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Literatura académica sobre el tema "Carcinoma colorettale (Colorectal cancer)"

Autor: Grafiati

Publicado: 10 de marzo de 2023

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Artículos de revistas sobre el tema "Carcinoma colorettale (Colorectal cancer)"

Masi, Gianluca y Alfredo Falcone. "Irinotecan nel Trattamento di Prima Linea del Carcinoma Colorettale Metastatico". Tumori Journal 91, n.º 2 (marzo de 2005): 5–18. http://dx.doi.org/10.1177/030089160509100229.

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Briganti, Laura, Mauro Palazzi y Mirna Severi. "L'adesione allo screening del tumore colorettale nell'Ausl di Cesena: metodologie di intervento". PSICOLOGIA DELLA SALUTE, n.º 2 (noviembre de 2009): 179–89. http://dx.doi.org/10.3280/pds2009-002012.

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- In March 2005 the Emilia Romagna region started a screening for the colorectal cancer prevention. Over a period of 2 years, all the target population of the region, between 50 and 69 years old, was asked to undergo a screening of their faeces. Within the Cesena Ausl, 36% of the target population replied to the call, against a regional average percentage estimated at 46%. As a result, a co-operation with the 4 local agencies dealing with cancers was started in Cesena Ausl. This was done in order to increase the compliance of the target population and it involved: ACISTOM, ARRT, IOR, LILT and Assiprov. This work was carried out through an analysis of the phenomenon, the organization of conferences, focus groups and other communicative activities for the population. After 2 years of work, the compliance in September 2008 was estimated to have increased up to 48% and is believed to be improving furthermore throughout the implementation of future work.Key words: screening, prevention, colorectal cancer, style of life, well-being promotion, action ResearchParole chiave: screening, prevenzione, tumore colorettale, stili di vita, promozione del benessere, ricerca intervento

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GUL, AYAZ, SYED IFTIKHAR ALAM, RASHID ASLAM y Waqar Alam. "COLORECTAL CARCINOMA". Professional Medical Journal 18, n.º 04 (10 de diciembre de 2011): 566–70. http://dx.doi.org/10.29309/tpmj/2011.18.04.2578.

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Objective: Colorectal cancer is the second commonest cause of death in the world. Its incidence in young patients is on rise. Objective: To determine the common types of colorectal carcinoma in patients below 40 years of age presenting to tertiary care level hospital. Study Design: Descriptive study Setting: It was carried out at Surgical Department, KTH, Peshawar Period: January 2007 to January 2008. Materials and methods: Total of 50 patients younger than forty years of age with colorectal cancer were included in study for the determination of histologic types. Results: There were 66% males and 34% were females. The commonest affected age group was 31-35 years old having 46% cases. On history 86% patients complained of altered bowel habits and on clinical examination anemia was present in 72% patients. Left and right sided tumors were found in 70% and 30% patients respectively. Adenocarcinoma was the commonest type found in 94% cases followed by lymphoma (4%). Conclusions: The incidence in young age group (≤ 39 years) was highest There was slight male preponderance. Adenocarcinoma was the commonest tumor.

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Gennatas, C. G., G. Papaxoinis, N. Tsavaris, D. Mouratidou, C. Andreadis, D. Voros, A. Fotopoulos, V. Smyrniotis y E. Mallas. "Advanced colorectal carcinoma". Journal of Clinical Oncology 22, n.º 14_suppl (15 de julio de 2004): 3655. http://dx.doi.org/10.1200/jco.2004.22.14_suppl.3655.

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Watson, Patrice, Kevin M. Lin, Miguel A. Rodriguez-Bigas, Tom Smyrk, Stephen Lemon, M. Shashidharan, Barbara Franklin, Beth Karr, Alan Thorson y Henry T. Lynch. "Colorectal carcinoma survival among hereditary nonpolyposis colorectal carcinoma family members". Cancer 83, n.º 2 (15 de julio de 1998): 259–66. http://dx.doi.org/10.1002/(sici)1097-0142(19980715)83:2<259::aid-cncr9>3.0.co;2-l.

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Lynch, HT y T. Smyrk. "Colorectal cancer, survival advantage, and hereditary nonpolyposis colorectal carcinoma". Gastroenterology 110, n.º 3 (marzo de 1996): 943–46. http://dx.doi.org/10.1053/gast.1996.v110.agast960943.

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Schmoll, H. J. "Colorectal Cancer: Colorectal carcinoma: Current problems and future perspectives". Annals of Oncology 5 (1994): S115—S121. http://dx.doi.org/10.1093/annonc/5.suppl_3.s115.

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Nottage, Kerri, Joshua McFarlane, Matthew J. Krasin, Chenghong Li, Deokumar Srivastava, Leslie L. Robison y Melissa M. Hudson. "Secondary Colorectal Carcinoma After Childhood Cancer". Journal of Clinical Oncology 30, n.º 20 (10 de julio de 2012): 2552–58. http://dx.doi.org/10.1200/jco.2011.37.8760.

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Purpose Colorectal carcinoma (CRC) has been described as a subsequent malignant neoplasm (SMN), although little is known about associated risk factors. We aimed to quantify the long-term risk of secondary CRC and identify treatment-related risk factors. Patients and Methods In this nested case-control study, 19 cases of adenocarcinoma of the colon or rectum were identified from 13,048 oncology patients treated for childhood cancer at St Jude Children's Research Hospital. Group 1 controls (n = 148) were matched for age at primary malignancy and follow-up interval. Group 2 controls (n = 72) were matched on primary diagnosis in addition to group 1 criteria. Exact conditional logistic regression was performed to calculate odds ratios (ORs) for chemotherapy and radiation exposure. Results Forty-year cumulative incidence of secondary CRC was 1.4%. Standardized incidence ratio was 10.9 (95% CI, 6.6 to 17.0) compared with that in the general US population. Secondary CRC was more likely in an irradiated segment of the colon (group 1 OR, 7.7; P = .001; group 2 OR, 15.4; P = .002). Risk increased by 70% with each 10-Gy increase in radiation dose. Increasing radiation volume increased risk (group 1 OR, 1.5; P < .001; group 2 OR, 1.8; P < .001). Alkylating agent exposure was associated with an 8.8-fold increased risk of secondary CRC (P = .03). Conclusion In matched analyses, radiation and alkylator exposure are associated with secondary CRC. This risk is proportional to dose and volume of radiation. Surveillance should be initiated at a young age among survivors receiving high-risk exposures.

