DrCleo Δημοσιεύτηκε 2 Νοεμβρίου 2012 Aναφορά Share Δημοσιεύτηκε 2 Νοεμβρίου 2012 ΠΡΩΤΑ ΑΠ' ΟΛΑ: ΠΑΤΑΜE FOLLOW THIS TOPIC Mετά από συζήτηση με κάποια παιδιά είπαμε να ανοίξουμε ένα φορουμ για να επικοινωνούμε. Επειδή το να κάνουμε ένα νέο φόρουμ επιβάλει συντήρηση, από γραφιστική, μπάνερς, έλεγχο των ποστ κλπ και επειδή είμαστε μόνο καμμιά τριανταριά είπα να ανοίξουμε απλά ένα νέο τομέα στο greekmeds. όποιος πάρα ταύτα θέλει να κάνουμε νέο/ ολοκαίνουργιο φόρουμ ας το πει, υπάρχουν εκατοντάδες apps για να γίνει αυτό http://www.greekmeds... +άνθρωπο +2011 Το μοναδικό που απαιτείται είναι ένας λογαριασμός στο http://www.greekmeds.gr εγώ για εγγραφή έβαλα τον λογαριασμό του παν/μιου. Σε περιπτωση που δεν δουλεύει το λινκ, τα keywords είναι πμσ νεοπλασματικη νόσος στον άνθρωπο ταξη 2011 http://www.greekmeds... +άνθρωπο +2011 Κλεόνικος Τσακιρης Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
DrCleo Δημοσιεύτηκε 4 Νοεμβρίου 2012 Author Aναφορά Share Δημοσιεύτηκε 4 Νοεμβρίου 2012 Κανω την αρχή ορισμένοι Online ατλαντες για ιστο-παθο Ωραία σελίδα από την Ρουμανία ιστο-παθο άτλαντας http://www.cumc.columbia.edu/dept/curric-pathology/pathology/pathology/pathoatlas/index.html του παν. Κολούμπια Εδω οι εικόνες είναι δευτερεύουσες μετά τις πληροφορίες cd markers Κλπ... http://www.path.uiowa.edu/virtualslidebox/iowa_histopathology/content_index_db.html το εικονικό κουτάκι με πλακάκια... πιο χρήσιμο απ'οτι φαίνεται.. σχεδόν καθόλου εικόνες, αλλά πολές πληροφορίες για τα νεοπλάσματα και το γενετικό τους υπόβαθρο... αμερικάνικη εταιρία αιματολογίας για λευκαιμίες και τέτοια ο online atlas, του πανεπιστημίου της Σαββάνα μάκρο/ μικρο παθολογίας http://library.med.utah.edu/WebPath/webpath.html ο ατλας ροντιν... ασπρόμαυρος... http://projects.galter.northwestern.edu/rhodin/ Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
DrTmr Δημοσιεύτηκε 4 Νοεμβρίου 2012 Aναφορά Share Δημοσιεύτηκε 4 Νοεμβρίου 2012 αντε με το καλο καλη αρχη! Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
Marialicious Δημοσιεύτηκε 4 Νοεμβρίου 2012 Aναφορά Share Δημοσιεύτηκε 4 Νοεμβρίου 2012 Και εγώ περίμενα να ποστάρεις κάτι σημαντικό DrTmr.Με απογοητεύεις....... Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
DrTmr Δημοσιεύτηκε 6 Νοεμβρίου 2012 Aναφορά Share Δημοσιεύτηκε 6 Νοεμβρίου 2012 σ λιγο καιροθα ανεβασω ολους τουσ τομους για να μην εχει κανεις παραπονο Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
DrTmr Δημοσιεύτηκε 6 Νοεμβρίου 2012 Aναφορά Share Δημοσιεύτηκε 6 Νοεμβρίου 2012 http://invenio.lib.auth.gr/record/125246/files/GRI-2011-5965.pdf διαβαστε για το nfkb απο εδω παιδια γιατι οπως μασ το δωσαν ειναι περιληψη Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
Stamor Δημοσιεύτηκε 6 Νοεμβρίου 2012 Aναφορά Share Δημοσιεύτηκε 6 Νοεμβρίου 2012 Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
DrCleo Δημοσιεύτηκε 8 Νοεμβρίου 2012 Author Aναφορά Share Δημοσιεύτηκε 8 Νοεμβρίου 2012 TO PDF ΑΠΟ ΤΗΝ ΧΘΕΣΙΝΗ (07// 11// 12) ΔΙΑΛΕΞΗ ΓΙΑ ΤΑ Κ.Α.Κ. 1 The Journal of Pathology 2012 Virtual Issue Number 2, March Stem cells, clonal expansion and cancer progression Compiled and annotated by Nadine T Gaisa, Institute of Pathology RWTH Aachen University, Aachen, Germany, and Malcolm R Alison, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK Setting the scene: stem cells in health and disease Stem cells have seemingly been isolated from every tissue of the body, although in certain organs in vivo, notably the heart and central nervous system, they do not appear to function in any useful way [1]. A critical feature of stem cell behaviour is their ability to self-renew, and logically this can be achieved by asymmetric division, whereby each stem cell divides to give rise to one daughter cell that remains a stem cell, while the other daughter cell becomes a transit amplifying (TA) cell. In reality, events are not so straightforward and within a tissue unit, e.g. a small intestinal crypt, stem cell number can also be maintained by symmetrical stem cell divisions that stochastically adopt either stem or TA fates. A further feature of most adult