deformation. Seventy-six normal subjects were divided into three age groups: young adults 15 to 39 years old (N = 26); middle-aged adults 40 to 59 years old (N = 22); and senior adults 60 to 78 years old (N = 28). Stimuli were circular or linear D4 (4th derivative of Gaussian) contours. A spatial two-alternative forced-choice staircase paradigm was used. In each trial, one deformed and one undeformed contour were presented on a screen. Subjects indicated which contour was deformed. Deformation detection thresholds were estimated by a maximum likelihood fitting procedure. We found that at a low modulation frequency (four cycles), the performance of detecting deformation does not change with age, and it does not correlate with either visual acuity or letter contrast sensitivity. At a higher modulation frequency (eight cycles), a significant difference between mean thresholds was found for young and senior adults. For circular D4, the mean threshold was elevated by 18%, from 7.6 sec arc (young adults) to 9.0 sec arc (senior adults). For linear D4, the mean threshold was elevated by 52%, from 5.8 sec arc to 8.8 sec arc. As a comparison, minimum angle of resolution was increased by 33%, and letter contrast threshold was elevated by 81%. The performance for linear D4 at higher modulation frequency was found to be significantly correlated with contrast threshold. These results provide further evidence to support the hypothesis that different mechanisms may be underlying the detection of circular and linear D4 contour deformation. The very small effect of aging on hyperacuity for radial deformation suggests that a global shape discrimination task could be a sensitive test for quantifying the early visual loss caused by eye diseases among seniors.

Adolescent↗

PubMed2001

Regulation of PDGFR-alpha in rat pulmonary myofibroblasts by staurosporine.

Upregulation of the platelet-derived growth factor (PDGF) receptor-alpha (PDGFR-alpha) is a mechanism of myofibroblast hyperplasia during pulmonary fibrosis. We previously identified interleukin (IL)-1beta as a major inducer of the PDGFR-alpha in rat pulmonary myofibroblasts in vitro. In this study, we report that staurosporine, a broad-spectrum kinase inhibitor, upregulates PDGFR-alpha gene expression and protein. A variety of other kinase inhibitors did not induce PDGFR-alpha expression. Staurosporine did not act via an IL-1beta autocrine loop because the IL-1 receptor antagonist protein did not block staurosporine-induced PDGFR-alpha expression. Furthermore, staurosporine did not activate a variety of signaling molecules that were activated by IL-1beta, including nuclear factor-kappaB, extracellular signal-regulated kinase, and c-Jun NH2-terminal kinase. However, both staurosporine- and IL-1beta-induced phosphorylation of p38 mitogen-activated protein kinase and upregulation of PDGFR-alpha by these two agents was inhibited by the p38 inhibitor SB-203580. Finally, staurosporine inhibited basal and PDGF-stimulated mitogenesis over the same concentration range that induced PDGFR-alpha expression. Collectively, these data demonstrate that staurosporine is a useful tool for elucidating the signaling mechanisms that regulate PDGFR expression in lung connective tissue cells and possibly for evaluating the role of the PDGFR-alpha as a growth arrest-specific gene.

Animals↗

PubMed2001

Detection of constrast-defined shape.

We assessed the accuracy of contrast-defined shape detection of stimuli of constant aspect ratio, namely, circular bandpass stimuli whose radii were sinusoidally varied about a mean radius. Performance for these contrast-defined shapes, which we show is determined by the global rather than the local attributes of the stimulus, is 2-8 times worse than that for their luminance-defined counterparts, suggesting separate processing limitations. By spatially and orientationally filtering the two-dimensional fractal-noise carriers of which these stimuli were composed, we determined whether there are specific rules concerning the spatial and orientational input to shape detectors from mechanisms sensitive to the carrier structure. The results suggest that second-order circularity detectors receive mixed input from spatial-frequency-tuned and orientationally tuned cells.

Contrast Sensitivity↗

PubMed2001

Digital signature technology for health care applications.

