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Introduction: Reticulocyte count and novel derived parameters provide insight into the effectiveness of erythropoiesis and may be useful tools in the classification and diagnosis of anemias. However, there is no standardisation, so we consider it necessary that each laboratory evaluates the parameters according to its own methodology and instrumentation and establishes its own reference ranges. Our aim was to establish the reference intervals (RIs) of reticulocyte profile provided by the Beckman Coulter DxH 900 haematological autoanalyzer in our reference population., Methods: One hundred and seventy-five healthy adults (18 to 62 years) were included. Subjects were collected from the blood donation centre of the Hospital Clínico San Carlos (Madrid, Spain) upon informed consent. Whole blood was collected and assayed for 14 haematological parameters on the Beckman Coulter DxH 900 analyzer in the haematology laboratory of the Clinical Analysis Department. RIs were established as per Clinical and Laboratory Standards Institute EP28-A3c guidelines using three different statistical approaches., Results: RIs estimated using the non-parametric method and the Harrell-Davis bootstrap method were very similar. RIs estimated by the robust method were narrower. Gender partitioning was required for two haematological parameters (low haemoglobin density (LHD) and microcytic anaemia factor (MAF)). The rest of the parameters did not need to be partitioned according to Lahti's method., Conclusion: RIs have been established for 14 hematologic parameters of the reticulocyte profile for the Beckman Coulter DxH 900 haematology analyzer using a healthy cohort of adult subjects., (© 2024 John Wiley & Sons Ltd.)

Objectives: Monocyte distribution width (MDW) is a new biomarker used as an early indicator of sepsis (ESId). It is often aids in the identification of patients who may develop sepsis. This study aims to establish the MDW reference interval (RI) within the healthy population of blood donors using EDTA-K 2 as anticoagulant. Many hospitals use this biomarker as a means of identifying patients who present to the hospital with sepsis., Methods: A total of 274 samples obtained from healthy donors were analyzed. MDW measurements were taken within 2 h post-extraction. The RI was estimated using various statistical methodologies, including the recommended CLSI EP28-A3c guideline, non-parametric and robust methods, along with the Harrell-Davis bootstrap method applied to the entire sample., Results: The RI estimated through non-parametric method was 14.77 CI90 % (14.36-14.97)-21.13 CI90 % (20.89-21.68); RI using the robust method was 15.64-19.05 and RI using the Harrell-Davis bootstrap method was 14.73 CI90 % (14.53-14.92)-21.14 CI90 % (20.88-21.40)., Conclusions: Based on clinical applicability, we recommend utilizing the RI derived from the non-parametric method, aligning with the CLSI recommendations. Furthermore, we consider that our results can be taken as a reference in other laboratories that serve a population similar to our study cohort., (© 2024 the author(s), published by De Gruyter, Berlin/Boston.)

Objective: The aim of the present study was to evaluate the diagnostic performance of monocyte distribution width (MDW) as a biomarker for sepsis diagnosis in severe patients attended in the Emergency Department for different conditions and not only infections., Methods: We performed an observational study in a consecutive prospective cohort including severe patients attending the Emergency Department with different conditions. MDW and other biomarkers were determined from samples obtained during the first care of patients. The diagnostic performance of the different biomarkers was determined based on the final diagnosis at patient discharge., Results: One hundred two patients, with a mean age of 76.7 (SD 16.5) years were included, 53 being (51.9%) male. Among the patients included, 65 (63.7%) had an infectious disease while the remaining had other different conditions. A MDW cut-off of 20.115 provided the best accuracy to identify infected patients, with a sensitivity of 89.2 (95% CI 79.4-94.7), a specificity of 89.2 (95% CI 75.3-95.7), a positive predictive value of 93.5 (95% CI 84.6-97.5), a negative predictive value of 82.5% (95% CI 68.0-91.3), a positive likelihood ratio of 8.25 (3.26-20.91), and a negative likelihood ratio of 0.12 (0.06-0.24). The area under the receiver operating characteristic curve for infection according to MDW was 0.943 (95% CI 0.897-0.989; p<0.001)., Conclusions: A MDW > 20.115 may be associated with infection and could help to distinguish between infected and non-infected patients in severe patients. These results must be confirmed in new studies due to the limited patient sample included., (©The Author 2023. Published by Sociedad Española de Quimioterapia. This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)(https://creativecommons.org/licenses/by-nc/4.0/).)

