A case of castration-refractory prostate cancer showing marked decrease of serum PSA level after zoledronic acid treatment with estramustine phosphate and prednisolone

A 66-year-old man was referred to our outpatient clinic for an elevated serum prostatic-specific antigen (PSA 4,319 ng/ mL). Magnetic resonance imaging (MRI) showed multiple metastatic lesions in the bones. The patient had received androgen deprivation therapy, but six months after treatment, he was diagnosed as having prostate cancer refractory to hormones. Combined treatment with docetaxel (DOC 30 mg/m2/week )and estramustine phosphate (EMP 560 mg/day) was initiated as first-line chemotherapy, but the treatment was discontinued because of side effects. Then, treatment with zoledronic acid was started(4 mg/4 weeks)and the PSA level decreased dramatically from 457.2 ng/mL to 5.5 ng/mL. Seven months after the diagnosis of CRPC, MRI showed a decrease ofbone metastases, and the PSA levels continued to decrease, eventually reaching 0.3 ng/mL. Zoledronic acid appears to not only show efficacy in preventing skeletal-related events, but has a potential antitumor effect in patients with metastatic CRPC.     

A case of hormone-refractory prostate cancer (HRPC) with tumor fever responding to docetaxel plus prednisolone therapy

We have experienced a patient with tumor fever from hormone-refractory prostate cancer (HRPC) who was treated successfully using docetaxel plus prednisolone therapy. A 65-year-old male was diagnosed with prostate cancer (T4 N1 M1b). He received androgen-ablation therapy. But six months later he was confirmed to show failure of the previous hormone therapy and disease progression even after anti-androgen withdrawal. Then docetaxel plus prednisolone therapy was started. After two courses of this therapy, the PSA level decreased by 50% or more, and after ten courses an improvement was seen on the bone scan. The patient has survived for twelve months after starting docetaxel plus prednisolone therapy, without serious adverse events.     

A Case of Bilateral Adrenal and Pleural Metastases from Prostate Cancer

Our case was 65 years old. At check-up, a high PSA level of 515 ng/ml was observed, the patient was diagnosed with having clinical stage D prostate cancer and a Maximum Androgen Blockade (MAB therapy) was started. In response to the exacerbated prostate cancer, we started a therapy involving the administration of 8 mg/kg body weight of dexamethasone and 55 mg/m² of docetaxel every 3 weeks. After completing 8 courses, an enlargement of the bilateral adrenal tumor was observed, and after completing 12 courses, a pleural tumor was discovered and the PSA level was also increased. The patient was therefore diagnosed with having bilateral adrenal metastasis and pleural metastasis of prostate cancer through diagnostic imaging. So far, there have been no reports of multiple occurrences of prostate cancer in the adrenal glands and the pleura, thus making this case the first such case.Key Words: Prostate cancer, Adrenal metastasis, Pleural metastases     

Biochemical markers for monitoring response to therapy: evidence for higher bone specificity by a novel marker compared with routine markers.

The aim of the present study was to compare a novel marker for high bone turnover with two routine markers for screening in prostate cancer patients. The markers were evaluated in two studies: (a) a cross-sectional study of 170 prostate cancer patients with local disease stratified by +/-lymph node metastases (N 0, N1) compared with controls and (b) a longitudinal study of 40 hormone refractory prostate cancer patients stratified by skeletal involvement and followed during docetaxel (+/-BM) and zoledronate (+BM) treatment. Presence or absence of bone metastases (BM) was assessed by imaging techniques (magnetic resonance imaging or X-ray) and technetium-99m scintigraphy. The serum or urinary levels of alpha C-telopeptide of collagen type I (alphaalphaCTX), prostate-specific antigen (PSA), and total alkaline phosphatase (tALP) were assessed. PSA was elevated in both N 0 and N1 patients compared with controls, whereas alphaalphaCTX was elevated only in N1 patients. tALP exhibited no difference in any of the groups. In the treatment study, PSA decreased with treatment in both the -BM and +BM groups compared with baseline values, showing similar effect of docetaxel or docetaxel/zoledronate treatment on this marker. On the contrary, alphaalphaCTX and tALP did not decrease with docetaxel treatment in the -BM group compared with baseline, whereas it decreased significantly with docetaxel/zoledronate treatment in the +BM group, already after 1 month of treatment for alphaalphaCTX. Results suggest that alphaalphaCTX is superior to PSA and tALP for identifying patients having a high risk of metastatic disease and for monitoring skeletal progression in +BM prostate cancer patients during treatment.     

