Σκοπός: Η μελέτη βιολογικών και θεραπευτικών συσχετισμών σε ασθενείς με ηπατοκυτταρικό καρκίνωμα και ο δυνητικός ρόλος της απόπτωσης. Ασθενείς και Μέθοδοι: Η μελέτη περιέλαβε 35 παρασκευάσματα μερικών ηπατεκτομών από ισάριθμους ασθενείς με ηπατοκυτταρικό καρκίνωμα, μη ινοπεταλιώδους τύπου, που αφαιρέθηκαν με ηπατεκτομή για θεραπευτικό σκοπό. Σε αυτούς τους όγκους εκτιμήθηκαν διάφορα μακροσκοπικά και μικροσκοπικά χαρακτηριστικά, διαβαθμίστηκαν και συσχετίστηκαν με το διάστημα ελεύθερο νόσου. Επιπρόσθετα, σε τομές παραφίνης εκτιμήθηκε η έκφραση του bcl-2 και του bax (ανοσοϊστοχημεία/mRNA in-situ υβριδισμός) και της πρωτεΐνης p53. Αποτελέσματα: Η αγγειακή διήθηση η οποία είναι ο ισχυρότερος προβλεπτικός παράγοντας υποτροπής της νόσου, σχετίζεται με το μέγεθος των όγκων, την ύπαρξη γιγαντοκυττάρων και νέκρωσης, τον επικρατούντα και το χειρότερο βαθμό διαφοροποίησης και τον αποπτωτικό/μιτωτικό δείκτη. Ο in-situ υβριδισμός ανέδειξε έκφραση του mRNA του bcl-2 σε 25 από τους 35 ασθενείς (70%). Η ανοσοϊστοχημική χρώση δεν ανέδειξε έκφραση της πρωτεΐνης του bcl-2 στα καρκινικά κύτταρα. Αντίθετα, το bax mRNA και η πρωτεΐνη bax έδειξαν παρόμοιο τρόπο έκφρασης και ανευρέθηκαν μέσα στα ηπατοκύτταρα και στα χολαγγεία. Η έκφραση του bax mRNA ήταν υψηλότερη σε όγκους καλής διαφοροποίησης. Η έκφραση του p53 ήταν μικρότερη στον μικροδοκιδώδη τύπο από το συμπαγή τύπο και ήταν υψηλότερη σε πτωχά διαφοροποιημένους όγκους από τους καλά ή μετρίως διαφοροποιημένους όγκους. Συμπεράσματα: Η ηπατική καρκινογένεση στον άνθρωπο είναι μια πολυπαραγοντική και πολυεστιακή διαδικασία. Η αγγειακή διήθηση σχετίζεται με τον αποπτωτικό/μιτωτικό δείκτη και υψηλότερος αποπτωτικός/μιτωτικό δείκτης σχετίζεται με καλύτερο ελεύθερο νόσου διάστημα. Επιπλέον, η πρωτεΐνη bcl-2 δεν εκφράζεται ενώ εκφράζεται το mRNA, το οποίο εισηγείται μετα-μεταφραστικό λάθος και δείχνει ότι το bcl-2 δεν παίζει σημαντικό ρόλο στην εξέλιξη του ηπατοκυτταρικού καρκινώματος. / Aim: The study of biologic and therapeutic correlations in patients with hepatocellular carcinomas and the potential role of apoptosis. Patients and Methods: The study included 35 partial hepatectomy specimens removed from equal number of patients with nonfibrolamellar hepatocellular carcinomas (HCCs) for therapeutic reasons. In these tumors several macroscopic and microscopic features were assessed, graded and correlated with disease free survival. In addition, in paraffin sections the expressions of bcl-2 and bax (protein immunohistochemistry / mRNA-in situ hybridization) and p53 protein were assessed. Results: Vascular invasion, which is the strongest predictor of disease recurrence, correlates significantly with tumor size, tumor giant cells and necrosis, the predominant and worst degree of differentiation, and the apoptosis/mitosis ratio. Immuno-histochemical staining failed to reveal any bcl-2 protein expression in tumor cells of HCC. In the contrary, bax MRNA and protein displayed somehow a similar pattern of expression. They were detected within hepatocytes, bile duct epithelial and cholangiolar epithelial cells. Ηigher bax mRNA expression was noted in grade I carcinomas. Expression of p53 protein was less in the microtrabecular type than in the solid type and it was higher in poorly differentiated tumors than in those that were well or moderately well differentiated. Conclusions: Liver carcinogenesis in humans is a multistep and multifocal process. Vascular invasion correlates with the apoptosis/mitosis ratio and a higher apoptosis/mitosis ratio correlates with improved disease free survival. In addition, bcl-2 gene is frequently present but its protein product is absent. This suggests a post-translational mechanism of bcl-2 protein degradation, indicating that bcl-2 does not play a substantial role in the progress of hepatocellular carcinoma.