BACKGROUND: The personal computer and the Internet have provided many useful services to both health care professionals and the general public. However, security remains a key factor that could limit their further growth potential. METHODS: We reviewed and assessed the potential use of the cryptographic technique to resolve security issues. We also analyzed services available in the current market environment and determined their viability in supporting health care applications. RESULTS: While the cryptographic application has a great potential in protecting security of health care information transmitted over the Internet, a nationwide security infrastructure is needed to support deployment of the technology. Although desirable, it could be cost prohibitive to build a national system to be dedicated for the health care purpose. CONCLUSIONS: A hybrid approach that involves the government's development of a dedicated security infrastructure for health care providers and the use of commercial off-the-shelf products and services by the general public offers the most cost-effective and viable approach.

Computer Security↗

PubMed2001

Retrohepatic vena cava and juxtahepatic venous injuries.

The daunting mortality encountered with retrohepatic vena cava and juxtahepatic venous trauma is testimony to the difficulties inherent in their management. For a successful outcome, the operating surgeon must be able to rapidly identify the nature of the injury and tailor the choice of procedure accordingly. Atriocaval shunting, balloon shunting, sequential vascular clamping, and perihepatic packing are all methods of treatment with which the surgeon must be familiar. In this review, we present a case of this injury caused by a gunshot wound. This serves as a useful starting point for a discussion of the techniques available for addressing this injury.

Adult↗

PubMed2001

Comparison of degradation reactions of Acid Yellow 61 in both oxidation processes of H2O2/UV and O3.

The comparison of degradation of Acid Yellow 61 as a model dye compound in both oxidation processes of H2O2/UV and O3 has been studied. When the decolorization rate of Acid Yellow 61 in both reactions presented similar, it was found there are some differences from the results of AOX removal and production of inorganic ions and organic acids. The results reveal that the H2O2/UV has beneficial effect on mineralization than O3 only for degradation of Acid Yellow 61 solution and it is possible for enhancement of method efficiency by taking longer reaction time and addition of high concentration of oxidants.

Benzene Derivatives↗

PubMed2000

Regulation of interleukin-1beta -induced platelet-derived growth factor receptor-alpha expression in rat pulmonary myofibroblasts by p38 mitogen-activated protein kinase.

The potential role of p38 mitogen-activated protein (MAP) kinase in platelet-derived growth factor receptor-alpha (PDGF-Ralpha) gene expression was investigated using cultured rat pulmonary myofibroblasts. p38 MAP kinase was constitutively expressed in myofibroblasts and activated by interleukin (IL)-1beta. A pyridinylimidazole compound, SB203580, completely inhibited the ability of p38 MAP kinase activity to phosphorylate PHAS-1 substrate. SB203580 inhibited IL-1beta-induced up-regulation of PDGF-Ralpha mRNA and protein in a concentration-dependent manner. Other kinase inhibitors, including the mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor PD98059, did not block up-regulation of PDGF-Ralpha. The IL-1beta-induced increase in the number of (125)I-PDGF-AA-binding sites at the cell surface was reduced >70% by pretreatment with SB203580. Accordingly, an enhancement of PDGF-AA-stimulated DNA synthesis following IL-1beta pretreatment was blocked >70% by SB203580. SB203580 did not affect IL-1beta-induced ERK activation, yet enhanced IL-1beta-induced JNK activation approximately 2-fold. Treatment of cells with SB203580 after inhibition of transcription by actinomycin D decreased the half-life of IL-1beta-induced PDGF-Ralpha mRNA from >4 to approximately 1.5 h. Moreover, pretreatment of cells with cycloheximide blocked induction of PDGF-Ralpha mRNA by IL-1beta, suggesting that de novo protein synthesis was required for PDGF-Ralpha mRNA stabilization. These data indicate that p38 MAP kinase regulates PDGF-Ralpha expression at the translational level by signaling the synthesis of an mRNA-stabilizing protein.

Animals↗

PubMed2000

Peroxynitrite targets the epidermal growth factor receptor, Raf-1, and MEK independently to activate MAPK.