Background and Aims: Gene p53 alteration is a genetic event described in the progression from adenoma to colorectal carcinoma. Most of the p53 mutations occur in exons 5 to 8 in highly preserved regions and in the three main structural domains of the p53 protein. It is possible that mutations affecting different structural regions may present different effects on the p53 protein function and, due to this, they may have different prognostic meaning., Materials and Methods: The study population consisted of 353 patients diagnosed with sporadic colorectal cancer. Mutations in 5-8 exons of p53 gene were detected by means of single strand conformation polymorphism (SSCP). All samples that showed different migration bands in SSCP were confirmed by sequencing., Results: A total of 69 patients (19.7%) showed alterations of the gene p53. It was observed that mutation in codon 175 in exon 5 was related to tumors located in the colon (p = 0.01) and the mutation in the codon 288 in exon 8 was related to rectal tumors (p = 0.02). In the study of overall survival, mutation in codon 175 of exon 5 conferred a better prognosis and alterations of exon 8 were related to a worse prognosis in different population subgroups: in men, in patients younger than 71 years old, in the tumors located in the proximal colon, the ones moderately differentiated, and those that are mucinous., Conclusion: According to this study, mutations in different exons of p53 are related to different phenotypes in colorectal cancer. These phenotypes could mean differences in the clinical evolution of the patients.

Objective: Renal carcinoma develops as a consequence of the accumulation of several genetic aberrations. Alterations in the p16 gene have been described in many tumors. Methylation of its promoter in CpG islands is the most common mechanism of inactivation of this gene. The aim of this study was to establish whether p16 gene methylation leads to a loss of the encoded protein in 57 patients with renal carcinoma, and if this aberration has any value in predicting disease progression in these patients., Methods: Gene promoter methylation was determined by deoxyribonucleic acid treated with sodium bisulfite to subsequently amplify methylated and unmethylated regions rich in CpG islands. The p16 protein product was detected for immunohistochemical examination., Results: Hypermethylation of the p16 gene was detected in 22.9% of the patients, none of whom had the protein product. A lack of p16 protein was confirmed in 52.9% of the tumors, indicating another genetic alteration or posttranscriptional modifications preventing the codification of this protein. Through multivariate analysis of overall survival, gene methylation was found to have independent prognostic value: the absence of alteration confers an undefined risk of death., Conclusions: Of the molecular modifications described for renal carcinoma, aberrations in the p16 gene are frequent. In these patients, methylation of the p16 gene promoter seems to afford a protective effect against the risk of death.

Background: The CellSearch System is a technique to detect circulating tumor cells (CTCs) in patients with cancer. Few data have been published concerning the role of CTCs detection by this method in colorectal cancer. The aim of this study was to correlate the presence of CTCs with the commonest clinical and morphological variables., Patients and Methods: Blood samples were collected from 97 patients and 30 healthy volunteers. Quantification of CTCs in 7.5 ml of blood was carried out with the CellSearch System. The results were expressed as number of CTCs/7.5 ml and the cut-off of >or=2 CTCs/7.5 ml was chosen to define the test as positive., Results: Positive CTCs were detected in 34 of 94 patients (36.2%). Correlation was not found among positive CTCs and location of primary tumor, increased carcinoembryonic antigen level, increased lactate dehydrogenase level or grade of differentiation. Only stage correlated with positive CTCs (20.7% in stage II, 24.1% in stage III and 60.7% in stage IV, P = 0.005)., Conclusions: CTCs detection by CellSearch is a highly reproducible method that correlates with stage but not with other clinical and morphological variables in patients with colorectal cancer. Colon cancer tumor cells are detectable in all stages. Further studies are warranted.