Atliktas perspektyvusis stebėjimo tyrimas, kurio metu buvo tirti sunkią galvos smegenų traumą patyrę vaikai, gydyti KMUK Vaikų intensyviosios terapijos skyriuje. Pacientų būklė pagal GBS vertinta išvykstant iš gydymo įstaigos ir po šešių mėnesių. Darbo tikslas Nustatyti sunkią galvos smegenų traumą patyrusių vaikų ligos baigčių prognozinius veiksnius. Darbo uždaviniai 1. Įvertinti ankstyvas ir vėlyvas sunkią galvos traumą patyrusių vaikų ligos baigtis. 2. Nustatyti sunkią galvos traumą patyrusių vaikų vidinio kaukolės slėgio ir smegenų perfuzinio slėgio ryšį su ligos baigtimis. 3. Nustatyti sunkią galvos traumą patyrusių vaikų traumos pobūdžio ryšį su ligos baigtimis. 4. Nustatyti paciento būkės vertinimo skalių ir laboratorinių tyrimų kritines reikšmes ir jų prognozinę vertę. 5. Nustatyti laboratorinių tyrimų kritines reikšmes ir jų prognozinę vertę. Išgyveno 80,5 proc. sunkią galvos smegenų traumą patyrusių vaikų. Išvykstant iš gydymo įstaigos 50 proc. pacientų, o po šešių mėnesių – 24,2 proc. pacientų traumos baigtis buvos bloga. Įtakos traumos baigtims turėjo kraujavimas po kietuoju smegenų dangalu, smegenų edema, kaukolės kaulų lūžiai. Nustatytos laktatų, gliukozės kiekio kraujo serume, vaikų traumų skalės, Glazgo komų skalės ir vaikų mirštamumo indekso 2 kritinės reikšmės, prognozuojančios mirtį, blogą baigtį išvykstant iš gydymo įstaigos ir po šešių mėnesių. Dekompresinė kraniotomija, atlikta, kai VKS = 24,5 mmHg,o SPS = 46.5 mmHg ligos baigčių nepakeitė. / The prospective observational study involved children after severe traumatic brain injury treated in Pediatric Intensive Care Unit of Kaunas University of Medicine Hospital. The outcome according to Glasgow Outcome Scale was assessed on discharge and after six months The aim of the study was to determine the prognostic factors in children after severe traumatic brain injury. The objectives of the study: 1. To evaluate early and late outcomes in children after severe traumatic brain injury 2. To evaluate the relation of intracranial pressure and cerebral perfusion pressure with outcome in children after severe traumatic brain injury. 3. To evaluate the relation between type of injury and outcome. 4. To determine the threshold values for trauma scoring scales and to evaluate their prognostic significance. 5. To determine the threshold values for laboratory findings and to evaluate their prognostic significance. The survival rate was 80.5 %.half of patients had bad outcome on discharge and 24.4 % – had bad outcome after six months. The prognostic factors of outcome for children after severe traumatic brain injury were subdural hemorrhage, cerebral edema and skull fracture. Threshold values of Pediatric Trauma Score, Glasgow Coma Score and Pediatric index of Mortality 2 for death and bad outcomes on discharge and after six months were ascertained. Decompressive craniectomy performed at ICP ≥ 24.5 mmHg, CPP ≤ 46.5 mmHg had no impact on outcome in children after severe traumatic... [to full text]

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Tyrimo tikslas - ištirti intensyvios terapijos ligonių slaugymo įtaką jų gydymo baigčiai ligoninėje. Tyrimo uždaviniai. Įvertinti intensyvios terapijos skyriaus ligonių gydymo rezultatus (mirštamumą, gydymo ligoninėje laiką, pakartotinių guldymų į intensyvios terapijos skyrių, kitų komplikacijų dažnumą). Nustatyti, kokią įtaką turi intensyvios terapijos ligonių slaugos intensyvumas jų gydymo baigčiai ligoninėje. Palyginti intensyvios terapijos skyriaus ligonių gydymo baigtį ligoninėje, priklausomai nuo jų slaugos intensyvumo intensyvios terapijos skyriuje. Tyrimo objektas. Ligonių slauga intensyvios terapijos skyriuje. Tyrimo metodai. Buvo atliktas retrospektyvinis tyrimas, pasirinkta dokumentų turinio statistinė duomenų analizė, į tyrimą buvo įtraukti 261 tiriamųjų