Clinical outcome of oral uracil/tegafur (UFT) therapy for patients with hormone refractory prostate cancer

There is no standard therapeutic strategy for advanced hormone refractory prostate cancer after the initial hormonal therapy fails. The objective of this study was to retrospectively evaluate the clinical outcome of the oral anticancer agent, uracil/tegafur (UFT) for patients with hormone refractory prostate cancer. This study included 68 patients with hormone refractory prostate cancer treated by oral administration of UFT (300-600 mg/day). All patients had previously received maximum androgen blockade (MAB) which failed. In this series, response was defined as more than 50% decrease from the baseline prostate specific antigen (PSA) value at the start of second line therapy. Upon initiating administration of UFT, a reduction in PSA value was observed in 41 of the 68 patients (60.3%), among whom 13 (19.1%) were regarded as responders; however, PSA value continued to increase in the remaining 27 (39.7%). Median duration of PSA response was 7 months (range 1-22 months). During the observation period, there were no severe side effects due to UFT administration, but 7 patients transiently presented appetite loss. Patients without bone metastasis at the initial diagnosis or whose serum PSA value at the start of UFT therapy was less than 2.0 ng/ml showed a significantly higher incidence of PSA response to UFT; however, other factors examined had no significant impact on PSA response to UFT. Furthermore, cause-specific survival in responders to UFT therapy was significantly better than that in non-responders. These findings suggest that administration of UFT after the failure of initial MAB therapy can achieve a comparatively favorable PSA response without severe side effects; therefore, it may be worthy to consider administering UFT to patients with hormone refractory prostate cancer.     

Chemo-endocrine therapy with low-dose cisplatin, UFT, and dexamethasone for hormone-refractory prostate cancer patients

Since September 2005, twenty-two patients with hormone-refractory prostate cancer (aged 55-81 years) were treated with LH-RH agonist and low-dose cisplatin, UFT, and dexamethasone after proving resistant to estramustine phosphate therapy. The regimen of this therapy consists of 5 mg/body of cisplatin intravenously once a week, 300 mg/day of UFT and 1 mg/day of dexamethasone orally, every day. All patients suffered from clinical progression such as local recurrence in 11 patients who had already received radiation therapy, lymph node metastasis in 7 patients, and bone metastasis in 15 patients. Initial PSA value ranged from 1.7 ng/mL to 215.1 ng/mL. The PSA response rate, which decreased more than 50% in PSA values was 72. 7% (16/22). The follow-up term ranged from 2 to 43 months, and nine patients died of cancer progression. The median time to progression was 11 months, and median overall survival was 19 months. There were no severe adverse effects, and stoppages of the therapy for 13 patients were all due to disease progression. Following this therapy, 9 patients received best supportive care and 4 patients received docetaxel chemotherapy. We considered this therapy to be effective for patients with hormone-refractory prostate cancer because it maintained their good QOL.     

Testicular Metastasis of Prostate Cancer: A Case Report

The incidence of secondary neoplasms of the testis during autopsies is approximately 2.5%. Although most secondary testicular metastases are due to prostate cancer, only a few patients with prostate cancer have clinically manifested testicular metastasis. We report the case of a prostate cancer patient with testicular metastasis who was diagnosed after the presence of a palpable mass in the right testis. A 56-year-old Japanese male presented to our hospital with an elevated serum prostate-specific antigen (PSA) level of 137 ng/ml. He was diagnosed with stage IV (T3N1M1b) prostate cancer and received androgen deprivation therapy, followed by various hormonal manipulations. His serum PSA level was undetectable for 1 year. No distant metastases were detected during imaging examinations. He received radiation therapy; however, his serum PSA level increased gradually. Four months later, he presented with right testicular swelling. Computed tomography revealed a heterogenous mass in the right testis and a right high inguinal orchiectomy was performed. Histopathological analysis showed that the right testis was infiltrated with metastatic adenocarcinoma with a Gleason score of 8. This is a rare case of right testicular metastasis in a patient with prostate cancer. Testicular metastasis of prostate cancer can be aggressive and metastasize.Key Words: Prostate cancer, Testicular metastasis, Orchiectomy     

Docetaxel followed by hormone therapy in men experiencing increasing prostate-specific antigen after primary local treatments for prostate cancer.