tissue stem cells is their multipotentiality; the ability of a single stem cell to produce all the cell lineages that occur within its location. This can be demonstrated both in vitro and in vivo, the latter using lineage labelling with genetic markers (see below). Continually renewing populations are thus hierarchically organised, with stem, TA and differentiating compartments. Adult stem cells are also implicated in disease; metaplasia is likely due to a change in the local milieu of the stem cell niche, commonly brought about by chronic inflammation, and there is good experimental evidence that some cancers, notably in the intestine, are initiated most effectively by ‘driver’ mutations in stem cells. On the other hand, cancer may also be initiated in cells further down the hierarchy, considered likely for the origin of many leukaemias and some solid tumours, e.g. breast carcinomas (see below). Thus, due to the involvement of adult stem cells in many pathological situations, stem cells across a broad range of tissues were the focus of the 2009 Annual Review issue of the Journal of Pathology [2]. It has also become apparent that tumours themselves can be hierarchically organised, with cancer stem cells (CSCs) fuelling the growth of tumours [3] and this topic is also discussed in this Virtual Issue. 1. Attributes of adult stem cells Malcolm R Alison and Shahriar Islam The Journal of Pathology 2009; 217: 144-160. (Invited review) 2. Stem cells in pathobiology and regenerative medicine Malcolm R Alison The Journal of Pathology 2009, 217, 141-143. (Introductory article) 2 3. Cancer stem cells: problems for therapy? Malcolm R Alison, Susan M Lim and Linda J Nicholson The Journal of Pathology 2011; 223: 147-161. (Invited review) Tissue-specific stem cells with regard to clonal tissue architecture and multipotentiality Epithelial tissues are specialized cellular systems composed by single or multiple cell types organized in a specific manner in order to accomplish highly specialized functions. These epithelia are maintained by tissuespecific stem cells and their progeny, and the continuous turnover of epithelial cells guarantees a constant tissue function. It is commonly believed, somewhat mistakenly, that stem cell identification can only be ascertained if the isolated cell in question can be expanded in vitro or be transplanted in vivo, demonstrating self-renewal and multipotentiality. However, as pointed out by Allan Spradling [4], such assays may simply unearth differentiation potential that is not normally displayed by the stem cell in vivo where stem cell behaviour is governed by the niche. So what alternative assays are available? In mice, lineage labelling can be achieved by crossing mice with a Cre-inducible knock-in allele (in a gene exclusively expressed in stem cells) with a lacZ or GFP reporter strain – the gold standard of stem cell identification. Until recently, lineage labelling using genetic markers in humans has been elusive, but now it is possible to identify clonal populations based on the occurrence of ‘neutral’ passenger mutations in mitochondrial DNA (mtDNA). Spradling further emphasises the need to study stem cells in their undisturbed state, and likens studies using mtDNA mutations as clonal markers to “peering through a living tissue microscope” [4]. A series of articles focus on the localization of tissue-specific stem cells and their progeny in humans with respect to clonal epithelial architecture by means of this mtDNA sequencing of cells within histochemically identified areas of mtDNA encoded cytochrome c oxidase (CCO) enzyme deficiency. Gutierrez-Gonzales, et al. show that each cell within a CCO-defective small intestinal crypt carries an identical mtDNA mutation and therefore the crypt is monoclonal, derived from a common stem cell [5]. Small patches of enzyme-deficient intestinal crypts must form by crypt fission of the initially enzyme-deficient crypt since all crypts in the patch carry the same mutation. However, as multiple stem cells are present in a crypt, partially deficient