265 research outputs found
E-cadherin adhesion molecule and syndecan-1 expression in various thyroid pathologies
Cadherins and syndecans are transmembrane glycoproteins implicated in cell-cell and cell-matrix adhesion. Impairment of cadherin and syndecan mediated adhesion is likely to constitute one of the main factors leading to the reduced cell-cell and cell-matrix adhesion characteristics of tumor cells and play a pivotal role in the acquisition of invasive and metastatic proprieties by neoplastic epithelial cells. Aim: To elucidate the role and alterations of syndecan-1 expression in comparison with those of E-cadherin in normal and pathological thyroid glands (TG). Methods: A total of 55 TG carcinomas, 40 TG adenomas, 40 cases of hyperplastic TG disorders and 20 cases of normal TG autopsy samples, were evaluated by immunohistochemistry. The staining intensity, and localization of syndecan-1 and E-cadherin in sequential sections were examined, and semi-quantified. Results: Immunostaining of syndecan-1 and E-cadherin was strong in normal follicular TG epithelial cells, and located mainly in basolateral membrane. No significant change was seen in either molecule in hyperplastic TG disorders compared with TG adenomas. A significant reduction in expression of both syndecan-1 and E-cadherin was seen in well-differentiated TG carcinomas as compared with normal TG epithelium (p = 0.0001 and p = 0.032, respectively). Similarly, there was a significant reduction of both molecules expression in poorly differentiated and anaplastic TG carcinomas compared to well differentiated tumors (syndecan-1: p = 0.0037; and E-cadherin: p = 0.075). Conclusion: Decreased E-cadherin and syndecan-1 expression along with decreasing cellular differentiation may be involved in the complex mechanism of progression of TG pathology.ΠΠ°Π΄Π³Π΅ΡΠΈΠ½Ρ ΠΈ ΡΠΈΠ½Π΄Π΅ΠΊΠ°Π½Ρ β ΡΡΠΎ ΡΡΠ°Π½ΡΠΌΠ΅ΠΌΠ±ΡΠ°Π½Π½ΡΠ΅ Π³Π»ΠΈΠΊΠΎΠΏΡΠΎΡΠ΅ΠΈΠ½Ρ, ΡΡΠ°ΡΡΠ²ΡΡΡΠΈΠ΅ Π² ΠΌΠ΅ΠΆΠΊΠ»Π΅ΡΠΎΡΠ½ΠΎΠΉ Π°Π΄Π³Π΅Π·ΠΈΠΈ ΠΈ Π°Π΄Π³Π΅Π·ΠΈΠΈ ΠΊΠ»Π΅ΡΠΎΠΊ
ΠΊ ΠΌΠ°ΡΡΠΈΠΊΡΡ. ΠΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΡΡΠΈΡ
ΠΌΠΎΠ»Π΅ΠΊΡΠ» ΠΈΠ³ΡΠ°ΡΡ Π³Π»Π°Π²Π½ΡΡ ΡΠΎΠ»Ρ Π² ΠΏΡΠΈΠΎΠ±ΡΠ΅ΡΠ΅Π½ΠΈΠΈ ΠΈΠ½Π²Π°Π·ΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΈ ΠΌΠ΅ΡΠ°ΡΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ
ΠΏΠΎΡΠ΅Π½ΡΠΈΠ°Π»Π° Π·Π»ΠΎΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎ ΡΡΠ°Π½ΡΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½Π½ΡΠΌΠΈ ΡΠΏΠΈΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΠΌΠΈ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌΠΈ. Π¦Π΅Π»Ρ: ΠΎΡΠ΅Π½ΠΊΠ° ΡΠΎΠ»ΠΈ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ ΡΠΈΠ½Π΄Π΅ΠΊΠ°Π½Π°-1
ΠΈ Π-ΠΊΠ°Π΄Π³Π΅ΡΠΈΠ½Π° Π² ΡΠΊΠ°Π½ΠΈ ΡΠΈΡΠΎΠ²ΠΈΠ΄Π½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ Π² Π½ΠΎΡΠΌΠ΅ ΠΈ ΠΏΡΠΈ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΠΈ. ΠΠ΅ΡΠΎΠ΄Ρ: ΠΎΠ±ΡΠ°Π·ΡΡ ΡΠΊΠ°Π½ΠΈ Π΄Π»Ρ ΠΈΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ
ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ Π²Π·ΡΠ»ΠΈ Ρ 55 Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠ°ΠΊΠΎΠΌ ΡΠΈΡΠΎΠ²ΠΈΠ΄Π½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ (Π©Π), 40 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² β Ρ Π°Π΄Π΅Π½ΠΎΠΌΠΎΠΉ Π©Π, 40 β Ρ Π³ΠΈΠΏΠ΅ΡΠΏΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ
ΠΏΡΠΎΡΠ΅ΡΡΠ°ΠΌΠΈ Π©Π, ΠΊΠΎΠ½ΡΡΠΎΠ»Π΅ΠΌ ΡΠ»ΡΠΆΠΈΠ»ΠΈ 20 ΠΎΠ±ΡΠ°Π·ΡΠΎΠ² Π½Π΅ΠΈΠ·ΠΌΠ΅Π½Π΅Π½Π½ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ Π©Π (Π°ΡΡΠΎΠΏΡΠΈΡ). Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ:
ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ ΡΠΈΠ½Π΄Π΅ΠΊΠ°Π½Π°-1 ΠΈ Π-ΠΊΠ°Π΄Π³Π΅ΡΠΈΠ½Π° Π² Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΡ
ΡΠΎΠ»Π»ΠΈΠΊΡΠ»ΡΡΠ½ΡΡ
ΡΠΏΠΈΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΊΠ°Ρ
Π©Π Π²ΡΡΠ°ΠΆΠ΅Π½Π° ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΠΎ,
Ρ ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎΠΉ Π»ΠΎΠΊΠ°Π»ΠΈΠ·Π°ΡΠΈΠ΅ΠΉ Π² Π±Π°Π·ΠΎΠ»Π°ΡΠ΅ΡΠ°Π»ΡΠ½ΠΎΠΉ ΠΌΠ΅ΠΌΠ±ΡΠ°Π½Π΅. ΠΠ΅ ΠΎΡΠΌΠ΅ΡΠ°Π»ΠΈ ΡΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΡΠ°Π·Π»ΠΈΡΠΈΠΉ Π² ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ
ΠΎΠ±Π΅ΠΈΡ
ΠΌΠΎΠ»Π΅ΠΊΡΠ» ΠΏΡΠΈ Π³ΠΈΠΏΠ΅ΡΠΏΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΡΠΎΡΠ΅ΡΡΠ°Ρ
ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ Π°Π΄Π΅Π½ΠΎΠΌΠ°ΠΌΠΈ Π©Π. ΠΠ΄Π½Π°ΠΊΠΎ ΡΠ°ΠΊΠΎΠ²Π°Ρ Π·Π½Π°ΡΠΈΡΠ΅Π»ΡΠ½ΠΎ ΡΠ½ΠΈΠΆΠ΅Π½Π°
Π² ΠΎΠ±ΡΠ°Π·ΡΠ°Ρ
Π²ΡΡΠΎΠΊΠΎΠ΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΠΊΠ°ΡΡΠΈΠ½ΠΎΠΌΡ ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΠΌ ΡΠΏΠΈΡΠ΅Π»ΠΈΠ΅ΠΌ Π©Π (p = 0,0001 ΠΈ p = 0,032
ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎ), Π° ΡΠ°ΠΊΠΆΠ΅ ΠΏΡΠΈ Π½ΠΈΠ·ΠΊΠΎΠ΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΌ ΠΈ Π°Π½Π°ΠΏΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΎΠΌ ΡΠ°ΠΊΠ΅ ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ Π²ΡΡΠΎΠΊΠΎΠ΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΡΠΌΠΈ
ΠΎΠΏΡΡ
ΠΎΠ»ΡΠΌΠΈ Π©Π (p = 0,0037 Π΄Π»Ρ ΡΠΈΠ½Π΄Π΅ΠΊΠ°Π½Π°-1 ΠΈ p = 0,075 Π΄Π»Ρ Π-ΠΊΠ°Π΄Π³Π΅ΡΠΈΠ½Π°). ΠΡΠ²ΠΎΠ΄Ρ: ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΠΈ
ΡΠΈΠ½Π΄Π΅ΠΊΠ°Π½Π°-1 ΠΈ Π-ΠΊΠ°Π΄Π³Π΅ΡΠΈΠ½Π°, ΡΠΎΠΏΡΠΎΠ²ΠΎΠΆΠ΄Π°ΡΡΠ΅Π΅ΡΡ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ΠΌ ΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΠΈ ΠΊΠ»Π΅ΡΠΎΠΊ ΠΊ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°ΡΠΈΠΈ, ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΡΠ°ΡΡΡΡ
ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠ° ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ Π©Π
Proteome Profiling of Breast Tumors by Gel Electrophoresis and Nanoscale Electrospray Ionization Mass Spectrometry
We have conducted proteome-wide analysis of fresh surgery specimens derived from breast cancer patients, using an approach that integrates size-based intact protein fractionation, nanoscale liquid separation of peptides, electrospray ion trap mass spectrometry, and bioinformatics. Through this approach, we have acquired a large amount of peptide fragmentation spectra from size-resolved fractions of the proteomes of several breast tumors, tissue peripheral to the tumor, and samples from patients undergoing noncancer surgery. Label-free quantitation was used to generate protein abundance maps for each proteome and perform comparative analyses. The mass spectrometry data revealed distinct qualitative and quantitative patterns distinguishing the tumors from healthy tissue as well as differences between metastatic and non-metastatic human breast cancers including many established and potential novel candidate protein biomarkers. Selected proteins were evaluated by Western blotting using tumors grouped according to histological grade, size, and receptor expression but differing in nodal status. Immunohistochemical analysis of a wide panel of breast tumors was conducted to assess expression in different types of breast cancers and the cellular distribution of the candidate proteins. These experiments provided further insights and an independent validation of the data obtained by mass spectrometry and revealed the potential of this approach for establishing multimodal markers for early metastasis, therapy outcomes, prognosis, and diagnosis in the future. Β© 2008 American Chemical Society