PURPOSE: Prostatectomy or radiation for localized prostate cancer (PC) can fail in up to 15% to 30% of patients. The purpose of this study was to determine feasibility, tolerability, and outcome of docetaxel followed by hormone therapy in men experiencing an increasing prostate-specific antigen (PSA) after their primary local treatments for PC. PATIENTS AND METHODS: Men with increasing serum PSA after prostatectomy or/and radiation were eligible. Serum PSA had to be > or = 4 ng/mL and serum testosterone had to be in the noncastrate range. Treatment included docetaxel 70 mg/m2 every 3 weeks for up to six cycles, followed by total androgen suppression (luteinizing hormone-releasing hormone agonist plus bicalutamide) and peripheral androgen blockade (finasteride plus bicalutamide) for 12 to 20 months. RESULTS: Thirty-nine men were enrolled; 32 had PSA-only failure, seven also had clinical metastasis. Baseline median PSA was 13.7 ng/mL. Serum PSA decreased > or = 50% in 17 of 35 patients (48.5%) and > or = 75% in seven of 35 patients (20%) with docetaxel. The PSA decreased to a median of 0.1 ng/mL with subsequent hormone therapy. In 28 of 33 patients the PSA increased (median, 0.41 ng/mL) at a median follow-up of 2.3 months after treatment. In contrast, in five of 33 men the PSA remains at 0.1 ng/mL at a median of 18.9 months after therapy; three of these five men had soft tissue metastasis at entry but remain in complete remission. The most common grade 3 to 4 toxicity was neutropenia (61.5%). CONCLUSION: Docetaxel followed by hormone therapy of limited duration may provide disease control in subgroups of men experiencing failure after local treatments for PC.     

Honokiol, a natural plant product, inhibits the bone metastatic growth of human prostate cancer cells

BACKGROUND: Honokiol, a soluble nontoxic natural product derived from Magnolia spp., has been shown to induce apoptosis in malignant cells. The effect of honokiol and the combined therapy with docetaxel on prostate cancer (PCa) growth and bone metastasis was investigated in experimental models. METHODS: The in vitro proapoptotic effects of honokiol on human androgen-dependent and -independent PCa, bone marrow, bone marrow-derived endothelial, and prostate stroma cells were investigated. Honokiol-induced activation of caspases was evaluated by Western blot and FACS analysis. To confirm the cytotoxicity of honokiol, mice bone was inoculated in vivo with androgen-independent PCa, C4-2 cells and the effects of honokiol and/or docetaxel on PCa growth in bone were evaluated. Daily honokiol (100 mg/kg) and/or weekly docetaxel (5 mg/kg) were injected intraperitoneally for 6 weeks. PCa growth in mouse bone was evaluated by radiography, serum prostate-specific antigen (PSA) and tissue immunohistochemistry. RESULTS: Honokiol induced apoptosis in all cell lines tested. In PCa cells honokiol induced apoptosis via the activation of caspases 3, 8, and 9 and the cleavage of poly-adenosine diphosphate ribose polymerase in a dose- and time-dependent manner. Honokiol was shown to inhibit the growth and depress serum PSA in mice harboring C4-2 xenografts in the skeleton and the combination with docetaxel showed additive effects that inhibited further growth without evidence of systemic toxicity. Immunohistochemical staining confirmed honokiol exhibited growth-inhibitory, apoptotic, and antiangiogenic effects on PCa xenografts. CONCLUSIONS: The combination of honokiol and low-dose docetaxel may be used to improve patient outcome in androgen-independent prostate cancer with bone metastasis.     

Natural history of rising serum prostate-specific antigen in men with castrate nonmetastatic prostate cancer.