crypts can be present, that with time will become totally deficient as a crypt becomes monoclonally converted by so-called niche succession. Furthermore, a number of crypts feed the epithelium of a single villus, therefore the villus epithelium is invariably polyclonal. All cell types of the intestinal epithelium were present within clonal fields (unequivocal evidence of multipotentiality – a key feature of stem cells) with the exception of Paneth cells that sometimes exhibited a nonclonal origin. Paneth cells are a long-lived cell population and this might explain the lack of clonality (or they might originate from a separate committed progenitor cell). Using the same methodological approach it has also been shown that urogenital epithelia have a clonal composition. The bladder mucosa consists of multiple, irregularly shaped, clonal fields growing out of basallylocated stem cells [6]. The progeny of urothelial stem cells grow preferentially vertically (in the direction of bladder lumen for differentiation), although lateral growth (covering a larger area) has been shown [6]. Mucosal invaginations, the so-called Brunn’s nests, were also clonal fields, again characterized by identical mtDNA mutations. In the prostate, Gaisa et al. describe CCO-deficient clonal epithelial areas composed of basal and intermediate epithelial cell layers, which can also expand to larger areas and stretch to whole prostatic glands [7]. This pattern is conserved in normal, atrophic and hypertrophic epithelia. Significantly the clonal areas consisted 3 of all the types of cells within the prostatic epithelium, confirming the existence of prostatic multipotential stem cells. Similar findings in prostatic epithelium are shown by Blackwood et al., who additionally point out that acini can be composed of both CCO-deficient and CCO-positive areas, seemingly caused by multiple stem cells within an acinus that has not yet monoclonally converted [8]. 4. The living-tissue microscope: the importance of studying stem cells in their natural, undisturbed microenvironment Allan C Spradling The Journal of Pathology 2011; 225: 161-162. (Perspective) 5. Analysis of the clonal architecture of the human small intestinal epithelium establishes a common stem cell for all lineages and reveals a mechanism for the fixation and spread of mutations Lydia Gutierrez-Gonzales, Maesha Deheragoda, George Elia, Simon J Leedham, Arjun Shankar, Charles Imber, Janusz Jankowski, Douglass M Turnbull, Marco Novelli, Nicholas A Wright, Stuart AC McDonald The Journal of Pathology 2009; 217: 489-496. (Original paper) 6. The human urothelium consists of multiple clonal units, each maintained by a stem cell Nadine T Gaisa, Trevor A Graham, Stuart AC McDonald, Sagrario Cañadillas-Lopez, Richard Poulsom, Axel Heidenreich, Gerhard Jakse, Paul J Tadrous, Ruth Knuechel, Nicholas A Wright The Journal of Pathology 2011; 225: 163-171. (Original paper) 7. Clonal architecture of human prostatic epithelium in benign and malignant conditions Nadine T Gaisa, Trevor A Graham, Stuart AC McDonald, Richard Poulsom, Axel Heidenreich, Gerhard Jakse, Ruth Knuechel, Nicholas A Wright The Journal of Pathology 2011; 225: 172-180. (Original paper) 8. In situ lineage tracking of human prostatic epithelial stem cell fate reveals a common clonal origin for basal and luminal cells John K Blackwood, Stuart C Williamson, Laura C Greaves, Laura Wilson, Anastasia C Rigas, Raveen Sandher, Robert S Pickard, Craig N Robson, Douglass M Turnbull, Robert W Taylor, Rakesh Heer The Journal of Pathology 2011; 225: 181-188. (Original paper) The founder cells of cancer: mutated stem/progenitor cells? In tissues with a continual turnover of cells, it is reasonable to presume that the initial genetic changes needed for successful tumour initiation must occur in stem or at least long-lived cells. These cells persist for sufficient time to accrue the requisite alterations to establish a ‘foothold’ against the prevailing cell escalator that leads to cell efflux. Daryl Shibata and colleagues suggest that we can study cell