Establishment and characterization of human bladder cancer cell lines BexBra1, BexBra2, and BexBra4.

Bladder cancer (BC) is the fourth most common cancer in the USA. In Brazil, BC represents 3% of the total existing carcinomas in the population and represents the second highest incidence among urological tumors. The majority of bladder cancer cell lines available were derived from Caucasians and established in the seventies or eighties. Thus, neoplasia development in these cells likely occurred in environment conditions vastly different than today. In the present study, we report the establishment and characterization of three Brazilian bladder cancer cell lines (BexBra1, BexBra2, and BexBra4). These cell lines may be helpful for dissecting the genetic and epigenetic aspects that trigger the progression of BC. Moreover, the development of a Brazilian representative of the disease will allow us to investigate the potential inter-racial differences of malignancy-associated phenotypes in bladder cancer.

Incidence of benign lesions according to tumor size in solid renal masses.

OBJECTIVE: The incidence of solid renal masses has increased sharply in recent years due to widespread use of abdominal imaging studies. The aim of the present study was to evaluate the incidence of benign lesions in solid renal masses according to tumor size. MATERIALS AND METHODS: The authors retrospectively reviewed the records of 305 patients with 328 renal solid masses treated by surgery. Based on a report by one pathologist, the specimen tumor size and the histology of each lesion were tabulated. The frequency of renal cell carcinoma and benign renal lesions was evaluated and a correlation between tumor size and pathological features of the masses was observed. RESULTS: The frequency of malignant lesions in the 328 renal masses was 83.2%. When lesions were stratified into groups with diameters 3 cm, the incidence of benign histology was 22.9% and 13.3%, respectively (p = 0.026). The odds ratios for finding a benign lesion in masses 3 cm. CONCLUSION: The incidence of benign lesions is significantly higher in renal masses smaller than 3 cm in diameter, which should be taken in account when the treatment of renal solid masses is planned.

Incidence of benign lesions according to tumor size in solid renal masses

Objective: The incidence of solid renal masses has increased sharply in recent years due to widespread use of abdominal imaging studies. The aim of the present study was to evaluate the incidence of benign lesions in solid renal masses according to tumor size. Materials and Methods: The authors retrospectively reviewed the records of 305 patients with 328 renal solid masses treated by surgery. Based on a report by one pathologist, the specimen tumor size and the histology of each lesion were tabulated. The frequency of renal cell carcinoma and benign renal lesions was evaluated and a correlation between tumor size and pathological features of the masses was observed. Results: The frequency of malignant lesions in the 328 renal masses was 83.2 percent. When lesions were stratified into groups with diameters ¡Ü 3 cm or > 3 cm, the incidence of benign histology was 22.9 percent and 13.3 percent, respectively (p = 0.026). The odds ratios for finding a benign lesion in masses ¡Ü 3 cm was 1.93 (IC 95 percent, 1.07 - 3.46) compared to masses > 3 cm. Conclusion: The incidence of benign lesions is significantly higher in renal masses smaller than 3 cm in diameter, which should be taken in account when the treatment of renal solid masses is planned.

An evaluation of the anti-neoplastic activity of curcumin in prostate cancer cell lines.

OBJECTIVE: The aim of our study is to investigate the anti-neoplastic effect of curcumin in prostate cancer cell lines. Specifically, we are using the LNCaP cell line and another prostate cell line developed in our laboratory, PcBra1. The PcBra1 cells were derived from a localized, obstructive prostate cancer with a Gleason score of 9 (4+5). MATERIALS AND METHODS: A prostate cancer cell line was isolated from a localized, obstructive prostate cancer with a Gleason score of 9 (4+5), and it was characterized using immunohistochemistry. After six passages, the new cell line was treated with varying doses of curcumin: 10 microM, 25 microM or 50 microM. Apoptosis was detected by flow cytometry using Annexin V FITC. For comparison, the same experiment was performed using the well-established metastatic prostate cancer cell line, LNCaP. RESULTS: Increasing concentrations of curcumin promoted more apoptosis in the PcBra1 cells. Exposure to 10 and 25 microM curcumin induced apoptosis in 31.9% and 52.2% of cells, respectively. Late apoptosis was induced in 37% of cells after treatment with 10 microM curcumin and 35% of cells with a 25 microM treatment. Necrosis accounted for less than 10% of the death in these cells at those two concentrations. When curcumin was used at 50 microM, apoptosis was observed in 64.3% of the cells. Including late apoptosis and necrosis, 98.6% of the cells died in response to 50 microM curcumin. Results with the LNCaP cells were similar although late apoptosis was the main phenomenon at 25 microM. CONCLUSION: We have shown that curcumin acts on localized prostate cancer to induce apoptosis and may therefore be an option as a future therapeutic agent.