Background and Objective: The aim of this study is the detection and quantification of circulating tumor cells (CTC) in patients diagnosed with colon cancer and to establish whether they are related to the main clinicopathologic variables for this type of carcinoma., Patients and Method: Twenty-five colon cancer patients and 30 healthy volunteers were analysed. The quantification was performed using the CellSpotter Analyzer (Veridex LLC), that allows immunomagnetic isolation and immunospecific labelling of the cells for their enumeration., Results: 72% of the colon cancer patients showed CTC and the mean number of cells found was 5 CTC/7.5 ml of peripheral blood. 52% of the samples contained 2 or more cells. Considering 2 cells as the cut-off point, a significant relationship with lactate dehydrogenase was found., Conclusions: This new technology which allows isolation and quantification of CTC in peripheral blood has proven to be valid for the detection of epithelial cells in colon cancer patients in every tumor stage. The results shown in this work confirm that cytokeratin 8, 18 and 19 are detected in CTC in this tumor type and will allow us to develop a protocol for the study of the relationship of quantification of theses cells and the clinical parameters involved in colon cancer.

Aim: To determine whether the telomerase activity is related to the Microsatellite instability (MSI) genetic pathway and whether it means a difference in the survival., Methods: The population consisted of 97 colorectal cancer patients. MSI determination was performed in accordance with the NCI criteria using PCR and Genescan. Telomerase activity was determined by the TRAP-assay, an ELISA procedure based on the amplification of telomeric repeat sequences., Results: 6.2% showed high MSI (MSI-H), 10.3% showed low MSI (MSI-L) and 83.5% did not show this alteration (MSS). Positive telomerase activity was detected in 92.8% of the patients. 83.3% of MSI-H tumors showed positive telomerase against 93.8% of MSS tumors. In the overall survival analysis the absence of telomerase activity conferred a better prognosis., Conclusion: Previous works have shown that tumors which develop via the MSI pathway present a better prognosis. No link between telomerase activity and MSI status is observed, although sample sizes are small. Patients with telomerase negative tumors had better overall survival than patients with telomerase positive tumors.

Background and Aims: Between 10 and 15% of all cases of colorectal cancer are the result of microsatellite instability (MSI) in the genetic pathway due to an alteration in the DNA repair genes. Tumors with high MSI are characterized by a better prognosis. The BRAF oncogene has been linked to the MSI pathway in tumorogenesis. The objective of this study was to determine whether alterations in BRAF are related to MSI and whether they can result in differences in survival rates., Methods: The study cohort comprised 351 patients diagnosed with sporadic colorectal cancer. MSI was determined in accordance with the National Cancer Institute's (NCI) recommendations by means of PCR and sequence analyses. Mutational analysis of the BRAF gene was performed by real-time PCR and subsequent sequencing of the altered samples. The methylation pattern of the hMLH1 gene was determined using methylation-specific PCR analyses of bisulfite-treated DNA and the results confirmed by sequencing., Results: Of the patients tested, 6.9% showed high MSI and 3.7% showed a BRAF gene mutation. hMLH1 methylation was observed in 67.2% of the patients with MSI and/or the BRAF alteration. The BRAF mutation was related to the MSI genetic pathway (P < 0.0001) and with hMLH1 methylation. In the analysis of overall survival only MSI had an independent prognostic value for the risk of death. Patients with the BRAF mutation showed a higher risk of death, although this association was found not to be statistically significant., Conclusions: There is a subgroup of carcinomas which develop via the MSI pathway that carry an alteration of the BRAF gene. This alteration confers a poorer outcome on these patients within the total group of patients with MSI who have a better prognosis. This hypothesis should be further investigated in a larger study population due to the low incidence of BRAF mutations in colorectal cancer.