ligonių, kurie nuo 2008-07-01 iki 2008-11-01 gydėsi 15 lovų I Reanimacijos - intensyvios terapijos skyriuje VUL Santariškių klinikose, ir kurie, perkėlus iš I RITS, tęsė gydymą Santariškių klinikose bendrosiose palatose. Ligoniai, gydyti I RITS trumpiau kaip 8 valandas, t. y. tie, kurių būklė aktyviai stebėta trumpą laiką arba kurie dėl ypač sunkios būklės greitai mirė, taip pat ligoniai kurie buvo iš I RITS iškelti į kitus stacionarus, į tyrimą nebuvo įtraukti. Slaugos procesas RITS buvo apskaičiuotas individualiai vienam pacientui, taikant validizuotą, iš anglų kalbos išverstą, Terapinių Intervencijų Apskaičiavimo Skalę – 28 (Therapeutic Inervention Scoring Sistem -28 (TISS-28)). Tyrimo duomenys buvo apdoroti ir... [toliau žr. visą tekstą] / Research objective – to analyze the influence of intensive care patients nursing on their hospital outcomes. Research tasks: To evaluate the results of treatment of intensive care unit patients (mortality, duration of stay in a hospital, frequency of repeated admissions to department of intensive care and other complications). To determine the influence of intensity of care delivered to intensive care patients to their hospital outcome. To compare hospital outcomes of intensive care unit patients according to intensity of care delivered to them in department of intensive care. Object of research: Nursing of patients in unit of intensive care. Method of research: There was a retrospective research accomplished and statistic analysis of document content chosen. The research included 261 surveyed patients who were treated in fifteen-bed Ist Department of Reanimation and Intensive Therapy of Vilnius University Hospital Santariškių klinikos and who continued treatment in general-purpose wards of Santariškių klinikos after transferring from Ist ICU. Patients who stayed in Ist ICU for less than 8 hours, i.e. those whose state was actively observed for a short period or those who died because of their particularly critical state and those who were transferred from Ist ICU to other hospitals, were excluded from the research. Nursing process in ICU was evaluated for each patient individually using Therapeutic Intervention Scoring System -28 (TISS-28). Main results of research:... [to full text]

The survival for high-grade glioma patients is poor and the treatment may cause severe side effects. A common obstacle in the treatment is chemoresistance. To improve the quality of life and prolong survival for these patients prognostic biomarkers and new approaches for chemotherapy are needed. To this end, a strategy to evade chemoresistance was evaluated by combining chemotherapeutic drugs with agents inhibiting resistance mechanisms identified by a bioinformatic analysis (paper I). The prognostic value of 13 different proteins was analyzed in this thesis (papers II-IV). Two of them, p38 mitogen-activated protein kinase (MAPK) and protein tyrosine phosphatase non-receptor type 6 (PTPN6, also known as SHP1) were analyzed for their potential as targets in combination chemotherapy (in paper III and IV, respectively).   We found that: PTPN6 expression and methylation status may be important for survival of anaplastic glioma patients, p38 MAPK phosphorylation may be a potential negative prognostic biomarker for high-grade glioma patients and FGF2 expression may be a potential negative prognostic biomarker for proneural glioma patients. PTPN6 may be a useful target for combination chemotherapy with cisplatin, melphalan or bortezomib in high-grade gliomas. The following drug combinations; camptothecin combined with an EGFR or RAC1 inhibitor, imatinib combined with a Notch or RAC1 inhibitor, temozolomide combined with an EGFR or FAK inhibitor and vandetanib combined with a p38 MAPK inhibitor may be useful combination chemotherapy for high-grade gliomas.