PURPOSE: To describe the natural history of nonmetastatic prostate cancer and rising prostate-specific antigen (PSA) despite androgen deprivation therapy. PATIENTS AND METHODS: The 201 patients in this report were the placebo control group from an aborted randomized controlled trial to evaluate the effects of zoledronic acid on time to first bone metastasis in men with prostate cancer, no bone metastases, and rising PSA despite androgen deprivation therapy. Relationships between baseline covariates and clinical outcomes were assessed by Cox proportional hazard analyses. Covariates in the model were baseline PSA, Gleason sum, history of bilateral orchiectomies, regional lymph node metastases at diagnosis, prior prostatectomy, time from androgen deprivation therapy to random assignment, time from diagnosis to random assignment, and PSA velocity. RESULTS: At 2 years, 33% of patients had developed bone metastases. Median bone metastasis-free survival was 30 months. Median time to first bone metastases and overall survival were not reached. Baseline PSA level greater than 10 ng/mL (relative risk, 3.18; 95% CI, 1.74 to 5.80; P < .001) and PSA velocity (4.34 for each 0.01 increase in PSA velocity; 95% CI, 2.30 to 8.21; P < .001) independently predicted shorter time to first bone metastasis. Baseline PSA and PSA velocity also independently predicted overall survival and metastasis-free survival. Other covariates did not consistently predict clinical outcomes. CONCLUSION: Men with nonmetastatic prostate cancer and rising PSA despite androgen deprivation therapy have a relatively indolent natural history. Baseline PSA and PSA velocity independently predict time to first bone metastasis and survival.     

A case of remnant gastric cancer with multiple bone metastasis and peritoneal dissemination; efficacy of combination therapy of docetaxel and TS-1

A 69-year-old female underwent radical surgery for advanced gastric cancer (Stage IIIA) 7 years ago. She was diagnosed as remnant gastric cancer with multiple bone metastasis and peritoneal dissemination. Treatment with docetaxel and TS-1 was started with the following regimen: daily oral administration of 100 mg/body TS-1 for 14 days, followed by a 7 day rest and infusion of 40 mg/m2 docetaxel on day 1. Two months after the initial administration of docetaxel/TS-1, the sites of the remnant gastric cancer and bone metastasis were reduced in size, and the ALP returned to almost the normal level. The site of peritoneal dissemination had disappeared. Currently (nine months after diagnosis), she is undergoing therapy with TS-1. The combination of docetaxel and TS-1 can be a new tool for the management of gastric cancer with bone metastasis.     

比卡鲁胺联合戈舍瑞林间断性治疗前列腺癌临床研究

目的:观察比卡鲁胺联合戈舍瑞林间断性治疗对前列腺癌患者血清PSA、f-PSA的影响,及对排尿梗阻症状、骨转移灶和骨痛感的疗效。方法:将本院2005年7月-2012年7月收治的前列腺癌患者84例分为手术去势组20例,持续药物去势组32例和间歇药物去势组32例。手术去势组病例行双侧睾丸切除术,并口服比卡鲁胺治疗,持续药物去势组予比卡鲁胺合戈舍瑞林治疗,间歇药物去势组给药同持续药物去势组,当患者血清PSA值降至0.2ng/ml以下时停止给药,PSA值重新升至4ng/ml以上时,再给药治疗。分别在治疗前、治疗后1、3、6、12个月时观察三组患者的血清PSA、f-PSA变化,及有排尿梗阻症状、骨转移灶和骨痛感患者的变化。结果:三组患者治疗后血清PSA、f-PSA值较本组治疗前均有明显下降（P＜0.01）。三组治疗后血清PSA、f-PSA值同时间组间比较无显著差异（P＞0.05）。三组治疗后有自觉排尿梗阻症状、有骨转移灶及有骨痛感的患者数较本组治疗前均有明显减少（P＜0.05）。结论:比卡鲁胺联合戈舍瑞林间断性疗法对前列腺癌的控制治疗可与持续疗法和手术去势疗法收到同样疗效。     