Background: The relationship between breast cancer and circadian rhythm variation has been extensively studied. Increased breast tumorigenesis has been reported in melatonin-suppressed experimental models and in observational studies., Objectives: Circulating Tumor Cells (CTC) circadian- rhythm may optimize the timing of therapies. This is a prospective experimental study to ascertain the day-time and night-time CTC levels in hospitalized metastasic breast cancer (MBC) patients., Material and Methods: CTC are isolated and enumerated from a 08:00 AM and 08:00 PM blood collections. 23 MBC and 23 healthy volunteers entered the study. 69 samples were collected (23 samples at 08:00 AM and 23 samples at 08:00 PM from MBC; 23 samples from healthy volunteers). Results from two patients were rejected due to sample processing errors. No CTC were isolated from healthy-volunteers., Results and Discussion: No-differences between daytime and night-time CTC were observed. Therefore, we could not ascertain CTC circadian-rhythm in hospitalized metastasic breast cancer patients.

Background: As the enzyme telomerase extends the life of the cell through its ability to lengthen telomeres, its activity in different types of tumor has been evaluated as a possible factor involved in tumorigenesis. The aim of this study was to assess the prognostic significance of telomerase activity in patients with colorectal carcinoma., Patients and Methods: Telomerase activity was determined in 103 patients undergoing surgery for colorectal cancer between 2001 and 2003. Telomerase activity was determined by an enzyme-linked immunoassay based on the amplification of telomeric repeat sequences (TRAP assay)., Results: 90% of our study population showed telomerase activity. Telomerase activity was related to tumor stage and site: a lower proportion of patients with stage A tumors showed telomerase activity compared to more advanced stages; and more patients with colon than with rectal carcinomas were telomerase positive. Multivariate analysis revealed that by adjusting for tumor stage, telomerase activity could be used to predict the risk of death or recurrence (p < 0.001)., Conclusions: Activation of telomerase seems to be a frequent event related to the stage of the tumor in colorectal tumorigenesis. Our findings suggest that telomerase activity can predict a greater risk of death or recurrence, irrespective of the more conventional prognostic factors.

Background and Objective: Two different pathways for the development of tumor have been described in colorectal carcinoma: the chromosomic instability, raised by suppressor genes and proto-oncogene alterations, and the microsatellite instability (MSI), caused by alterations in DNA repairing genes., Patients and Method: The frequency and the clinical meaning of the microsatellites instability pathway were determined in a consecutive prospective cohort of 106 patients who underwent surgical resection of colorectal carcinoma by a single surgeon. Microsatellite instability determination was established according to the criteria proposed by the National Cancer Institute in 1998., Results: 9.4% of patients had a high instability and it was low in 11.3%; both groups displayed different clinico-pathological characteristics (age, sex, tumor site and histologic type). In the multivariant analysis of overall survival and disease free survival, high instability exhibited prognostic value independent of the rest of variables evaluated (p < 0.0001)., Conclusions: The genetic alterations giving rise to microsatellite instability lead to a better prognosis in patients with colorectal cancer.

Background: Methylation of the CpG islands in the p16 gene promoter region is an important transcription repression mechanism that has been identified as an alternative mechanism for inactivating specific genes in cancer. Given that, DNA methylation is a common event in colorectal cancer., Materials and Methods: The aim of this study was to establish the methylation status of the p16 gene in 104 patients with colorectal carcinoma and evaluate its prognostic value. DNA was bisulfite-modified and analyzed for p16 promoter methylation by methylation-specific PCR., Results: Methylation of thep16 gene was determined in 18.3% of our patient population (19/104). The methylated state did not correlate with any clinicopathological factors. During a median follow-up period of 72 months, the overall survival rate for patients with gene methylation was 75% and without gene methylation it was 61% (p = 0.09)., Conclusions: Although not statistically significant, this difference indicates a clinically valuable tendency., (Copyright 2005 S. Karger AG, Basel.)