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Shah, Muhammad Fahd, Irum Sabir Ali y Ahmed Faraz. "COLORECTAL CANCER". Professional Medical Journal 23, n.º 06 (10 de junio de 2016): 687–92. http://dx.doi.org/10.29309/tpmj/2016.23.06.1608.

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Introduction: Colorectal cancer is a potentially fatal gastrointestinal disease andhas been studied extensively. In an effort to decrease the morbidity and mortality associatedwith this disease, studies have been performed to gain insight into the anatomic distribution,average age at presentation, mean age at presentation for different segments of colon involvedand intersex differences. Objective: The objective of this study is to determine the frequencyof sites of colorectal cancer involvement. Material and methods: Study design: Study wasdescriptive case series. Setting: General surgical department post graduate Lady ReadingHospital Peshawar. Period: From 01/01/2011 to 30/06/2012. Sample size: Sample size was416 using 3.57% proportion of descending colon5, 95% confidence level and 1.785% margin oferror under WHO software for sample size determination. Sampling technique: Consecutivenon probability sampling. Results: This study was carried out in 416 consecutive patients.These patients included 233 men (56 %) and 183 women (44%). Age varied from twelve yearsto seventy years. The commonest age group in the study at the time of presentation was63-72 years. Commonest site involved was rectum (26%) followed by sigmoid colon (16%).Bleeding per rectum was the commonest symptom (62.05%) followed by altered bowel habits(35.71%). Twelve patients (21.43%) presented with intestinal obstruction. Histopathologically,twenty patients had well differentiated adeno-carcinoma (35.72%) whereas eighteen patientshad anaplastic tumour (32.14%) and mucinous adeno-carcinoma was found in five patients(8.92%).Conclusion: Rectum is the most common site of tumour followed by left, right andtransverse colon respectively. The site of involvement affects the surgical procedure required.In conclusion the symptoms of colorectal cancer may not be representative of any anatomicalsite, by the time symptoms appear the lesion may have become invasive.

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Manxhuka-Kerliu, Suzana, Skender Telaku, Halil Ahmetaj, Arijeta Baruti, Sadushe Loxha y Agron Kerliu. "Colorectal Cancer: Prognostic Values". Bosnian Journal of Basic Medical Sciences 9, n.º 1 (20 de febrero de 2009): 19–24. http://dx.doi.org/10.17305/bjbms.2009.2851.

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After lung cancer colorectal cancer (Cc) is ranked the second, as a cause of cancer-related death. The purpose of this study was to analyze the Cc cases in our material with respect to all prognostic values including histological type and grade, vascular invasion, perineural invasion, and tumor border features. There were investigated 149 cases of resection specimen with colorectal cancer, which were fixed in buffered neutral formalin and embedded in paraffin. Tissue sections (4(µm thick) were cut and stained with H&E. Adenocarcinoma was the most frequent histological type found in 85,90% of cases, in 60,94% of males and 39,06% of females; squamous cell carcinoma in 7,38%, in 63,63% of males and 36,36% of females; mucinous carcinoma in 4,68%, in 57,15% of males and 42,85% of females; while adenosquamous carcinoma, undifferentiated carcinoma and carcinoma in situ in 0,71% of cases each. Dukes' classification was used in order to define the depth of invasion. Dukes B was found in 68,45% of cases, whereas in 31,54% of cases Dukes C was found. As far as histological grading is concerned, Cc was mostly with moderate differentiation (75,16%) with neither vascular nor perineural invasion. Resection margins were in all cases free of tumor. Our data indicate that the pathologic features of the resection specimen constitute the most powerful predictors of postoperative outcome in Cc. Dukes' stage and degree of differentiation provide independent prognostic information in Cc. However, differentiation should be assessed by the worst pattern.

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Tesis sobre el tema "Carcinoma colorettale (Colorectal cancer)"

Mescoli, Claudia. "FATTORI PROGNOSTICI DEL CARCINOMA COLO-RETTALE: IL FENOTIPO E IL RUOLO DELLE CELLULE TUMORALI ISOLATE STUDIO PROSPETTICO". Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3427520.