This dissertation presents a model-based reasoning architecture with a two fold purpose: to detect and classify component faults from observable system behavior, and to generate fault propagation models so as to make a more accurate estimation of current operational risks. It incorporates a novel approach to system level diagnostics by addressing the need to reason about low-level inaccessible components from observable high-level system behavior. In the field of complex system maintenance it can be invaluable as an aid to human operators. The first step is the compilation of the database of functional descriptions and associated fault-specific features for each of the system components. The system is then analyzed to extract structural information, which, in addition to the functional database, is used to create the structural and functional models. A fault-symptom matrix is constructed from the functional model and the features database. The fault threshold levels for these symptoms are founded on the nominal baseline data. Based on the fault-symptom matrix and these thresholds, a diagnostic decision tree is formulated in order to intelligently query about the system health. For each faulty candidate, a fault propagation tree is generated from the structural model. Finally, the overall system health status report includes both the faulty components and the associated at risk components, as predicted by the fault propagation model.

L’ensemble de ce travail vise à étudier les mécanismes de résistance aux thérapies anti-angiogéniques dans le traitement du cancer du rein à cellules claires (ccRCC). Nous avons mis en évidence que le bévacizumab (BVZ), un anticorps monoclonal humanisé anti-VEGF utilisé en clinique, accélère la croissance de ccRCC humain chez la souris nude. Ce modèle mime la phase d’échappement souvent observée chez les patients. Le traitement BVZ induit de la lymphangiogenèse associée à une surexpression du VEGF-C. Les cellules tumorales après traitement possèdent également des capacités d’invasion accrues. Ainsi, le traitement BVZ pourrait faciliter la progression tumorale et la formation de métastases dans les ccRCC. Le traitement entraine également une diminution de l’expression d’une phosphatase membranaire, la phospho-tyrosine phosphatase récepteur kappa (PTPR)impliquée dans le contrôle de l’activité de récepteurs à activité tyrosine kinase, comme le récepteur de l’EGF, du PDGF et de l’HGF. Ces récepteurs régulent la prolifération et la migration cellulaire. Le traitement BVZ faciliterait donc la croissance tumorale indépendante du VEGF. Enfin, le traitement induit une augmentation de la sécrétion de cytokines angiogéniques redondantes qui prennent le relais du VEGF, comme les cytokines CXCL7 et CXCL8, et facilitent le développement tumoral sous traitement BVZ. En particuliers, la cytokine CXCL7 et ses récepteurs CXCR1-2 ont un rôle central dans le développement des ccRCC. Cibler l’axe CXCL7/CXCR1-2 réduit efficacement la croissance tumorale. Les récepteurs cibles de PTPR, pour lesquels des inhibiteurs sont actuellement utilisés pour le traitement d’autres cancers, le VEGF-C et la cytokine CXCL7, pourraient donc constituer de nouveaux marqueurs prédictifs d’efficacité du BVZ et de nouvelles cibles thérapeutiques dans le traitement des ccRCC. La résistance au BVZ pourrait également s’expliquer par l’existence de formes "bénéfiques" anti-angiogéniques du VEGF qui sont reconnues par le BVZ avec la même affinité que les formes pro-angiogéniques. Nous avons mis en évidence qu’une immunisation prophylactique à l’aide d’un peptide spécifique du VEGF pro-angiogénique limite la croissance tumorale de ccRCC syngéniques de souris. De la même façon, en traitement curatif, l’utilisation d’anticorps spécifiques du VEGF pro-angiogénique bloque la croissance de ccRCC chez la souris nude sans induire les différents mécanismes d’échappement observés avec le BVZ. Ces résultats suggèrent la pertinence du ciblage spécifique des formes pro-angiogéniques de VEGF dans le traitement des ccRCC. / The aim of my work is to study resistance mechanisms to anti-angiogenic treatments of Clear Cell Renal Carcinoma (ccRCC). We observed that bevacizumab (BVZ) -a humanized monoclonal antibody targeting VEGF and currently used in the clinic- promotes the growth of human ccRCC xenografts in nude mice. This model mimics the “escape phase” widely observed in patients. BVZ treatment induces lymphangiogenesis and over-expression of VEGF-C. Tumor cells exposed to the