健择加顺铂全身化疗治疗激素非依赖性晚期前列腺癌的近期疗效

背景与目的:迄今为止,临床上仍需探索有效的治疗措施治疗激素非依赖性晚期前列腺癌。本研究拟探讨健择加顺铂治疗激素非依赖性晚期前列腺癌的临床效果及不良反应。方法:15例激素非依赖性晚期前列腺癌患者,全部经手术去势及不同程度的抗雄激素药物治疗后病情缓解,之后病情再进展,经全身骨扫描证实12例有多发性骨转移灶,其中并有肝脏、双侧肾上腺和颅内转移各1例,血PSA进行性升高。用健择1000mg/m2加生理盐水(NS)100ml静脉滴注,第1、8天各一秦自科,等.健择加顺铂全身化疗治次;DDP100mg/m2加NS500ml静脉滴注第1天,或者DDP30mg+NS250ml静脉滴注第1～5天;每28天为一个疗程。结果:10例患者的血PSA值降至正常水平(<4ng/L),4例PSA值下降超过50%,1例PSA值变化不明显。化疗前12例有骨转移灶疼痛(按VRS分级Ⅰ级4例、Ⅱ级5例、Ⅲ级3例),化疗后9例疼痛消失,另3例仍有疼痛(Ⅰ级2例、Ⅱ级1例)。多发性颅内转移灶中最大转移瘤直径由化疗前的3.0cm缩小至0.5cm,化疗后面瘫症状消失。肝脏转移瘤由原先的10.2cm缩小至3.3cm。双侧肾上腺多发性转移瘤化疗后总的肿瘤体积缩小1/3以上。随访3～29个月,平均15.2个月,2例患者死亡,中位生存期14.7个月。平均疼痛缓解期为13.6个月。PSA值降低的平均稳定期为12.3个月。本组病例最常见     

Sequencing of Cabazitaxel in Metastatic Castrate-Resistant Prostate Cancer: A Case Report

Prostate cancer is a common cancer in men; for metastatic disease, it has a 5-year survival rate of 30%. No FDA-approved therapy for castrate-resistant prostate cancer (CRPC) known to improve survival was available until 2004, when based on a significant survival benefit over mitoxantrone, docetaxel in combination with prednisone was approved. In combination with prednisone, cabazitaxel, which was approved in the United States in 2010, is indicated for patients with metastatic CRPC previously treated with a docetaxel-containing regimen. This case report describes the treatment of a man 58 years of age who was diagnosed with advanced prostate cancer in 2006. He was initially managed with radical prostatectomy followed by androgen deprivation therapy, but a rising prostate-specific antigen (PSA) level led to enrollment in a clinical trial of HE3235 for 6 months. Subsequently, with progression of disease, he was treated with docetaxel for 4 months and then palliative radiation therapy. Cabazitaxel was initiated in October 2010; his condition stabilized within weeks, and he experienced a progressive decline in his PSA level from a peak of 5,424 ng/ml. Continued treatment with cabazitaxel resulted in his being weaned off pain medications and resuming his normal activities. After 16 cycles of cabazitaxel, his PSA declined to 994 ng/ml as of January 2012. He tolerated the cabazitaxel well and occasionally received myeloid growth factors for treatment of neutropenia; otherwise, he experienced only mild diarrhea. This response to cabazitaxel is notable, particularly in light of prior failure of multiple therapies.Key Words: Cabazitaxel, Castrate-resistant prostate cancer (CRPC), Treatment sequencing     

Retrospective Study of Predictors of Bone Metastasis in Prostate Cancer Cases

Introduction: The purpose of this study was to identify clinical profiles of patients with low risk of having bonemetastases, for which bone scanning could be safely eliminated. Materials and Methods: This retrospective crosssectional study looked at prostate cancer patients seen in the Urology Departments in 2 tertiary centres over the11 year period starting from January 2000 to May 2011. Patient demographic data, levels of PSA at diagnosis,Gleason score for the biopsy core, T-staging as well as the lymph node status were recorded and analysed.Results: 258 men were included. The mean age of those 90 men (34.9%) with bone metastasis was 69.2±7.3 years.. Logistic regression found that PSA level (P=0.000) at diagnosis and patient’s nodal-stage (P=0.02) were theonly two independent variables able to predict the probability of bone metastasis among the newly diagnosedprostate cancer patients. Among thowse with a low PSA level less than 20ng/ml, and less than 10ng/ml, bonemetastasis were detected in 10.3% (12 out of 117) and 9.7% (7 out of 72), respectively. However, by combiningPSA level of 10ng/ml or lower, and nodal negative as the two criteria to predict negative bone scan, a relativelyhigh negative predictive value of 93.8% was obtained. The probability of bone metastasis in prostate cancercan be calculated with this formula: -1.069+0.007(PSA value, ng/ml)+1.021(Nodal status, 0 or 1)=x Probabilityof bone metastasis=2.718x/1+2.718x. Conclusion: Newly diagnosed prostate cancer patients with a PSA level of10ng/ml or lower and negative nodes have a very low risk of bone metastasis (negative predictive value 93.8%)and therefore bone scans may not be necessary.     