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AIM.To date, lymph node (LN) involvement is the most important prognostic factor in patients undergoing radical surgery for CRC, and pN+ve status identifies patients who require adjuvant chemotherapy. About 20-30% of patients with pathological-negative LNs (pN0), however, develop recurrent disease. Thus, there is a subgroup of pN0-CRC patients harbouring occult metastatic disease that is undetected by the current pathological and clinical evaluations. The need for more accurate prognostic factors has addressed the aim of this study to look for new morphologic reliable markers. PATIENTS AND METHODS. The study included: - Group A: 1606 consecutive pN0-CRC patients surgically treated at the University of Padova between 2002 and 2008; - Group B: 944 pN0-CRC patients (obtained from group A); - Group C: 361 consecutive pN0-CRC patients (obtained from group B, ruling out rectal carcinomas undergone neoadjuvant radio-chemotherapy) in order to immunohistochemically assess the prevalence of ITC and the clinical outcome of pN0-ITC+ve-CRC patients. All the 1606 surgical resections were sampled and diagnosed at the Pathology Department according to a standardized precedure in order to recorder the clinico-pathological features. From 361 pN0 cases, ITC detection has been performed on serial sections (at different levels: 80-100 μm) of the 5920 originally dissected (formalin fixed paraffin embedded) lymph nodes. Each section has been stained with appropriate antibodies to reveal the presence of tumoral cells undetected at the routine observation. The clinico-pathological features has been compared between each other and the clinical outcome. RESULTS. (a) The importance of histopathological variables (Infiltration Depth, Lymphonodal Status, Growth Pattern, Vascular Invasion, Rectal localization, Tumoral de- differentiation Grade ) as prognostic factors has been confirmed; (b) Independent paramenters influencing relapse in negative nodes are : Tumoral de differentiation Grade, Histotype, Growth Pattern and peri and intra neoplastic inflammation; (c) Multivariate Analisys shows that ITC presence in nodes of CRC pN0 patients is the only variable significantly influencing prognosis. CONCLUSIONS. The present study confirms the importance of those histopathological parameters which are not primary involved in patient stratification risk of relapsing disease, in particular of ITC. Our results elucidate the role of ITC as prognostic factors clinically significant and they suggest the possible utilization of ITC as selection criteria in pN0 patients for adiuvant therapy.
SCOPO. Il carcinoma del colon-retto (CCR) è la seconda neoplasia maligna causa di morte nel mondo occidentale. La presenza di metastasi nei linfonodi regionali è il fattore prognostico più importante e, distinguendo lo stadio III (pN1/2) dagli stadi I e II (pN0) (in assenza di metastasi extranodali) identifica i pazienti da sottoporre a terapia adiuvante. Tuttavia, il 20-30% dei pazienti senza metastasi linfonodali (pN0) sviluppa malattia recidiva. Esiste, pertanto, tra gli stadi precoci, un sottogruppo di soggetti “portatori” di metastasi occulte che non sono identificabili con le comuni tecniche di valutazione. La necessità di nuovi e più accurati fattori prognostici ha indirizzato lo scopo di questo lavoro alla ricerca di parametri morfologici clinicamente rilevanti per lo sviluppo di nuove strategie terapeutiche. PAZIENTI E METODI. Lo studio include: - Gruppo A: 1606 pazienti consecutivi con CCR sottoposti a resezione curativa; - Gruppo B: 944 pazienti pN0 (estratti dal gruppo A); - Gruppo C: 361 pazienti consecutivi pN0 (estratti dal gruppo B, escludendo i cancri rettali sottoposti a terapia neo-adiuvante) nei cui linfonodi è stata indagata la presenza/prevalenza di Cellule Tumorali Isolate. 1606 resezioni consecutive colo-rettali sono state campionate e refertate secondo un protocollo standardizzato per raccoglierne le caratteristiche clinico-patologiche. Da 361 resezioni colo-rettali, campionate e refertate come sopra, sono stati analizzati con metodica immunoistochimica (anticorpo anti-citocheratina MNF116) 5920 linfonodi, per ognuno dei quali sono state esaminate due sezioni a distanza di 80-100 μm. Le caratteristiche clinico-patologiche sono state comparate tra loro e con i risultati dell’ outcome secondo i parametri “ricorrenza di malattia” e “decesso per malattia”. RISULTATI. (a) L’importanza di variabili isto-patologiche (Profondità d’infiltrazione, Status Linfonodale, Pattern di crescita, presenza di Invasione Vascolare, insorgenza in Sede Rettale, Grado di de-differenziazione tumorale) come fattori prognostici è stata consolidata; (b) Parametri indipendenti che influenzano la recidiva in assenza di metastasi linfonodali sono : Grado di de-differenziazione tumorale , Istotipo, Pattern di crescita e Reazione flogistica intra e peritumorale; (c) Analisi in multivariata dimostrano che la presenza di ITC nei linfonodi di pazienti con CCR pN0 è l’unica variabile che influenza significativamente la prognosi. CONCLUSIONI. Il presente studio conferma l’importanza di parametri isto-patologici “secondari” nella stratificazione del rischio di ricorrenza di malattia, in particolare delle Cellule Tumorali Isolate. I risultati ottenuti chiariscono il ruolo delle ITC come indicatori prognostici clinicamente rilevanti e ne suggeriscono il possibile utilizzo come criterio di selezione di pazienti pN0 da sottoporre a terapia adiuvante.

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Bertazza, Loris. "Analisi delle Cellule Tumorali Circolanti nel carcinoma gastrico e nelle metastasi epatiche da cancro del colon-retto: ruolo di Survivin e CD133 come fattori prognostici". Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3427460.