treatment acquire an increased spreading capacity. Hence, BVZ might promote tumor progression and metastasis formation of ccRCC. Furthermore, this treatment decreases the expression of the receptor phosphor tyrosine phosphatase kappa (PTRP). This phosphatase is involved in the regulation of tyrosine kinase receptors controlling growth and migration, among others EGF, PDGF and HGF receptors. Thus, BVZ might promote tumor growth independently of VEGF. Moreover, the treatment increases secretion of redundant cytokines like CXCL7 and CXCL8. By their ability to exert similar effect as VEGF, these cytokines promote tumor development under BVZ treatment. In particular, CXCL7 and its receptors CXCR1 and CXCR2, play a central role in the development of ccRCC. Targeting this pathway efficiently reduces tumor growth. Target receptors of PTRP for which inhibitors are currently used for other cancers, VEGF-C and CXCL7 could therefore be regarded as new predictive markers for BVZ efficiency and may be considered as potential therapeutic targets. Resistance to BVZ could also be explained by the presence of "beneficial" forms of anti-angiogenic VEGF recognized by the BVZ with the same affinity as the pro-angiogenic forms. We have demonstrated that prophylactic immunization with a pro-angiogenic VEGF-specific peptide limits tumor growth of murine syngeneic ccRCC. Similarly, in curative therapy, antibodies specific for pro-angiogenic VEGF block growth of ccRCC in nude mice without inducing the escape mechanisms observed with BVZ. These results highlight the relevance of targeting such pro-angiogenic forms of VEGF for the treatment of ccRCC.

Os marcadores prognósticos em mastologia têm sido utilizados como apoio diagnóstico para prever o comportamento dos neoplasmas mamários (prognóstico) e determinar a provável resposta ao tratamento pré ou pós-cirúrgico. Estudos têm sido feitos sobre o prognóstico dos tumores mamários caninos (TMCs) que apresentam semelhanças e diferenças com tumores mamários humanos. Além disso, esses tumores exibem, com alta freqüência, proliferação de células mioepiteliais que podem sofrer metaplasia, acompanhada de alterações moleculares. O presente estudo teve o objetivo de verificar a expressão imuno-histoquímica e a associação de diferentes marcadores utilizados como prognósticos nos tumores de mama humana (RE, RP, c-erbB-2 e Ki-67) e marcadores mioepiteliais (p63, CK5 e vimentina) nos TMCs. O primeiro artigo analisa a expressão desses marcadores em 35 tumores encontrados em onze fêmeas caninas nas quais foram identificados tumores malignos múltiplos nas glândulas mamárias. Cada tipo histológico analisado em fêmeas portadoras de tumores múltiplos expressou marcadores prognósticos e mioepiteliais peculiares à sua histogênese, porém houve associação dessa expressão apenas em alguns tipos celulares presentes nos TMCs. Os tumores com componente epitelial carcinomatoso não apresentaram diferenças significativas, no entanto, nos tumores com componente complexo e misto, ocorreu associação entre a expressão da p63, CK5 e vimentina. No conjunto de marcadores estudados, a p63 e a CK5 mostram-se promissoras na elucidação da transformação das células mioepiteliais concomitante à invasão tumoral e com relação à expressão da vimentina que se mostrou bem evidenciada durante a transformação da célula mioepitelial proliferada a célula participante do mesênquima do neoplasma invasor em mamas de caninos, ao menos nos aspectos de expressão molecular e morfológica. O segundo artigo analisa os marcadores mioepiteliais em 82 casos de TMCs malignos. Este estudo comprovou a freqüência e a associação da expressão desses marcadores em determinados tipos histológicos tumorais e celulares, permitindo a identificação das células mioepiteliais em transformação na maior parte dos TMCs malignos, notadamente, os que apresentam componente mesenquimal metaplásico. Mais estudos devem ser feitos na tentativa de verificar a significância da expressão encontrada no comportamento biológico desses tumores. / Prognostic markers in mastology have been used as diagnostic support, to predict the behavior of mammary neoplasias (prognosis) and to determine their possible response to treatment before or after surgery. Studies have been conducted on the prognosis of canine mammary gland tumors (MGTs), which show similarities to and differences from human breast tumors. In addition, these tumors often show proliferation of myoepithelial cells, which may undergo metaplasia, accompanied by molecular