Activation of ERK-1 and -2 by H(2)O(2) in a variety of cell types requires epidermal growth factor receptor (EGFR) phosphorylation. In this study, we investigated the activation of ERK by ONOO(-) in cultured rat lung myofibroblasts. Western blot analysis using anti-phospho-ERK antibodies along with an ERK kinase assay using the phosphorylated heat- and acid-stable protein (PHAS-1) substrate demonstrated that ERK activation peaked within 15 min after ONOO(-) treatment and was maximally activated with 100 micrometer ONOO(-). Activation of ERK by ONOO(-) and H(2)O(2) was blocked by the antioxidant N-acetyl-l-cysteine. Catalase blocked ERK activation by H(2)O(2), but not by ONOO(-), demonstrating that the effect of ONOO(-) was not due to the generation of H(2)O(2). Both H(2)O(2) and ONOO(-) induced phosphorylation of EGFR in Western blot experiments using an anti-phospho-EGFR antibody. However, the EGFR tyrosine kinase inhibitor AG1478 abolished ERK activation by H(2)O(2), but not by ONOO(-). Both H(2)O(2) and ONOO(-) activated Raf-1. However, the Raf inhibitor forskolin blocked ERK activation by H(2)O(2), but not by ONOO(-). The MEK inhibitor PD98059 inhibited ERK activation by both H(2)O(2) and ONOO(-). Moreover, ONOO(-) or H(2)O(2) caused a cytotoxic response of myofibroblasts that was prevented by preincubation with PD98059. In a cell-free kinase assay, ONOO(-) (but not H(2)O(2)) induced autophosphorylation and nitration of a glutathione S-transferase-MEK-1 fusion protein. Collectively, these data indicate that ONOO(-) activates EGFR and Raf-1, but these signaling intermediates are not required for ONOO(-)-induced ERK activation. However, MEK-1 activation is required for ONOO(-)-induced ERK activation in myofibroblasts. In contrast, H(2)O(2)-induced ERK activation is dependent on EGFR activation, which then leads to downstream Raf-1 and MEK-1 activation.

Animals↗

PubMed2000

Suramin analogs inhibit human angiogenesis in vitro.

BACKGROUND: Suramin is a polysulfonated naphthylurea that inhibits tumor cell proliferation and angiogenesis, but the widespread use of this drug has been limited by significant neurologic toxicity. A series of suramin analogs that may exhibit less toxicity in vivo have been synthesized. We hypothesized that these novel analogs would have antiangiogenic properties equal to or greater than those of suramin when evaluated in an in vitro human placental vein angiogenesis model. METHODS: Human placental veins (n = 72 per group) were cultured in a 0.3% fibrin clot for a period of 14 days. Three suramin analogs (NF 145, NF 248, NF 293) and suramin were tested at 56 and 560 microM concentrations to determine their effect on the development of an angiogenic response. Experiments were repeated for each analog on veins from three different placentas. The percentage of wells that initiated an angiogenic response was calculated and compared with initiation in a control group (n = 141). RESULTS: The three suramin analogs inhibited angiogenesis in a dose-dependent fashion, with all compounds exhibiting near-complete inhibition of angiogenesis at 560 microM. The effects of these analogs were equal to or greater than those of suramin. CONCLUSION: Suramin analogs with structural alterations inhibit human angiogenesis at concentrations equivalent to those seen in vivo. These analogs may be more effective antiangiogenic agents than suramin and may have less potential for toxicity.

Animals↗

PubMed2000

Activation of Stat3 preassembled with platelet-derived growth factor beta receptors requires Src kinase activity.