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Background At present the only prognostic system routinely employed for the management of gastric cancer patients is the TNM staging classification, that identifies broad risk categories with a significant prognostic variability within each stage, which makes TNM a suboptimal predictive tool on the single patient basis. Only 10-20% of patients with liver metastases from colorectal cancer is resectable with radical intent and 60-70% will develop a relapse despite apparently curative surgery. Both these classes of patients therefore would benefit from additional treatments after surgery such as adjuvant chemotherapy. We need new prognostic factors that can identify patients at high risk to be submitted to treatment. Aim of the study To study circulating tumor cells by gene profiling the peripheral blood in order to identify prognostic biomarkers that add independent prognostic power to the conventional staging systems. This might allow for a better stratification of patients’ risk and thus a better therapeutic management of gastric cancer and metastatic colorectal cancer patients, especially in the adjuvant setting. Patients, materials and methods 70 patients, affected with gastric adenocarcinoma at different TNM stages of disease who underwent radical surgery and 50 patients undergoing liver resection for metastases from colorectal cancer (stage IV) were enrolled in the study. Immediately before surgery, a sample of peripheral blood was withdrawn from each patient. For each sample, RNA was extracted and utilized for quantitative real time PCR evaluation of the expression of the following genes: CK19, CEA, VEGF, and Survivin for gastric cancer patients; CK19, CK20, CEA, VEGF, EGFR, CD133 and Survivin for colorectal liver metastases patients. Univariate and multivariate survival analysis was performed to investigate on the prognostic role of these biomarkers. Results After stepwise variable selection, Cox multivariate analysis of survival showed a significant association between overall survival and both TNM stage ad Survivin gene expression levels in peripheral blood of gastric cancer patients, while multivariate analysis confirmed the statistically significant association between both the radical resection and the transcriptional levels of CD133 and overall survival in colorectal liver metastases patients. In addition, Survivin transcriptional levels were higher in patients with gastric cancer as compared to the calibrator reference (obtained from the peripheral blood of healthy donors) in 98.6% of cases; analogously, CK19 was upregulated in 97.1% of cases. These findings support the hypothesis that the peripheral blood gene profile might be utilized also as a diagnostic marker in gastric cancer. Concluding remarks The positive findings of this pilot study are the basis for larger prospective studies in larger groups of gastric cancer and colorectal liver metastases patients, aimed to validate the prognostic power of Survivin and CD33 expression in peripheral blood of these two groups, respectively. Moreover it would be interesting to further explore also the potential diagnostic value of the peripheral blood gene profile in gastric cancer.
Presupposti dello studio Attualmente l'unico sistema prognostico utilizzato in clinica per i pazienti con cancro gastrico è la stadiazione TNM, che crea classi di rischio con prognosi significativamente diversa, ma con un’alta variabilità del rischio all’interno delle singole classi, risultando così uno strumento prognostico non ottimale a livello di singolo paziente. Solo il 10-20% dei pazienti con metastasi epatiche da carcinoma del colon-retto (CRC) risulta resecabile con intento radicale e di questi il 60-70% svilupperà una recidiva nonostante l’intervento potenzialmente curativo. Entrambe queste classi di pazienti necessitano di trattamenti aggiuntivi alla chirurgia come la chemioterapia adiuvante. Sono quindi necessari fattori prognostici nuovi, che permettano di individuare i pazienti ad alto rischio da indirizzare alla terapia. Scopo dello studio Studiare le cellule tumorali circolanti, attraverso il profilo di espressione genica nel sangue periferico, per individuare fattori prognostici indipendenti, in modo da rendere migliore la stratificazione del rischio e di conseguenza la cura dei pazienti con adenocarcinoma gastrico e con metastasi epatiche da carcinoma del colon-retto, con particolare riguardo alla selezione dei pazienti da trattare con terapia adiuvante. Pazienti, materiali e metodi Nello studio sono stati inclusi 70 pazienti con adenocarcinoma gastrico in diverso stadio TNM sottoposti a gastrectomia con intento radicale e 50 pazienti con metastasi epatiche da CRC sottoposti a chirurgia. Prima dell’intervento chirurgico, a ogni paziente è stato eseguito un prelievo di sangue venoso periferico, se ne è estratto l’RNA totale ed il corrispondente cDNA è stato utilizzato per l’analisi di espressione genica mediante PCR quantitativa. Per i pazienti con carcinoma gastrico sono stati valutati i geni CK19, CEA, VEGF, Survivin; per i pazienti con metastasi epatiche da CRC sono stati valutati i geni CK19, CK20, CEA, VEGF, EGFR, CD133 e Survivin. Per valutare il ruolo prognostico di ogni marcatore sono state effettuate le analisi di sopravvivenza uni- e multivariata. Risultati All’analisi multivariata secondo Cox della sopravvivenza globale, dopo selezione stepwise, sono risultati fattori prognostici indipendenti per i pazienti con cancro gastrico la stadiazione TNM e l’espressione del gene codificante per Survivin, mentre per i pazienti con CRC metastatico sono risultati fattori prognostici indipendenti la radicalità dell’intervento e l’espressione di CD133 nel sangue periferico. Inoltre Survivin era maggiormente espressa nei pazienti con carcinoma gastrico rispetto al calibratore (ottenuto dal sangue di donatori sani) nel 98.6% dei casi; analogamente CK19 era maggiormente espressa nel 97.1% dei casi. Questi dati supportano la possibilità dell’utilizzo dell’espressione genica nel sangue periferico anche come marcatore diagnostico del carcinoma gastrico. Conclusioni I risultati positivi di queste analisi costituiscono la base per la conduzione di più ampi studi prospettici nelle due patologie considerate, al fine di poter validare il valore prognostico dell’espressione di Survivin e CD133 nel sangue periferico dei pazienti rispettivamente con carcinoma gastrico e con CRC metastatico. Sarebbe inoltre di sicuro interesse confermare il significato diagnostico del profilo genico del sangue periferico nel cancro gastrico.

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La, Morella Carla Maria Alessia. "La fibrinogenemia nel K colorettale (prospettive come fattore prognostico)". Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/949.

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Scopo della presente tesi è quello di valutare, in base ai dati della letteratura, se l iperfibrinogenemia costituisca un elemento clinicamente rilevante ai fini predittivi della recidiva del carcinoma colorettale. Viene inoltre presentata la casistica relativa ai casi di CRC operati presso la Clinica Chirurgica II (Direttore Prof. Salvatore Berretta) del P.O. Policlinico dal 2001 al 2010.

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Schutte, Berend. "Cancer cell ploidy and proliferation in colorectal carcinoma". Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1987. http://arno.unimaas.nl/show.cgi?fid=5360.

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Gruppo, Mario. "Subclinical myopathy and colorectal cancer: identification and role of new muscle damage and regeneration biomarkers". Doctoral thesis, Università degli studi di Padova, 2015. http://hdl.handle.net/11577/3424623.