alterations. The aim of the present study was to check the immunohistochemical expression and the association between different markers used as prognostic factors in human breast tumors (ER, RP, c-erbB-2 and Ki-67) and myoepithelial markers (p63, CK5 and vimentin) in MGTs. The first article analyzes the expression of these markers in 35 tumors in 11 female dogs, where multiple tumors were identified in the mammary glands. Each histological type analyzed in the female dogs with multiple tumors expressed prognostic and myoepithelial markers that were peculiar to their histogenesis, but the association of this expression was observed only in some cell types of MGTs. Tumors with a carcinomatous epithelial component did not have significant differences, but tumors with complex and mixed components showed association between the expressions of p63, CK5 and vimentin. Of the group of investigated markers, p63 and CK5 proved to be promising tools in elucidating the transformation of myoepithelial cells concomitantly to tumor invasion and in terms of vimentin expression, which was quite pronounced in this transformation from proliferating myoepithelial cells into cells that participate in the mesenchyma of the invasive neoplasia in canine mammary glands, at least with regard to the aspects of molecular and morphological expression. The second article analyzes myoepithelial markers in 82 cases of malignant MGTs. This study corroborated the frequency and association of the expression of these markers in certain histological tumor and cell types, allowing for the identification of myoepithelial cells in transformation in most malignant MGTs, chiefly those with a metaplastic mesenchymal component. Further studies are necessary in order to assess the importance of expression found in the biological behavior of these tumors.

Advanced understanding of the global carbon budget requires large-scale and long-term information on forest carbon pools and fluxes. In situ and remote sensing measurements have greatly enhanced monitoring of forest carbon dynamics, but incomplete data coverage in space and time results in significant uncertainties in carbon accounting. Although theoretical and mechanistic models have enabled continental-scale and global mapping, robust predictions of forest carbon dynamics are difficult without initialization, adjustment, and parameterization using observations. Therefore, this dissertation is focused on a synergistic combination of lidar measurements and modeling that incorporates biophysical principles underlying forest growth. First, spaceborne lidar data from the Geoscience Laser Altimeter System (GLAS) were analyzed for monitoring and modeling of forest heights over the U.S. Mainland. Results showed the best GLAS metric representing the within-footprint heights to be dependent on topography. Insufficient data sampling by the GLAS sensor was problematic for spatially-complete carbon quantification. A modeling approach, called Allometric Scaling and Resource Limitations (ASRL), successfully alleviated this problem. The metabolic scaling theory and water-energy balance equations embedded within the model also provided a generalized mechanistic understanding of valid relationships between forest structure and geo-predictors including topographic and climatic variables. Second, the ASRL model was refined and applied to predict large-scale patterns of forest structure. This research successfully expanded model applicability by including eco-regional and forest-type variations, and disturbance history. Baseline maps (circa 2005; 1-km2 grids) of forest heights and aboveground biomass were generated over the U.S. Mainland. The Pacific Northwest/California forests were simulated as the most favorable region for hosting large trees, consistent with observations. Through sensitivity and uncertainty analyses, this research found that the refined ASRL model showed promise for prognostic applications, in contrast to conventional black-box approaches. The model predicted temporal evolution of forest carbon stocks during the 21st century. The results demonstrate the effects of CO2 fertilization and climate feedbacks across water- and energy-limited environments. This dissertation documents the complex mechanisms determining forest structure, given availability of local resources. These mechanisms can be used to monitor and forecast forest carbon pools in combination with satellite observations to advance our understanding of the global carbon cycle.