An evaluation of the anti-neoplastic activity of curcumin in prostate cancer cell lines

OBJECTIVE: The aim of our study is to investigate the anti-neoplastic effect of curcumin in prostate cancer cell lines. Specifically, we are using the LNCaP cell line and another prostate cell line developed in our laboratory, PcBra1. The PcBra1 cells were derived from a localized, obstructive prostate cancer with a Gleason score of 9 (4+5). MATERIAL AND METHODS: A prostate cancer cell line was isolated from a localized, obstructive prostate cancer with a Gleason score of 9 (4+5), and it was characterized using immunohistochemistry. After six passages, the new cell line was treated with varying doses of curcumin: 10 µM, 25 µM or 50 µM. Apoptosis was detected by flow cytometry using Annexin V FITC. For comparison, the same experiment was performed using the well-established metastatic prostate cancer cell line, LNCaP. RESULTS: Increasing concentrations of curcumin promoted more apoptosis in the PcBra1 cells. Exposure to 10 and 25 µM curcumin induced apoptosis in 31.9 percent and 52.2 percent of cells, respectively. Late apoptosis was induced in 37 percent of cells after treatment with 10 µM curcumin and 35 percent of cells with a 25 µM treatment. Necrosis accounted for less than 10 percent of the death in these cells at those two concentrations. When curcumin was used at 50 µM, apoptosis was observed in 64.3 percent of the cells. Including late apoptosis and necrosis, 98.6 percent of the cells died in response to 50 µM curcumin. Results with the LNCaP cells were similar although late apoptosis was the main phenomenon at 25 µM. CONCLUSION: We have shown that curcumin acts on localized prostate cancer to induce apoptosis and may therefore be an option as a future therapeutic agent.

Pretreatment tumor volume estimation based on total serum psa in patients with localized prostate cancer.

OBJECTIVES: To establish a formula that estimates tumor volume in localized prostate cancer based on serum prostate specific antigen levels. One of the main prognostic variables in localized prostate cancer is tumor volume, which can be precisely defined only after prostate extirpation. The present study defines a simple method that allows for estimation of tumor volume before treatment, which can help to establish a better therapeutic strategy for each patient. METHODS: From 1997 to 2002, 735 patients with prostate cancer of stagesT1c-T2c without any previous treatment were submitted to radical prostatectomy. Surgical specimens were evaluated by the same pathologist and the total tumor volume (in cc) and the relative tumor volume (as the percent of the total prostate volume) were determined using the grid morphometric method. Pretreatment serum prostate specific antigen was correlated with tumor volume in each patient using a linear regression model. RESULTS: There were positive correlations between the serum levels of prostate specific antigen and the total tumor volume in cc (p<0.001) and the relative tumor volume as a percentage (p<0.001). For each ng/ml unit increment of serum prostate specific antigen, there was a 0.302 cc increase in total tumor volume and a 0.7% increase in relative tumor volume. Total and percent tumor volume could be calculated, respectively, using the formulas Volume (cc) = 3.476 + 0.302 x PSA (ng/ml) and Volume (%) = 11.331 + 0.704 x prostate specific antigen (ng/ml). CONCLUSIONS: Tumor volume in patients with prostate cancer can be determined before treatment based on the serum prostate specific antigen levels.

Pretreatment tumor volume estimation based on total serum psa in patients with localized prostate cancer

OBJECTIVES: To establish a formula that estimates tumor volume in localized prostate cancer based on serum prostate specific antigen levels. One of the main prognostic variables in localized prostate cancer is tumor volume, which can be precisely defined only after prostate extirpation. The present study defines a simple method that allows for estimation of tumor volume before treatment, which can help to establish a better therapeutic strategy for each patient. METHODS: From 1997 to 2002, 735 patients with prostate cancer of stagesT1c-T2c without any previous treatment were submitted to radical prostatectomy. Surgical specimens were evaluated by the same pathologist and the total tumor volume (in cc) and the relative tumor volume (as the percent of the total prostate volume) were determined using the grid morphometric method. Pretreatment serum prostate specific antigen was correlated with tumor volume in each patient using a linear regression model. RESULTS: There were positive correlations between the serum levels of prostate specific antigen and the total tumor volume in cc (p<0.001) and the relative tumor volume as a percentage (p<0.001). For each ng/ml unit increment of serum prostate specific antigen, there was a 0.302 cc increase in total tumor volume and a 0.7 percent increase in relative tumor volume. Total and percent tumor volume could be calculated, respectively, using the formulas Volume (cc) = 3.476 + 0.302 x PSA (ng/ml) and Volume ( percent) = 11.331 + 0.704 x prostate specific antigen (ng/ml). CONCLUSIONS: Tumor volume in patients with prostate cancer can be determined before treatment based on the serum prostate specific antigen levels.