Laminin isoform expression in breast tumors
Certain laminins of vascular basement membranes have been identified in human breast tumors and brain gliomas that share the same Ξ²1 chain. These laminins are new carcinoma angiogenic markers and might represent potential targets for antiangiogenic therapy
Tumor-associated Tenascin-C isoforms promote breast cancer cell invasion and growth by MMP-dependent and independent mechanisms
Metallothionein genes: no association with Crohn's disease in a New Zealand population
Metallothioneins (MTs) are excellent candidate genes for Inflammatory Bowel Disease (IBD) and have previously been shown to have altered expression in both animal and human studies of IBD. This is the first study to examine genetic variants within the MT genes and aims to determine whether such genetic variants have an important role in this disease. 28 tag SNPs in genes MT1 (subtypes A, B, E, F, G, H, M, X), MT2, MT3 and MT4 were selected for genotyping in a well-characterized New Zealand dataset consisting of 406 patients with Crohn's Disease and 638 controls. We did not find any evidence of association for MT genetic variation with CD. The lack of association indicates that genetic variants in the MT genes do not play a significant role in predisposing to CD in the New Zealand population
Dysplasia of the Upper Aerodigestive Tract Squamous Epithelium
Dysplasia of the oral, laryngeal and oropharyngeal stratified squamous epithelia is a microscopically defined change that may occur in clinically identifiable lesions including erythroplakia, leukoplakia and erythroleukoplakia, lesions that convey a heightened risk for carcinomatous progression. Dysplastic lesions have been classified microscopically according to degree of cytologic atypia and changes in architectural patterns, usually on a three part or four part gradation scale. Vocal cord epithelial lesions are graded according to either the Ljubljana or the World Health Organization (WHO) system whereas oral dysplasias are generally classified according to WHO criteria. Cytologically atypical cells are considered to represent precancerous changes predicting an increase risk for carcinomatous transformation. Inter- and intra-rater reliability studies among pathologists have disclosed low correlation coefficients for four part grading systems, whereas improved agreement is achieved (kappa correlation values) using the Ljubljana systems. Evidence forwarded by some studies supports the prognostic value of progressively severe dysplastic changes for carcinomatous transformation; however, some studies indicate that the presence of a clinically defined lesion without microscopic evidence of dysplasia also connotes increased risk for carcinomatous transformation. Loss of heterozygosity (LOH) at 3p and 9p microsatellite domains, DNA ploidy analysis and nuclear image analyses may have predictive value as molecular and histomorphological biomarkers
Androgenic dependence of exophytic tumor growth in a transgenic mouse model of bladder cancer: a role for thrombospondin-1