The amplification and/or overexpression of the c-erbB-2/neu oncogene may play a role in tumor development and progression. The aim of this prospective study was to evaluate the prognostic value of p185 protein in colorectal cancer using immunohistochemical techniques. We analyzed 106 colorectal tumor tissue specimens from patients who had been operated on by the same surgeon and subjected to a median follow-up of 3 years. Thirty-three per cent of patients showed p185 overexpression related to an advanced stage of the disease. In patients with adenocarcinoma tumors of the colon without distant metastases, p185 detection was found to be of clinical prognostic relevance (p = 0.06).

This study was designed to establish the role of microsatellite instability (MSI) in the development of sporadic tumors of the ovary. The instability of 6 microsatellites (BAT25, BAT26, NME1, D17S250, D5S346 and D2S123) was determined by comparing MSI in healthy and tumoral tissue in each of 40 patients undergoing surgery for a sporadic ovarian tumor. BAT26 and D2S123 instability was detected in borderline tumors, and ovarian carcinomas were found to present instability in the microsatellites BAT25, NME1 and D17S250. Our findings indicate that microsatellite instability lacks a significant role in the appearance or progression of sporadic ovarian tumors.

To investigate the possible role of genomic aberrations of chromosome 9p21 in the tumorigenesis of human renal cell carcinoma (RCC), 40 sporadic RCCs were studied using PCR analyses. The tumours were predominantly low stage and low grade. Loss of heterozygosity (LOH) was observed in nine of 39 informative cases, but no homozygous deletion was noticed. Hypermethylation of the promoter region of p16 occurred in eight of the 40 RCCs. No correlation was found between hypermethylation of the p16 gene and LOH on 9p21. A similar level of LOH and methylation was observed in the 40 RCCS regardless of histology, grade and stage. These results suggest that inactivation of p16 and the possibility of other unknown tumour suppressor genes located on other chromosomes could be involved in the pathogenesis of RCC.

The p16INK4a gene, localized within chromosome 9p21, has been identified as a cyclin-dependent kinase inhibitor and may negatively regulate the cell cycle acting as a tumor suppressor. Genetic alterations involving the 9p21 region are common in human cancers. A consecutive series of 64 untreated patients (median of follow up 53 months) undergoing surgical resection for locally advanced laryngeal squamous-cell carcinomas (LSCCs) has been studied prospectively. Our purpose was to investigate p16 alterations (9p21 allelic loss, hypermethylation and point mutations) and their possible association with clinico-pathological data and flow cytometric variables (DNA-ploidy and S-phase fraction (SPF)), and to determine the possible prognostic role of this gene in these tumors. PCR-based techniques were used for investigating 9p21 loss of heterozygosity (LOH) and methylation promoter status of the p16 gene. p16 mutations were detected by PCR-SSCP (single strand conformation polymorphism) and sequencing. 9p21 LOH was detected in 16/62 (26%) informative tumors, point mutations in 5% (3/64) and hypermethylation in 9% (6/64) of the cases. p16 alterations were significantly associated with high SPF and DNA-aneuploidy. By univariate analysis, poor histologic differentiation, stage IV, DNA-aneuploidy and p16 point mutations proved to be significantly related to quicker relapse, whereas these same factors, and in addition high SPF, 9p21 LOH and any p16 alterations were significantly related to shorter overall survival. By Cox proportional hazards analysis only histologic grade (G3) and p16 point mutations were independently related to both disease relapse and death. Our study has identified p16 point mutations as important biomolecular indicators in LSCCs., (Copyright 2002 Wiley-Liss, Inc.)