Members of the STAT family of transcriptional regulators modulate the expression of a variety of gene products that promote cell proliferation, survival and transformation. Although initially identified as mediators of cytokine signaling, the STAT proteins are also activated by, and thus may contribute to the actions of, polypeptide growth factors. To define the mechanism by which these factors activate STATs, we examined the process of Stat3 activation in Balb/c-3T3 fibroblasts treated with platelet-derived growth factor (PDGF). As STATs are activated by tyrosine phosphorylation, and as PDGF receptors are ligand-activated tyrosine kinases, we considered the possibility that Stat3 interacts with and is phosphorylated by PDGF receptors. We find that Stat3 associates with PDGF beta receptors in both the presence and, surprisingly, the absence of PDGF. Moreover, Stat3 was phosphorylated on tyrosine in PDGF beta receptor immunoprecipitates of PDGF-treated but not untreated cells. Although required, receptor activation was insufficient for Stat3 activation. When added to cells in combination with a pharmacologic agent (PD180970) that specifically inhibits the activity of Src family tyrosine kinases, PDGF did not activate Stat3 as monitored by electrophoretic mobility shift assay. PD180970 did not affect MAPK activation by PDGF or the JAK-dependent activation of Stat3 by interleukin-6. The necessity of Src activity for Stat3 activation by PDGF was further evidenced by data showing the presence of Src in complexes containing both Stat3 and PDGF beta receptors in PDGF-treated cells. These results suggest a novel mechanism of STAT activation in which inactive Stat3 pre-assembles with inactive PDGF receptors, and in response to ligand binding and in a manner dependent on Src kinase activity, is rapidly phosphorylated and activated. Additional data demonstrate that Src kinase activity is also required for PDGF stimulation of DNA synthesis in density-arrested cells.

3T3 Cells↗

PubMed2000

Growth factors and epithelial-stromal interactions in prostate cancer development.

Epithelial-stromal interactions are important not only in growth, development, and functional cytodifferentiation of the prostate but also in derangements of prostate gland such as BPH and prostate carcinoma. This chapter explores the roles of epithelium and stroma during this delicate process and highlights the role and mutual influence of each on the other. It also examines the importance of ECM in mediating the effects of androgens and drawn attention to estrogen and genetic factors in the process. During this process of epithelial-stromal interaction, growth factors play a central role in mediating the interactions. This chapter focuses on the role of several growth factors including epidermal growth factor, fibroblast growth factor, transforming growth factor alpha, transforming growth factor beta, insulin-like growth factor-1, vascular endothelial growth factor, nerve growth factor, platelet-derived growth factor, and hepatocyte growth factor. This chapter emphasizes the importance of epithelial-stromal interactions in tumorigenesis and highlights the switch of paracrine to autocrine mode during the process of carcinogenesis.

Animals↗

PubMed2000

Gastric adenomas and superficial adenocarcinomas display distinct patterns of mucin carbohydrate and core protein expression.

AIMS: To investigate the histogenetic relationship between gastric epithelial neoplasms we studied differences in expression of mucin carbohydrate antigens and mucin core protein, in normal and metaplastic gastric mucosa, and in gastric adenomas and superficial adenocarcinomas. METHODS AND RESULTS: We generated four monoclonal antibodies, including HGM72/75 against human gastric mucin and HCM14/21 against human colonic mucin, and investigated immunoreactivities of these antibodies and MUC2 protein expression in normal and metaplastic gastric mucosa, adenomas (15 samples) and superficial adenocarcinomas (intestinal-type, 77; diffuse-type, 59 samples). HGM72 reacted with mucous neck cells of the fundic glands and with pyloric glandular cells whereas HGM75 stained foveolar cells and metaplastic goblet cells. Weak binding of HCM14/21 and strong staining with MUC2 were found in metaplastic goblet cells. Binding of HGM75, HCM14, MUC2, but not HGM72 was high in adenomas. An equivalent staining with HGM72 and HGM75 with low expression of MUC2 and HCM14 was shown in intestinal-type carcinomas while the diffuse-type demonstrated more strong reactivity with HGM75 than with HGM72, MUC2 and HCM14. Little binding of HCM21 was observed in any specimens. CONCLUSIONS: This study demonstrates that adenomas predominantly have a intestinal phenotype, but both types of adenocarcinomas retain some cells with a gastric phenotype during the early steps of neoplastic development.

Adenocarcinoma↗