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Background Skeletal muscle is the major reservoir of body proteins and it can be affected in conditions associated to altered protein turnover and metabolism such as cancer. Although severe wasting is seen primarily in patients with advanced malignancy, some of them present degree of wasting at the onset of disease. Autophagy has been recently described to play a relevant role in muscle wasting. Materials and Methods We performed morphometric studies and immunohistochemical analyses on intraoperative rectus abdominis muscle biopsies from 50 consecutive weight stable colorectal patients and 25 weight-stable patients operated for non-inflammatory benign diseases with no clinical signs of myopathies. Biochemical and molecular analyses have been performed in order to evaluate protein profile, the presence of autophagy induction and their correlation with clinical outcome. Results In cancer patients, we observed a subclinical myopathy characterized by an abnormal distribution of myonuclei relocated from the periphery inside the myofiber. The percentage of myofibers with abnormally located myonuclei was significantly higher in patients compared to controls. Analyses on serum samples showed that, in the absence of systemic inflammation, in the prevalence of cancer patients the levels of albumin and prealbumin were below the normal range and the mean value was significantly lower compared to that detected in controls. Molecular analyses showed an accumulation of p62, a typical marker of autophagy induction, significantly higher in cancer patients compared to controls. We found an inverse correlation between the number of abnormally nucleated myofibers and the presence of lymph node metastasis. Cancer relapse was correlated with low serum levels of prealbumin and high levels of p62 in myofibers of cancer patients. Conclusions Colorectal cancer patients have a subclinical myopathy characterized by myofibers with internally located myonuclei. In the absence of inflammation, cancer patients show low levels of prealbumin and albumin as markers of altered protein turnover and persistent high levels of p62 in myofibers as expression of autophagy induction with an impairment in physiological autophagic flux. Up to now our data indicate that skeletal muscle fibers show nuclear abnormalities that seems to be associated to a better prognosis, while the presence of an altered protein turnover at an early stage of disease, with an impairment in the physiological autophagic flux, that could be predictive of cancer relapse and onset of cancer cachexia.
Introduzione Il muscolo scheletrico rappresenta la principale riserva proteica del corpo e può essere compromesso in varie affezioni metaboliche e di alterato turnover proteico, quale il cancro. Benchè una severa perdita di massa sia generalmente presente in quadri neoplastici avanzati, in alcuni casi può essere già evidente in una fase di malattia iniziale. L’autofagia è stata recentemente descritta come uno dei possibili fattori responsabili del processo catabolico. Materiali e Metodi 50 pazienti sottoposti ad intervento chirurgico per neoplasia colorettale e 25 pazienti operati per patologia benigna non infiammatoria, in assenza di segni clinici di miopatia, sono stati sottoposti a biopsia muscolare su cui sono state eseguite analisi di carattere morfometrico ed istochimico. Sono state, inoltre, eseguite analisi biochimiche e molecolari al fine di valutare l’assetto proteico e lo stato di attivazione del processo autofagico e la loro correlazione con l’outcome clinico dei pazienti. Risultati Nei pazienti neoplastici abbiamo riscontrato la presenza di una miopatia subclinica, caratterizzata dalla presenza di fibre muscolari con un’anomala localizzazione del nucleo cellulare al centro della fibra, significativamente maggiore rispetto ai controlli. L’analisi dell’assetto proteico ha dimostrato valori sierici di albumina e prealbumina significativamente più bassi nei pazienti oncologici, mentre l’analisi molecolare ha documentato elevati livelli di p62 nelle fibre muscolari dei pazienti affetti da carcinoma colorettale, rispetto ai controlli. La valutazione dell’outcome clinico ha dimostrato una correlazione inversa tra la percentuale di miofibre anomale e l’insorgenza di metastasi linfonodali, mentre bassi livelli sierici di prealbumina ed alti livelli di p62 nelle fibre muscolari sono risultati correlati con un aumentato rischio di ripresa di malattia Conclusioni I pazienti affetti da carcinoma colorettale presentano una miopatia subclinica già all’insorgenza della malattia, caratterizzata dalla presenza di fibre con alterata posizione del nucleo nella cellula. In assenza di infiammazione sistemica e tissutale, i pazienti oncologici presentano bassi livelli sierici di albumina e prealbumina, come espressione di un alterato turnover proteico, nonché elevati livelli di p62 nelle fibre muscolari, a dimostrazione dell’attivazione del processo autofagico che risulta tuttavia compromesso. Tali dati suggeriscono, pertanto, un verosimile ruolo protettivo per le anomalie nucleari descritte, mentre un alterato turnover proteico ed una compromissione del normale flusso autofagico, in concomitanza dell’insorgenza della neoplasia, costituiscono un potenziale fattore predittivo negativo in termini di ripresa di malattia ed evoluzione verso uno stato cachettico.

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Barrow, Emma. "Cancer risk and biomarker analysis in mismatch repair deficient colorectal carcinoma". Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516737.