Objective: To determine the loss of heterozygosity (LOH) on 9p21 (locus D9S1747) in patients with renal carcinoma by analysis of microsatellite polymorphisms., Methods: 40 patients with sporadic renal cancer were studied. LOH on 9p21 was performed by analysis of microsatellite polymorphisms., Results: 23.7% showed LOH on 9p21. No correlation was found between this genetic alteration and tumor features., Conclusions: LOH on 9p21 was found in 23.7% of the patients in this series. LOH was found in 26.9% of renal cell carcinomas, 25% of papillary carcinomas and 25% of Bellini duct carcinomas. LOH was not found in the other histological types.

3% of human cancers are renal cell carcinomas (RCC). The most common chromosome abnormality found in this tumor is loss of heterozygosity (LOH) on the short arm of chromosome 3, which suggests that there must be one or more tumor suppressor genes between 3p14 and 3p21 near the VHL gene which play a relevant role in renal cancer development. DNA from normal and tumor tissue from 40 patients at various stages of RCC was analyzed for LOH at three microsatellites mapped to 3p (3p14.1-14.3; 3p21.2-21.3 and 3p25) by polymerase chain reaction). 42.5% of the tumors studied showed LOH on at least one locus. 30% showed LOH on only one locus; 5% on two loci and 7.5% on the three loci tested. LOH occurred only on nonpapillary tumors (p = 0.03). Interestingly, all the tumors with LOH on 3p21 were >/=25 mm (p = 0.04; relative risk 1.76, confidence interval: 1.3-2.3)., (Copyright 2000 S. Karger AG, Basel.)

Objective: To determine the methylation status of the tumor suppressor gene p16 in patients with renal carcinoma by analysis of microsatellite polymorphisms., Methods: 40 patients with sporadic renal cancer were studied. Tumor and normal tissue from each patient were tested for methylation status of the p16 gene by analysis of microsatellite polymorphisms., Results: 20% showed methylation of p16. No correlation was found between this genetic alteration and tumor features., Conclusions: Methylation of p16 was found in 20% of the patients in this series. According to the analysis, 18.5% of renal cell carcinomas showed methylation, 50% of chromophobe cell carcinomas and 25% of carcinomas of Bellini's tubules. The rest of the histological types showed no methylation.

Objective: To determine the utility of p185 oncogene in the biological characterization of transitional cell carcinoma and in the prediction of recurrence, and to analyze survival at 5 years mean follow-up., Methods: A prospective clinical cohort study was conducted on 81 patients. Tissue specimens were obtained between November 1992 and November 1993. The study comprised two groups: nontumoral bladder tissue specimens from 20 patients (group I) and tissue specimens from 61 patients with bladder carcinoma (group II). p185 expression was determined by enzyme immunoanalysis (EIA). A statistical analysis of the results was performed., Results: p185 oncoprotein levels were higher in patients with recurrence (1098.97 HNU/mg protein vs. 924.54 HNU/mg). Although higher levels of p185 were found in the patients that had died vs those who are alive, the differences were not statistically significant for overall survival or stratification by tumor grade or infiltration (p = 0.556; ns)., Conclusions: Determination of p185 oncoprotein was found to be useful in the prediction of tumor recurrence at 5 years mean follow-up.

The expression of p53 protein was examined in a series of 111 colorectal cancer adenocarcinomas with a long follow-up. A quantitative luminometric immunoassay (LIA) was used for the measurement of wild-type and mutant p53 protein in extracts from colorectal tumour cytosols, p53 being detected in 42% of the samples (range 0.0-52 ng (mg-1)). Using an arbitrary cut-off value of 2.7 ng mg(-1), 25% of the tumours were classified as manifesting high p53 levels. There was no association of p53 expression with patient age, sex, serum preoperative carcinoembryonic antigen (CEA) levels, tumour site and size, nodal status or TNM stage. Significant and independent correlation was found to exist between high p53 levels and prolonged disease-free survival (P = 0.05) at a median follow-up of 60 months. This survival advantage was most apparent among stage III cancer patients. The results from this study would suggest that expression of high p53 levels appear to be useful in selecting a group of colorectal cancer patients with a better prognosis.