Clinical Usefulness of Serum Carboxyterminal Propeptide of Type I Procollagen and Pyridinoline Cross-linked Carboxyterminal Telopeptide of Type I Collagen in Patients with Prostate Cancer

A study was undertaken to evaluate the clinical usefulness ofmeasurements of serum concentrations of the carboxyterminalpropeptide of type I procollagen (PICP) and the pyridinolinecross-linked carboxyterminal telopeptide of type I collagen(ICTP) as parameters of bone metastasis in patients with prostatecancer. Serum PICP, ICTP, prostate-specific antigen (PSA), andalkaline phosphatase (ALP) were evaluated in 82 patients withprostate cancer and 26 patients with benign prostatic hyperplasia(BPH). These markers were measured serially in 16 prostate cancerpatients during treatment. The serum levels of PICP, ICTP, ALP,and PSA were significantly higher in prostate cancer patientswith bone metastasis than in patients with either BPH or prostatecancer without bone metastasis. Although the rate of detectionof bone metastasis with PICP and ICTP was slightly lower thanthat with PSA determined by the receiver operating characteristiccurve, the correlation between both PICP and ICTP and the extentof disease was much higher than that of PSA. PICP and ICTP levelsvaried with ALP and PSA levels, the patient's clinical courseafter the start of endocrine therapy and the progression ofbone metastasis. The levels of PICP and ICTP did not changesubstantially in patients who developed local regrowth or lymphnode metastasis, and decreased as bone metastases respondedto radiotherapy. PICP and ICTP thus reflect the metastatic burdenin bone and are useful for monitoring the response of bone metastasisto therapy.     

激素抵抗性前列腺癌化疗15例报告

目的：探讨多西紫杉醇联合泼尼松治疗内分泌治疗失败前列腺癌的应用价值。方法：入选15例非激素依赖性前列腺癌患者,给予多西紫杉醇75 mg/m^2,第1天;泼尼松5 mg bid,第1-21天,21天为1个周期,每例接受化疗6-10个周期不等。结果：本组病例随访6-87周,中位61周。其中26.7%（4/15）完全缓解,46.7%（7/15）部分缓解,20.0%（3/15）稳定,6.66%（1/15）进展。缓解和稳定患者的PSA进展中位时间是40.3周（13-67周）。8例骨痛患者中5例疼痛缓解。 中位生存期大于12个月。不良反应可耐受。结论：多西紫杉醇联合泼尼松治疗激素抵抗性前列腺癌有较好疗效,不良反应轻。     

血清缓激肽与前列腺癌的相关性研究

目的 探讨血清缓激肽在前列腺癌的诊断及鉴别诊断中的临床应用价值.方法 收集68例前列腺癌患者和32例前列腺增生患者,以同期体检的健康男性32例为对照组,收集其血清,酶联免疫吸附试验(enzymelinked immuno sorbent assay,ELISA)法检测血清中的缓激肽水平,比较各组血清缓激肽水平的差异以及前列腺癌患者在不同年龄、临床分期、病理分期(Gleason评分)、前列腺特异抗原(prostate specific antigen,PSA)水平、肿瘤体积以及骨转移、淋巴结转移、局部侵犯与否状态下血清缓激肽水平的差异.比较血清缓激肽与PSA联合诊断前列腺癌和PSA独立诊断前列腺癌的敏感度差异.结果 前列腺癌组血清缓激肽水平[(16.44 ±0.91) μg/L]低于对照组[(19.72±1.10) μg/L]和前列腺增生组[(20.93±1.80) μg/L],差异均具有统计学意义(均P＜0.05).在肿瘤体积较大的前列腺癌患者血清缓激肽水平较低(P＜0.05),而血清缓激肽水平在年龄、肿瘤临床分期、病理分期(Gleason评分)、PSA水平及骨转移、淋巴结转移、局部侵犯与否方面比较差异均无统计学意义(均P＞0.05).血清缓激肽与PSA联合诊断前列腺癌较单独诊断敏感度提高(P＜0.05).结论 前列腺癌患者血清缓激肽表达水平较低,且与肿瘤体积相关.血清缓激肽与PSA联合诊断前列腺癌敏感度较单独诊断高.     