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Lynch Syndrome is caused by mutations in the DNA mismatch repair (MMR) genes; MLH1, MSH2, MSH6 and PMS2. An accurate estimation of cancer risk for MMR mutation carriers is essential for counselling and screening. United Kingdom (UK) specific cancer risks for MMR mutation carriers and cumulative colorectal cancer risks by decade have not been described to date. Using data from 121 Lynch Syndrome families, the cumulative lifetime risks of Lynch Syndrome spectrum cancers in mutation carriers were calculated, correcting for ascertainment bias. This data provides reassurance that current UK screening guidelines are appropriate. For colorectal cancer, tables of risk by decade were compiled for carriers of the different gene mutations. This novel data represents a useful counselling tool. Despite an increased cancer risk, individuals with Lynch Syndrome lack clear phenotypic characteristics. Mutation carrier identification is desirable as screening reduces mortality. After counselling and assessment of family history against clinical criteria, molecular diagnosis of tumour tissue is performed. Immunohistochemistry (IHe) of the MMR proteins has great potential as a method of identifying the most likely mutation and guiding mutation analyse. However IHC of the MMR proteins is not yet well established and problems have been reported with staining and slide interpretation. IHC slide assessment methods in the reported literature have been qualitative. This thesis describes the development and validation of a robust, semiquantitative scoring technique to be used in the assessment of IHC stained tumour sections from patients with possible Lynch Syndrome. Colorectal tumour sections from 51 MMR mutation carriers were stained with 3,3' Diaminobenzidine (DAB) using antibodies against the MMR proteins. Slide assessment was semiquantified using a 0-12 scale, and was found to be highly sensitive and specific for the identification of mutation carriers. It was found however, that protein expression may occur in the context of known pathogenic mutations, a potential pitfall in the screening process. Two quantitative techniques of slide assessment that could potentially obviate the need for human operator slide analysis were explored. Semiconductor quantum dots (QOs) are quantifiable fluorescent labels that can be used for multiplex staining. Quantitative QO IHC was compared to quantitative DAB IHC. Both are novel methodologies. Tumour sections from 36 mutation carriers were stained using each method, and multispectral analysis of the slides was performed. Quantitative analysis of the DAB stained slides was less sensitive than semi-quantitative analysis in this study, but was sufficiently sensitive to be used as a pre-screen in Lynch Syndrome. However despite the potential advantages of quantitative QD staining, it was less sensitive and specific than quantitative DAB IHC. The development of automated DAB IHC staining and quantitative multispectral slide analysis may enable future high throughput IHC for MMR mutation carrier identification. Around 15% of sporadic colorectal cancers develop along the MSI pathway due epigenetic MLH1 inactivation. The evidence suggests that patients with such tumours do not benefit from 5-Fluorouracil based chemotherapy. The cost effectiveness of identifying patients with such tumours was explored. Potential chemotherapeutic savings are substantial, supporting the introduction of this biomarker into clinical practice. The improved diagnostic accuracy of semi-quantitative IHC slide assessment and the potential for automation of quantitative IHC slide assessment would facilitate the introduction of this service.

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Fernando, Winnie Collet. "Molecular Pathogenesis of Serrated Carcinoma of the Colon". Thesis, Griffith University, 2014. http://hdl.handle.net/10072/367873.

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Colorectal cancer (CRC) progresses from precursor lesions or polyps via two main pathways – the traditional and serrated pathway. The traditional pathway is the conventional type, while the serrated neoplastic pathway has been recently identified and is not well characterised. The aim of this study was to evaluate molecular factors associated with the serrated pathway and study its progression from a serrated polyp to colorectal cancer using patient samples and mouse models. The first part of the study was to evaluate CIMP status of all the serrated polyp subtypes and its association with functionally important genes such as MLH1, p16 and IGFBP7 in patient samples. The mouse models were then utilized to assess the contribution of BRAF V600E mutation along with the cell cycle regulators and tumour suppressor genes, p16Ink4a and p19Arf in the initiation and progression of CRC. The CIMP study was a prospective study in which the real-time based MethyLight assay was employed to evaluate CIMP and methylation status of p16, IGFBP7 and MLH1 in 154 serrated polyps and 63 adenomas. Samples were subjected to bisulfite modification and methylation levels were assessed using the Weisenberger et al panel of methylation markers (IGF2, SOCS1, NEUROG1, RUNX3 and CACNA1G) with ALU as the reference gene.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
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Jankowski, Janusz Antoni Zygmunt. "Constitutive gene expression during colorectal tumorigenesis : in vivo and in vitro". Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321753.

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Melville, D. M. "The cancer risk in ulcerative colitis : the accuracy of markers of premalignant change and their value in clinical practice". Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235940.

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Majorana, Alessandra. "Alterazioni specifiche del trascrittoma dei microrna e struttura globale del network in carcinoma colorettale dopo trattamento con Cetuximab". Thesis, American Association for Cancer Research, 2011. http://hdl.handle.net/10761/129.