OBJETIVO: Determinar o impacto de fatores prognósticos na sobrevida de pacientes com metástases hepáticas ressecadas e originadas de câncer colorretal. CASUISTICA E MÉTODOS: Foram analisados os prontuários de 28 pacientes submetidos a ressecção hepática de metástases de câncer colorretal de Abril /1992 a Setembro /2001. Foram realizadas 38 ressecções (8 pacientes com mais de uma ressecção no mesmo tempo cirúrgico e 2 pacientes submetidos a re-ressecções). Todos haviam sido submetidos previamente à ressecção do tumor primário. Utilizou-se um protocolo de rastreamento de metástases hepáticas que incluiu revisões clinicas trimestrais, ecografia abdominal e dosagem de CEA até completarem-se 5 anos de seguimento e, após, semestralmente. Os fatores prognósticos estudados foram: estágio do tumor primário, tamanho das metástases > 5cm, intervalo entre ressecção do tumor primário e surgimento da metástase <1 ano, CEA>100ng/ml, margens cirúrgicas <1cm e doença metastática extra-hepática. O estudo foi retrospectivo e a análise estatística foi feita através da curva de Kaplan-Meier, do log rank e da regressão de Cox. RESULTADOS: A morbidade foi 39,3% e a mortalidade operatória foi 3,6%.A sobrevida em 5 anos foi de 35%. Os fatores prognósticos independentes adversos foram: intervalo <1 ano entre ressecção do tumor primário e surgimento da metástase (p=0,047 e RR 11,56) e doença metastática extra-hepática (p=0,004 e RR=57,28). CONCLUSÕES: A ressecção hepática de metástases de câncer colorretal é um procedimento seguro com sobrevida em 5 anos acima dos 30%. Foram fatores prognósticos independentes adversos: doença metastática extra-hepática e intervalo<1ano entre ressecção do tumor primário e surgimento da metástase. / Prognostic factors following liver resection for hepatic metastases from colorectal cancer. BACKGROUND: To determine the impact of prognostic factors on survival of patients with metastases from colorectal cancer that underwent liver resection. METHODS: The records of 28 patients that underwent liver resection for metastases from colorectal cancer between April /1992 and September/2001 were retrospectively analized. Thirty-eight resections were performed (more than one resection in eight patients and two patients underwent re-resections). The primary tumor was resected in all the patients. A screening protocol for liver metastases including clinical examinations every three months, abdominal ultrassonography and CEA level until five years of follow-up and after every six months, was applied. The prognostic factors analized regarding the impact on survival were: Dukes C stage of primary tumor, size of metastasis > 5cm, a disease-free interval from primary tumor to metastasis < 1 year, CEA level > 100ng/ml, resection margins < 1cm and extrahepatic disease. The Kaplan-Meier curves, log rank and Cox regression were used for the statistical analysis. RESULTS: Perioperative morbidity and mortality were 39,3% and 3,6% respectively. The 5-year survival rate was 35%. The independent prognostic factors were: disease-free interval from primary tumor to metastasis < 1year (p=0,047; RR=11,56) and extrahepatic metastatic disease (p=0,004; RR=57,28). CONCLUSIONS: The liver resection for metastases from colorectal cancer is a safe procedure with more than 30% 5-year survival .Disease- free interval from primary tumor to metastasis < 1year and extrahepatic disease were independent prognostic factors.