genealogy by reading its genome, in particular the methylation status of certain CpG sites in the promoter regions of non-expressed genes should increase with chronological and mitotic age, effectively functioning as a mitotic clock since de novo methylation appears to only occur at cell division [9]. Employing this logic they find that older individuals have mitotically older colorectal cancers, presumably because they arise from mitotically older colorectal stem cells [10]. Additionally the methylation status of the cancer was slightly higher than in the normal crypts from the same individual, possibly because extra divisions are required to drive cancer progression. 4 While the founder cell of many cancers might well be a mutated adult stem cell, and indeed patients with cancers having a stem cell gene expression profile tend to have the poorest prognosis, there is a strong case for some cancers arising from more differentiated cells along the stem cell – terminally differentiated cell pathway. This idea was first proposed many years ago by Barry Pierce in his hypothesis of ‘blocked ontogeny’ or ‘maturation arrest’ of stem cell differentiation. Bombonati and Sgroi propose such a scenario for the origins of breast cancer; they describe an evolutionary tree for the development of the various sub-types breast cancer based on genomic, transcriptomic, morphological and immunophenotypic data, speculating that stem cells, progenitor cells and even differentiated cells may be the founder cells of the various sub-types [11]. On the other hand, van Deurzen and colleagues caution against this histogenetic interpretation in all cases of breast cancer, noting that some metaplastic breast carcinomas may arise by dedifferentiation, since there can be phenotypic heterogeneity between the primary tumour (ductal phenotype) and the metastasis (metaplastic phenotype) [12]. Thus, the metaplastic phenotype may be a late-stage change rather than signifying a basal-like stem cell origin. 9. Inferring human stem cell behaviour from epigenetic drift D Shibata The Journal of Pathology 2009: 217: 199-205. (Invited review) 10. Older individuals appear to acquire mitotically older colorectal cancers Yen-Jung Woo, Kimberly D Siegmund, Simon Tavaré and Darryl Shibata The Journal of Pathology 2009; 217: 483-488. (Original paper) 11. The molecular pathology of breast cancer progression Alessandro Bombonati and Dennis C Sgroi The Journal of Pathology 2011; 223: 307-317. (Invited review) 12. Metaplastic breast carcinoma: tumour histogenesis or dedifferentiation? Carolien HM van Deurzen, Andrew HS Lee, Muhammad S Gill, Marian BE Menke-Pluijmers, Agnes Jager, Ian O Ellis and Emad A Rakha The Journal of Pathology 2011; 224: 434-437. (Hypothesis) Field cancerization and pre-invasive growth Propagation theories of pre-invasive cells are particularly interesting in organs where a ‘field cancerization’ event is presumed. According to this theory, epithelial cells harbouring a critical mutation may migrate a considerable distance without breaching the basement membrane, a phenomenon that could explain the occurrence of synchronous and metachronous carcinomas. Genomic evidence of pre-invasive clonal expansion and progression in bronchial dysplasia has been investigated by McCaughan et al. with a digital PCR technique [13]. Using amplicon boundaries as markers of clonality, multiple biopsies in a longitudinal bronchoscopic study were used. They demonstrated that field cancerization occurs at a pre-invasive stage and pre-invasive lesions and subsequent cancers are clonally related (identical amplicon boundaries). However, the degree of 3q amplification and the internal structure varied within serial lesions. Additionally, in this cohort, the degree of 3q amplification (implicating SOX2) corresponded to clinical progression. 