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Il carcinoma del colon-retto (CRC) e' una delle neoplasie piu' frequenti nel mondo occidentale e rappresenta un problema socio-sanitario di notevole rilievo. E' noto che non tutti i pazienti affetti da CRC rispondono in modo positivo alla terapia con i piu' comuni agenti antitumorali (es. Cetuximab): vi sono infatti dei fattori genetici predittivi della risposta, tra i quali sicuramente uno dei piu' noti e' lo stato mutazionale di KRAS. Tuttavia, questo approccio diagnostico molecolare e' comunque invasivo, poiche' presuppone un prelievo bioptico. Per questa ragione, diversi gruppi di ricercatori stanno cercando di individuare biomarcatori che, oltre ad essere specifici, siano identificabili con procedure non invasive. Indubbiamente, tra i possibili marcatori, i microRNA (miRNA) rivestono un ruolo particolarmente rilevante. I miRNA sono piccole molecole di RNA non codificante che svolgono un ruolo critico nella regolazione dell ' espressione genica in tutti i processi cellulari. Ad oggi, sono stati pubblicati diversi dati che suggeriscono come il profilo di espressione dei miRNA vari in modo specifico nei diversi tipi di cellule neoplastiche, in correlazione con il fenotipo del tumore e con la sua evoluzione. L' oggetto di questa tesi e' stato lo studio della relazione tra risposta terapeutica e modifiche del trascrittoma dei miRNA nel tumore colorettale (CRC), che ad oggi rimane sconosciuta. Per raggiungere questo obiettivo abbiamo effettuato il profiling dell'espressione di 667 miRNA in due linee cellulari umane CRC, una sensibile e l'altra resistente al Cetuximab (Caco-2 e HCT-116, rispettivamente) mediante RT-PCR con sonde TaqMan. Le Caco-2 e le HCT-116 esprimono diversi set di miRNA dopo il trattamento: in particolare, mentre nelle Caco-2 sono differenzialmente espressi 21 miRNA (DE miRNA), nelle HCT-116 i DE miRNA sono 22 (t-test, p <0.01). Testando l'espressione dei DE miRNA in campioni paraffinati di pazienti affetti da CRC, abbiamo scoperto che il miR-146b-3p e il miR-486-5p sono piu' abbondanti nei campioni con il gene KRAS mutato rispetto a quelli wild-type (test di Wilcoxon, p <0.05). Dall' analisi dei cluster e delle famiglie geniche dei DE miRNA e' emerso che miRNA localizzati in stretta prossimita' genomica o appartenenti alla stessa famiglia mantengono spesso lo stesso trend di espressione in seguito al trattamento. Secondo dati di letteratura, il 67% dei DE miRNA e' coinvolto nel cancro, incluso il CRC, mentre 19 targets dei DE miRNA sono stati precedentemente associati alla pathway del Cetuximab e del CRC, come ad esempio KRAS (targets dei DE miRNA let-7b e let-7e), PTEN e PIK3R1 (entrambi targets del miR-486-5p). Abbiamo identificato 25 fattori di trascrizione che putativamente controllerebbero questi DE miRNA; 11 di questi sono gia' stati individuati per essere coinvolti nella patogenesi del CRC, come ad esempio MYC, che controlla positivamente l ' espressione del miR-17* (un marcatore del CRC i cui livelli sono abbondanti in biopsie e plasma di pazienti). Sulla base di questi dati, suggeriamo che la sottoespressione di let-7b e let-7e e la sovraespressione del miR-17* potrebbero far considerare questi miRNA come marcatori molecolari candidati per la resistenza al Cetuximab. L'analisi funzionale globale delle network dei targets dei DE miRNA ha mostrato una significativa sovra-rappresentazione di processi biologici correlati al cancro, all' angiogenesi e alla risposta immunitaria, e di moduli centrati sui nodi critici coinvolti nell' internalizzazione di EGFR e sua degradazione ubiquitina-mediata. L'identificazione di miRNA la cui espressione e' legata all' efficacia della terapia, dovrebbe quindi consentire di predire la risposta dei pazienti al trattamento e potrebbe condurre ad una migliore comprensione dei meccanismi molecolari della risposta farmacologica. Il lavoro esposto in questa tesi e' stato pubblicato nel 2010 su Molecular Cancer Therapeutics (E-pub 29 Settembre).
The relationship between therapeutic response and modifications of miRNA transcriptome in Colorectal Cancer (CRC) remains unknown. We investigated this issue by profiling the expression of 667 miRNAs in two human CRC cell lines, one sensitive and the other resistant to cetuximab(Caco-2 and HCT-116, respectively) through TaqMan RT-PCR. Caco-2 and HCT-116 expressed different sets of miRNAs after treatment: specifically, 21 and 22 miRNAs were differentially expressed (DE) in Caco-2 or HCT-116, respectively (t-test, p<0.01). By testing the expression of DE miRNAs in CRC patients, we found that miR-146b-3p and miR-486-5p are more abundant in KRAS mutated samples respect to wild-type ones (Wilcoxon test, p<0.05). 67% of DE miRNAs were involved in cancer, including CRC, while 19 miRNA targets had been previously reported to be involved in the cetuximab pathway and CRC. We identified 25 TFs putatively controlling these miRNAs, 11 of which already reported to be involved in CRC. Based on these data, we suggest that the down regulation of let-7b and let-7e (targeting KRAS) and the up regulation of miR-17* (a CRC marker) could be considered as candidate molecular markers of cetuximab resistance. Global network functional analysis, based on miRNA targets, showed a significant overrepresentation of cancer-related biological processes and networks centered on critical nodes involved in EGFR internalization and ubiquitin-mediated degradation. The identification of miRNAs, whose expression is linked to the efficacy of therapy, should allow to predict the response of patients to treatment and possibly lead to a better understanding of the molecular mechanisms of drug response.

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Más fuentes

Libros sobre el tema "Carcinoma colorettale (Colorectal cancer)"

1950-, Seitz H. K., Simanowski U. A. 1949- y Wright Nicholas A, eds. Colorectal cancer: From pathogenesis to prevention? Berlin: Springer-Verlag, 1989.

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Hayat, M. A. Handbook of Immunohistochemistry and in Situ Hybridization of Human Carcinomas: Molecular Pathology, Colorectal Carcinoma, and Prostate Carcinoma. Burlington: Elsevier, 2005.

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1950-, Maguire Robert T. y Van Nostrand Douglas, eds. Diagnosis of colorectal and ovarian carcinoma: Application of immunoscintigraphic technology. New York: M. Dekker, 1992.

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Colorectal Cancer Gastrointestinal Carcinoma. Springer, 2009.

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Wright, Nicholas A., Helmut K. Seitz, B. C. Morson y Ulrich A. Simanowski. Colorectal Cancer: From Pathogenesis to Prevention? Springer London, Limited, 2012.

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Seitz, H. K. y U. A. Simanowski. Colorectal Cancer: From Pathogenesis to Prevention? Springer-Verlag Telos, 1989.

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Wright, Nicholas A., Helmut K. Seitz, B. C. Morson y Ulrich A. Simanowski. Colorectal Cancer: From Pathogenesis to Prevention? Springer Berlin / Heidelberg, 2012.

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Hayat, M. A. Handbook of Immunohistochemistry and in Situ Hybridization of Human Carcinomas, Volume 2: Molecular Pathology, Colorectal Carcinoma, and Prostate Carcinoma. Academic Press, 2005.

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Hayat, M. A. Handbook of Immunohistochemistry and in Situ Hybridization of Human Carcinomas, Volume 2: Molecular Pathology, Colorectal Carcinoma, and Prostate Carcinoma. Academic Press, 2005.

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Maguire, Robert T. y Douglas Van Nostrand. Diagnosis of Colorectal and Ovarian Carcinoma: Application of Immunoscintigraphic Technology (Targeted Diagnosis and Therapy). Marcel Dekker, 1992.

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Capítulos de libros sobre el tema "Carcinoma colorettale (Colorectal cancer)"

Hermanek, P. y L. H. Sobin. "Colorectal Carcinoma". En Prognostic Factors in Cancer, 64–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79395-0_7.