Background: Recent advances on carcinogenesis have led to the recognition of different patterns of behaviour of non-small cell lung cancers apart from those guided by the TNM staging system and the histologic subtype. The frequent genetic loss on chromosome 3p in all kinds of lung carcinoma leads to the suspect of the presence of a tumor suppressor gene located in that place. The aim of this work was to compare the different clinical features and evolution after treatment of the patients with non small cell lung carcinoma with and without loss of heterozygosity (LOH) on 3p., Patients and Method: Forty-five operated on non-small cell lung cancer patients were evaluated. The mean age was 64.4 years and all the patients were male. Seven patients had been previously treated for another epithelial neoplasm. 82.2% of the patients were heavy tobacco smokers. Most of the tumors (62.2%) were squamous cell carcinomas. Samples of tumoral and non tumoral lung tissue were immediately frozen after surgery. DNA from the tissue was extracted; then PCR amplification of microsatellites in regions 3p14 and 3p21 was performed. To determine the LOH in the regions analyzed a polyacrylamide gel electrophoresis was performed., Results: Twenty-five percent of the informative samples for 3p14 and 21.9% for 3p21 showed LOH. There was an statistical relationship between the LOH on 3p14 and the history of tobacco smoking and the adenocarcinoma histologic subtype (p < 0.05). There was a higher number of relapses and a shorter disease-free interval in those patients harboring 3p21 LOH., Conclusions: LOH on 3p can be detected in non-small cell lung carcinoma. Patients with loss of heterozygosity on 3p21 have a worse evolution after a curative intended surgical resection.

Objective: Mutations in the p53 gene are frequently detected in some types of malignant tumors (bladder, prostate, kidney, lung, breast, colon and rectum). This study analyzed the utility of p53 quantitation in transitional cell carcinoma of the bladder and evaluated the results at 5 years., Methods: A prospective clinical cohort study was conducted on 81 patients. The study comprised two groups: nontumoral bladder tissue specimens from 20 patients (group I) and tissue specimens from 61 patients with bladder carcinoma (group II). In both groups the tissue specimens were obtained between November 1992 and November 1993, including the follow-up period until July 1998. p53 expression was determined by a quantitative method based on immunoluminiscence (LIA-MAT p53)., Results: p53 expression was higher in bladder carcinoma than in healthy urothelial tissue; higher values of p53 were found for infiltrating and undifferentiated tumors. The p53 values were higher in patients with tumor recurrence than in those without (NS). The Bonferroni multiple comparisons test showed a higher mortality in patients with p53 > 0.9 than in patients who are alive or have died from other causes (p = 0.000)., Conclusion: The results show that p53 LIA-MAT is an independent prognostic factor at a cutoff of 0.9 and permits identification of a subgroup of patients at high risk.

Objective: Renal cancer accounts for 2% of tumors. The most common chromosome abnormality found in renal cancer is the loss of heterozygosity (LOH) on the short arm of chromosome 3 (3p), which suggests that near the gene responsible for von Hippel-Lindau disease, there may be one or more tumor suppressor genes between 3p14 and 3p21 with a relevant role in the development of renal cancer., Methods: 41 patients with sporadic renal cancer were tested for three microsatellites mapped to the short arm of chromosome 3 (3p14.1-3p14.3, 3p21.2-3p21.3 and 3p25) by polymerase chain reaction. The results were compared with patient habits and tumor features., Results/conclusions: 43.9% of the patients showed LOH on at least one locus. Thirty-four percent showed LOH only on one locus, 4.9% on two loci and 7.3% on the three loci tested. All the patients who showed LOH on 3p21 had a tumor size greater than 25 mm. There is a risk 1.76 times higher of no loss in tumors less than 25 mm in size than in tumors greater than 25 mm (Cl 95% 1.33-2.33).