Bone scanning--who needs it among patients with newly diagnosed prostate cancer?

BACKGROUND: We evaluated the relationship between serum PSA and clinical variables to eliminate bone scanning in patients with prostate cancer having a low probability of bone metastasis. METHODS: The study included 366 patients with newly diagnosed prostate cancer between 1999 and 2005. Bone metastasis was studied for its correlation with various clinical and pathological variables in these patients. RESULTS: Bone metastasis was found in 28 (7.7%) of 366 patients. Fourteen patients had skeletal symptoms related to bone metastasis. The risk for bone metastases increased considerably with increases of PSA level, clinical T stage and Gleason score. The metastasis was not found in 161 patients with serum PSA concentration of 10 ng/ml or lower. In 95 patients with the concentration between 10 and 20 ng/ml only two had the metastasis. These two patients had T2 disease and Gleason scores of 7 or greater. In 204 patients with clinical stage T1 disease, one (0.5%) had the metastasis. In 117 patients with Gleason scores of 6 or less, the metastasis was found in two (1.7%). CONCLUSIONS: For patients with serum PSA levels of 10 ng/ml or lower, bone scanning may be eliminated because of the negligible risk of bone metastases. In addition, scanning may not be necessary for those with PSA levels between 10 and 20 ng/ml, when they have T1 disease and Gleason scores of 6 or lower.     

多西他赛加泼尼松3周方案失败后联合雌二醇氮芥治疗激素难治性前列腺癌

目的激素难治性前列腺癌（ hormone refractory prostate cancer, HRPC）的治疗，在2004年取得了突破性进展，TAX327研究证实多西他赛联合泼尼松3wk方案可以延长病人的生存期，从而确立了其一线标准化疗方案的地位。但是，多西他赛联合泼尼松方案失败后的治疗选择仍然是一难题，为此，我们观察多西他赛联合雌二醇氮芥及泼尼松三联方案在一线标准方案失败后治疗HRPC的疗效和安全性。方法2005年11月至2007年3月，6例HRPC在多西他赛联合泼尼松3wk方案治疗过程中病情恶化（血PSA升高）时，用多西他赛联合雌二醇氮芥及泼尼松治疗。治疗方案：多西他赛75mg／m^2，d1，强的松5mg bid，d1起连续应用，雌二醇氮芥280mg，2次，d，d1起连用5d。21d为1疗程。病人平均年龄75．8a，血睾酮维持去势水平，WHO体力状态评分≤2，骨髓、心、肝、肾等重要脏器功能正常。估计生存时间〉3mo。疗效及不良反应判断标准：①血PSA下降〉50％，且维持〉3wk判断为有效。②可测量病灶按RECIST实体瘤评价标准评价。③骨痛者按主诉疼痛程度分级法（VRS）评价，评分下降1级为有效。④不良反应按WHO不良反应标准评定。结果6例共完成27个疗程。PSA有效5例，有效率为83.3％。有效病人PSA从治疗前的10．9～606．2（223．6±218．0）mg／mL下降到治疗后最低1．1～127．6（61．5±50．4）ng／mL。1例肺转移者，转移灶为稳定。1例骨痛者VRS疼痛评分从Ⅱ下降到Ⅰ。到分析日止，已死亡1例。此例从诊断激素非依赖前列腺癌到死亡共53mo。5例存活者从诊断激素非依赖前列腺癌起已存活14～36mo。主要不良反应为骨髓抑制（100％），脱发（100％），乏力（67％）等。结论多西他赛联合雌二醇氮芥及泼尼松三联方案对多西他赛联合泼尼松3wk方案治疗失败后的病人疗效肯定，毒副反应可以耐受，值得进一步观察?