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Liu, K. C. y N. A. Wright. "Histogenesis of Colorectal Carcinoma". En Colorectal Cancer, 313–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85930-4_21.

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Kirkland, S. C. "Cell Differentiation in Colorectal Carcinoma". En Colorectal Cancer, 322–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85930-4_22.

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Hardcastle, Jack Donald. "Follow-up After Treatment of Carcinoma". En Colorectal Cancer, 29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78225-1_9.

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Soto, Jorge A. "Imaging of Colorectal Carcinoma". En Cancer Treatment and Research, 255–80. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-75587-8_10.

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Eva, Bandres, Bitarte Nerea, Natalia Ramirez, Zarate Ruth y Garcia-Foncillas Jesus. "Colorectal Carcinoma: Identification of MicroRNAs Using Real-Time Polymerase Chain Reaction". En Colorectal Cancer, 83–102. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9545-0_6.

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Smyrk, Thomas C., Henry T. Lynch, Patrice A. Watson y Henry D. Appelman. "Histologic Features of Hereditary Nonpolyposis Colorectal Carcinoma". En Hereditary Colorectal Cancer, 357–62. Tokyo: Springer Japan, 1990. http://dx.doi.org/10.1007/978-4-431-68337-7_52.

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Watanabe, Hidenobu, Yoichi Ajioka, Mitsuya Iwafuchi, Teiichi Motoyama, Noriko Ishihara y Jiro Hitomi. "Histogenesis of Gastrointestinal Carcinoma in Peutz-Jeghers Polyp". En Hereditary Colorectal Cancer, 337–42. Tokyo: Springer Japan, 1990. http://dx.doi.org/10.1007/978-4-431-68337-7_49.

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Hamilton, Stanley R. y Scott E. Kern. "Clinical and Pathological Associations with Molecular Genetic Alterations in Colorectal Carcinoma". En Hereditary Colorectal Cancer, 517–18. Tokyo: Springer Japan, 1990. http://dx.doi.org/10.1007/978-4-431-68337-7_76.

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Tsuji, Yoshiyuki. "A Monoclonal Antibody C12 Against Endometrial Carcinoma, Recognize Polyfucosyl Lactosamine-Bearing Glycoprotein". En Hereditary Colorectal Cancer, 131–34. Tokyo: Springer Japan, 1990. http://dx.doi.org/10.1007/978-4-431-68337-7_20.

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Actas de conferencias sobre el tema "Carcinoma colorettale (Colorectal cancer)"

Bernard, Stefanus y David Agustriawan. "Identification of microRNA Targeting Cancer Gene of Colorectal Carcinoma in Caucasian Population". En 2019 International Conference on Information and Communications Technology (ICOIACT). IEEE, 2019. http://dx.doi.org/10.1109/icoiact46704.2019.8938488.

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Dangles-Marie, Virginie. "Abstract IA05: PDX in colorectal cancer and carcinoma of the anal canal". En Abstracts: Patient-Derived Cancer Models: Present and Future Applications from Basic Science to the Clinic; February 11-14, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.pdx16-ia05.

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Carvalho, Beatriz, Begoña Diosdado, Jochim S. Terhaar Sive Droste, Anne S. Bolijn, Meike de Wit, Myrthe van Burink, Remond JA Fijneman, Nicole CT van Grieken y Gerrit A. Meijer. "Abstract A04: Chromosomal aberrations implicated in colorectal adenoma to carcinoma progression as markers of high-risk colorectal adenomas". En Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-a04.

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Stanczak, Aleksandra, Rafal Stec, Lubomir Bodnar, Wojciech Olszewski, Marzena Ciechowicz, Wojciech Kozlowski, Cezary Szczylik, Monika Lamparska‐Przybysz y Maciej Wieczorek. "Abstract B33: Prognostic role of Wnt/beta‐catenin pathway in colorectal carcinoma". En Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b33.

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Abreu, Francine B., Erika MM Santos, Benedito M. Rossi, Ana C. Krepischi, Maria I. Achatz, Dirce M. Carraro, Ricardo R. Brentani, Luiz P. Kowalski y Silvia R. Rogatto. "Abstract A24: Germline deletion at 3p12.3 in patients with hereditary breast and colorectal carcinoma". En Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a24.

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Jia, Jemianne, Minzhi Xing, Xiaoxi Ling, Mingfeng Bai y Hyun S. Kim. "Abstract 4407: Novel mitochondria-targeted Doxorubicin Prodrug for colorectal cancer and hepatocellular carcinoma: In vitro studies". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4407.

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Eisele, Yannick, Patrick M. Mallea, Biljana Gigic, W. Zac Stephens, Christy A. Warby, Kate Buhrke, Tengda Lin et al. "Abstract A01: Fusobacterium nucleatum and clinicopathologic features of colorectal carcinoma: Results from the ColoCare Study". En Abstracts: AACR Special Conference on the Microbiome, Viruses, and Cancer; February 21-24, 2020; Orlando, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.mvc2020-a01.

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Broek, Evert van den, Maurits J. J. Dijkstra, Quirinus J. M. Voorham, Beatriz Carvalho, Mark A. van de Wiel, Sanne Abeln, Gerrit A. Meijer y Remond J. A. Fijneman. "Abstract A07: Detection of structural variants and recurrent breakpoint genes in colorectal adenoma-to-carcinoma progression". En Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-a07.

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Kim, Han Sang, Wonkyu Kim, Chang Gon Kim, Jinseon Yoo, Soonmyung Paik, Eui-Cheol Shin, Tae-Min Kim, Hoguen Kim y Joong Bae Ahn. "Abstract C132:Fusobacterium nucleatumin colorectal carcinoma and expression of multiple immune checkpoint molecules on T cells". En Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-c132.

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Chen, Yen-Chou, Ching Huai Ko, Shing Chuan Shen y Liang Yo Yang. "Abstract C34: The role of COX-2/PGE2 in gossypol-induced apoptosis of colorectal carcinoma cells". En Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-c34.

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