<p>Abstract</p> <p>Background</p> <p>Steroid hormones influence mitogenic signaling pathways, apoptosis, and cell cycle checkpoints, and it has long been known that incidence of bladder cancer (BC) in men is several times greater than in women, a difference that cannot be attributed to environmental or lifestyle factors alone. Castration reduces incidence of chemically-induced BC in rodents. It is unclear if this effect is due to hormonal influences on activation/deactivation of carcinogens or a direct effect on urothelial cell proliferation or other malignant processes. We examined the effect of castration on BC growth in UPII-SV40T transgenic mice, which express SV40 T antigen specifically in urothelium and reliably develop BC. Furthermore, because BC growth in UPII-SV40T mice is exophytic, we speculated BC growth was dependent on angiogenesis and angiogenesis was, in turn, androgen responsive.</p> <p>Methods</p> <p>Flat panel detector-based cone beam computed tomography (FPDCT) was used to longitudinally measure exophytic BC growth in UPII-SV40T male mice sham-operated, castrated, or castrated and supplemented with dihydrotestosterone (DHT). Human normal bladder and BC biopsies and mouse bladder were examined quantitatively for thrombospondin-1 (TSP1) protein expression.</p> <p>Results</p> <p>Mice castrated at 24 weeks of age had decreased BC volumes at 32 weeks compared to intact mice (p = 0.0071) and castrated mice administered DHT (p = 0.0233; one-way ANOVA, JMP 6.0.3, SAS Institute, Inc.). Bladder cancer cell lines responded to DHT treatment with increased proliferation, regardless of androgen receptor expression levels. TSP1, an anti-angiogenic factor whose expression is inhibited by androgens, had decreased expression in bladders of UPII-SV40T mice compared to wild-type. Castration increased TSP1 levels in UPII-SV40T mice compared to intact mice. TSP1 protein expression was higher in 8 of 10 human bladder biopsies of normal versus malignant tissue from the same patients.</p> <p>Conclusion</p> <p>FPDCT allows longitudinal monitoring of exophytic tumor growth in the UPII-SV40T model of BC that bypasses need for chemical carcinogens, which confound analysis of androgen effects. Androgens increase tumor cell growth <it>in vitro </it>and <it>in vivo </it>and decrease TSP1 expression, possibly explaining the therapeutic effect of castration. This effect may, in part, explain gender differences in BC incidence and implies anti-androgenic therapies may be effective in preventing and treating BC.</p
Correlation of BRCA1, TXR1 and TSP1 mRNA expression with treatment outcome to docetaxel-based first-line chemotherapy in patients with advanced/metastatic non-small-cell lung cancer
Gastric adenocarcinoma in a patient re-infected with H. pylori after regression of MALT lymphoma with successful anti-H. pylori therapy and gastric resection: a case report
BACKGROUND: Helicobacter pylori (H. pylori) has been etiologically linked with primary gastric lymphoma (PGL) and gastric carcinoma (GC). There are a few reports of occurrence of both diseases in the same patient with H. pylori infection. CASE PRESENTATION: We report a patient with PGL in whom the tumor regressed after surgical resection combined with eradication of H. pylori infection. However, he developed GC on follow up; this was temporally associated with recrudescence / re-infection of H. pylori. This is perhaps first report of such occurrence. CONCLUSIONS: Possible cause and effect relationship between H. pylori infection and both PGL and GC is discussed. This case also documents a unique problem in management of PGL in tropical countries where re-infection with H. pylori is supposed to be high
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