5 Brabletz et al. highlight the well known role of Wnt signalling in normal intestinal stem cell maintenance and tumour initiation (APC loss) [14]. They review the existence of two different stem cell populations in the small intestine; Bmi1-expressing slow cycling cells located about 4-5 cell positions (+4-5 cells) above the crypt base, and fast cycling crypt base columnar cells that express the Wnt target gene Lgr5, since found to cooperate in Wnt signalling following binding of its ligand, R-spondin1. In Familial Adenomatous Polyposis (FAP) they note an accelerated crypt fission rate, clearly a mechanism to facilitate field cancerization in the colonic mucosa. 13. Genomic evidence of pre-invasive clonal expansion, dispersal and progression in bronchial dysplasia Frank McCaughan, Christodoulos P Pipinikas, Sam M Jones, Jeremy George, Pamela H Rabbitts, Paul H Dear Journal of Pathology 2011; 224: 153-159. (Original paper) 14. Gastrointestinal stem cells in development and cancer S Brabeletz, O Schmalhofer, T Brabletz Journal of Pathology 2009; 217: 307-317. (Invited review) Cancer stem cells, tumour progression and metastasis Though still a contentious issue, most oncologists and pathologists embrace the concept of cancer stem cells (CSCs) in malignancy, in that tumours are hierarchically organised. A plethora of markers have been proposed for their prospective isolation [3], often based upon expression of a cell surface marker or the expression of the aldehyde dehydrogenase (ALDH) family of detoxifying enzymes [15]. In many cases the relevance of a particular marker to stem cell function remains elusive, no more so than with CD133; in colon cancer CD133 expression strongly correlates with metastatic disease in the liver, but siRNA-mediated knock-down of CD133 in colorectal cancer cell lines has no effect on proliferation, colony formation, migration and invasion [16]? Other problems exist, in Barrett’s oesophageal adenocarcinoma, serial dilution transplantation assays have suggested that CSCs exist at a frequency of 1:64,000 cells, but cells sorted on the basis of either CD24, CD29, CD34, CD44, CD133, CD166 or EpCAM failed to enrich for tumour-initiating ability [17], despite most of these markers being expressed -catenin, perhaps expression of Wnt target genes, e.g. Lgr5, might be illuminating? Many papers have reported gene expression signatures that purport to predict prognosis in cancer patients, in particular the colony formation efficiency of bulk tumour cells is often negatively correlated with patient survival, presumably because of a higher frequency of CSCs. Interestingly, Kok et al. describe a gene set in mammospheres derived from ER-positive breast cancer cell lines that predicts survival in patients with ER-positive breast cancer [18], possibly related to the quiescent nature of the CSCs in the mammosphere cultures. There is an increasing realisation that the stem cell state is not ‘fixed’ but a rather a more fluid state, often influenced by extrinsic factors produced by the adjacent tumour stroma [19]. A common occurrence is the induction of epithelial-mesenchymal transition (EMT) in the tumour cells at the invasive margin, often associated with the nuclear accumulation of -catenin, which Brabletz and colleagues propose endows colorectal cancer cells with a migratory CSC phenotype [14]; a similar mechanism has been proposed by the Weinberg lab for the generation of breast CSCs. So if CSCs, particularly those at the tumour margins, are responsible for invasion and 6 metastasis, how can we target them? Targeting CSCs in solid tumours [3] and haematological malignancies [20] seems the way forward, but CSCs are notoriously chemo- and radio-resistant. Alternatively, Lo and colleagues highlight the growing realisation that microRNAs (miRs) are important regulators of tumour behaviour [21]; miR200c was able to inhibit EMT in head and neck squamous cell carcinoma (HNSC) cells, reducing expression of the usual culprits promoting EMT (ZEB1, Snail, N-cadherin), and also improving the survival of mice transplanted with CD44+ALDH+ cells from HNSCCs. Unravelling the origins of metastasis has long been a challenge. Theories and strategies for tracing the origins of tumour spread (e.g. detection of amplifications by FISH or allelic imbalances via PCR or mutation sequencing) are the focus of a review by Nguyen [22]. They discuss aspects of tumour heterogeneity with respect to the different time course and the genetic ancestry of metastasis. Metastasis-inducing (genetic) events (e.g. HER2 amplification in breast cancer, TMPRSS2-ETS gene fusion in prostate cancer), clonal primary tumours and metastasis versus divergent tumours and metastasis are depicted. Nguyen points out the role of CSCs as metastasis-founding cells and discusses possible perspectives for cancer therapy. Sayagués and co-workers provide a more detailed look at the correlation between intratumoral cytogenetic heterogeneity and metastasis in colorectal cancer and liver metastasis [23]. By interphase in situ hybridization they show complex karyotypes with numerical/structural abnormalities for 7 or more different chromosomes/chromosomal regions both in the primary tumour and metastasis. Nearly all tumours harboured two or more tumour cell clones, and metastases contained clones similar to the primary tumour. In about 75% of metastatic tumours, the predominant tumour cell clone was also highly represented in the primary tumour, but in a few cases, a minor clone present in the primary tumour became the dominant one in the metastasis. The authors report some known important cytogenetic abnormalities in metastases of colorectal cancer, but they also describe new ones involving chromosome 5, 10q23, 14q32, 15q22, and 19q13. Continuing on the theme of clonal diversity, Geyer and colleagues enquired if morphologically distinct tumour subclones in metaplastic breast cancers are underpinned by different genetic aberrations [24]. Each component was microdissected and analysed using high-resolution array-comparative genomic hybridization, immunohistochemistry, in situ hybridization, TP53 sequencing and by the human androgen receptor (HUMARA) X-chromosome inactivation assay. The majority of cases harboured similar immunohistochemical and genomic profiles in the distinct tumour components, thus indicating a clonal relationship. However, specific genetic aberrations in divergent components could also be found, pointing to a gain of different genetic aberrations at an early stage of tumorigenesis, presumably underpinning the morphological diversity. Metastases showed a clonal nature with the primary tumour, although additional specific genetic aberrations were also present, thus supporting the theory of clonal/Darwinian evolution in tumours. 15. Finding cancer stem cells: are aldehyde dehydrogenases fit for purpose? Malcolm R Alison, Naomi J Guppy, Susan M Lim and Linda J Nicholson The Journal of Pathology 2010; 222: 335-344. (Invited review) 16. The cancer stem cell marker CD133 has high prognostic impact but unknown functional relevance for the metastasis of human colon cancer David Horst, Silvio K Scheel, Sibylle Liebmann, Jens Neumann, Susanne Maatz, Thomas Kirchner and Andreas Jung 7 The Journal of Pathology 2009; 219: 427-434. (Original paper) 17. Barrett’s oesophageal adenocarcinoma encompasses tumour-initiating cells that do not express common cancer stem cell markers Brechtje A Grotenhuis, Winand NM Dinjens, Bas PL Wijnhoven, Petra Sonneveld, Andrea Sacchetti, Patrick F Franken, Herman van Dekken, Hugo W Tilanus, J Jan B van Lanschot and Riccardo Fodde The Journal of Pathology 2010: 221: 379-389. (Original paper) 18. Mammosphere-derived gene set predicts outcome in patients with ER-positive breast cancer Marleen Kok, Rutger H Koornstra, Tania C Margarido, Renske Fles, Nicola J Armstrong, Sabine C Linn, Laura J Van‘t Veer and Britta Weigelt The Journal of Pathology 2009; 218: 316-326. (Original paper) 19. Jekyll and Hyde: the role of the microenvironment on the progression of cancer Michael Allen and J Louise Jones The Journal of Pathology 2011; 223: 162-176. (Invited review) 20. Targeted therapy in haematological malignancies Ashley Hamilton, Paolo Gallipoli, Emma Nicholson and Tessa L Holyoake The Journal of Pathology 2010; 220: 404-418. (Review article) 21. MicroRNA-200c attenuates tumour growth and metastasis of presumptive head and neck squamous cell carcinoma stem cells Wen-Liang Lo, Cheng-Chia Yu, Guang-Yuh Chiou, Yi-Wei Chen, Pin-I Huang, Chian-Shiu Chien, Ling-Ming Tseng, Pen-Yuan Chu, ## no greeklish please! ## - ## no greeklish please! ## - ## no greeklish please! ## - oxi fragolevantika grapste kalytera sta agglika - fragolevantika grapste kalytera ## no greeklish please! ## - oxi fragolevantika grapste kalytera sta agglika - agglika - fragolevantika grapste kalytera ## no greeklish please! ## - oxi fragolevantika grapste kalytera sta agglika - agglika --Hsi Lu, Kuo-Wei Chang, Shou-Yen Kao and Shih-Hwa Chiou The Journal of Pathology 2011; 223: 482-495. (Original paper) 22. Tracing the origins of metastasis Don X Nguyen The Journal of Pathology 2011; 223: 195-204. (Invited review) 23. Intratumoural cytogenetic heterogeneity of sporadic colorectal carcinomas suggests several pathways to liver metastasis José M Sayagués, María del Mar Abad, Herann Barquero Melchor, María L Gutierrez, Marìa Gonzàles - Gonzàles, Evan Jensen, Oscar Bengoechea, Emilio Fonseca, Alberto Orfao, Luis Muñoz-Bellvis The Journal of Pathology 2010; 221: 308-319. (Original paper) 24. Molecular analysis reveals a genetic basis for the phenotypic diversity of metaplastic breast carcinomas Felipe C Geyer, Britta Weigelt, Rachael Natrajan, Maryou BL Lambros, Dario de Biase, Radost Vatcheva, Kay Savage, Alan Mackay, Alan Ashworth, Jorge S Reis-Filho Journal of Pathology 2010; 220: 562-573. (Original paper) 8 Conclusion After reading this Virtual Issue we hope the reader appreciates the role of stem cells in all aspects of tissue architecture and maintenance, as well as tumour development, tumour initiation, tumour growth and metastasis. Both solid tumours and haematological malignancies appear to be hierarchically organized, being driven by a sub-population of CSCs. The precise identity of these CSCs in most tumours is still unclear, possibly because our present assays (colony formation in vitro and xenografting assays in immunodeficient mice) are far from satisfactory. It is also apparent that many tumours evolve in a Darwinian fashion, with further genetic change giving rise to new clones that either out-compete, co-exist or cooperate with the preceding clone(s). Tumour stroma is an important modulator of tumour growth and this influence extends to inducing EMT, seemingly associated with invasion and metastasis. Questions The following questions can be answered by reading and reflecting upon the above annotation and the papers that are cited within it. Within the Royal College of Pathologists Continuing Professional Development (CPD) scheme, CPD points may be earned by writing reflective notes on the papers in this Virtual Issue and the questions are designed to act as a focus for this activity. To do this, you may wish to use the Royal College of Pathologists' reflective notes form. Question 1 Outline the major changes in gene expression that result in epithelial-mesenchymal transition (EMT); what is the significance of EMT for tumour cells? Question 2 Describe how CSCs are prospectively isolated and assessed for clonogenic and tumorigenic efficacy. Question 3 Outline the characteristics of the two distinct populations of stem cells found in the small intestinal crypt. Question 4 Discuss current concepts regarding the histogenesis of the various sub-types of human breast cancer. Question 5 Cancer stem cells are often remarkably radio- and chemo-resistant: outline mechanisms responsible for such resistance. Question 6 What do you understand by the term ‘field cancerization’. What can be the consequence of such a process? www.thejournalofpathology.com Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
DrCleo Δημοσιεύτηκε 29 Δεκεμβρίου 2012 Author Aναφορά Share Δημοσιεύτηκε 29 Δεκεμβρίου 2012 στατικη κυτταρομετρια http://www.youtube.c...bed/g2y88CRI9XE http://www.youtube.com/embed/g2y88CRI9XE Link to comment Μοιράσου σε άλλους δικτυακούς τόπους More sharing options...
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