Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153690 (bone metastases)
 6,382 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prognosis in prostate cancer is determined, in greater part, by the presence of metastases. Bone metastases can occur in any part of the skeleton even, for example, at the base of the skull. We present a case of a 78 year old male who, in December 2001, presented with paralysis of the third cranial nerve. The NMR and CAT scans were normal and circulating levels of PSA were elevated. He was referred to the Urology Service where the treatment guidelines included complete androgen block. Subsequently, he developed retro-orbital pain, divergent strabismus and palpebral ptosis. CAT and NMR indicated a soft tissue mass at the sphenoid level. Treatment was Gamma Knife Radio-surgery. Since August 2004, in conjunction with the latest rise in PSA, the patients general status deteriorated considerably and he was referred to the Oncology Service. There was an increase in the paralysis of the third, fourth and sixth cranial nerve (complete left ophthalmoplegia) and left-central facial paralysis. Metastases from prostate cancer can be disseminated via the lymphatic or the blood system. Currently, there are more metastases from large-size tumours. Metastases are critical in prostate cancer because of their adverse effect on the patients survival. Measurements of circulating levels of prostate specific antigen and prostate acid phosphatase are very useful in the clinical diagnosis of the primary tumour, or its metastases.
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PMID:[Ophthalmoplegia in a patient with prostate cancer and bone metastases]. 1623 78

Prostate cancer is a major public health problem of the male population in all the developed countries. This non-skin cancer is the foremost one facing man today. Prostate cancer has become the second leading cause of cancer death2. In this study we investigated changes in the prostate carcinoma incidence and manifestation during a thirty-three years period. The study included 1226 cases of prostate cancer diagnosed from 1972 to 2005 in the Primorsko-Goranska County, Croatia. The age-adjusted incidence of prostate cancer increased from 1.69 per 100,000 men annually in 1972 to 137.58 per 100,000 men annually in 2005, which is an 81.4-fold increase. The percentage ofpatients with bone metastases on the first medical examination decreased from 1972 (75%) to 2005 (15%). The most of the patients with bone metastases at the first medical examination were between 30 and 50 years old. Early detection measures, such as prostate specific antigen testing and transrectal ultrasound guided prostate biopsy combined with the raised public awareness of the disease, most probably resulted in an increase of incidence.
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PMID:Epidemiology of prostate cancer in the mediterranean population of Croatia--a thirty-three year retrospective study. 1759 7

A 76-year-old man had been treated with maximum androgen blockade therapy for a poorly-differentiated prostate adenocarcinoma (T3cN1M0, prostate specific antigen (PSA) 65 ng/ml, Gleason Score 4+5=9) since September 2002. By August 2003, his serum PSA levels were undetectable and the lymph node swelling had vanished. However, in December 2004, his serum PSA levels started rising gradually up to 0.66 ng/ml. Radiation therapy on the prostate was then performed (66 Gy). At that time, no metastasis was detected by computed tomography and bone scintigraphy. In August 2005, multiple bone metastases were detected. Immunohistochemical examination of a biopsy specimen from the bone lesion revealed a small cell carcinoma/neuroendocrine cell carcinoma. He died with undetectable PSA levels (less than 0.008 ng/ml) in December 2005. The autopsy showed multiple organ metastases including bone, liver, lungs and others. The immunohistochemical examination revealed pure small cell carcinoma in all metastatic lesions. A precise histological examination of the lungs using a 1 cm serial section could not reveal any tumors compatible with primary lung cancer. We concluded from the clinical history and autopsy findings that his initial poorly-differentiated adenocarcinoma of the prostate dedifferentiated into a pure small cell carcinoma with neuroendocrine differentiation.
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PMID:[Small cell carcinoma of the prostate: a case report]. 1793 47

Prostate cancer (PCa) is the second leading cause of death in men aged 40 years and older ]and prognostic indices are useful in suggesting its proper treatment. The aim of this study was to evaluate the prognostic value of Gleason score (GS), TNM staging system, initial serum prostate specific antigen (PSA) and bone scintigraphy (BS) in patients with PCa under hormonal palliative treatment, in the development and progression of recurrent PCa. Our methods were as follows: Between January 2005 and December 2007, we have studied at the University General Hospital of Alexandroupolis fourty patients of mean age 77+/-7.2 years with advanced PCa under palliative treatment with antiandrogens and luteinizing hormone-releasing hormone analogues. PCa was diagnosed histologically, based on the TNM system after transrectal ultrasonography guided biopsy. The Gleason score assessment was made as described by others. Metastases were confirmed by a positive bone scintigraphy with 925 MBq (99m)Tc-MDP using a tomographic gamma camera, computerized axial tomography or magnetic resonance imagining. Measurements of PSA were conducted by the radioimmunoassay method. We also examined 20 healthy blood donors (median age 45+/-6.1 years) as controls, in order to estimate the cut-off value of PSA. Our results show the following: Thirteen of our patients had 1-6 "hot" spots and 27 had more than 6 "hot" spots in the bone scan. The median Gleason score was 7 (modal Gleason score 3+4). Serum PSA levels were higher in patients with PCa and bone metastases in comparison to those with PCa without bone metastases. Very high values of PSA (more than 50 ng/ml) were found in patients with multiple bone metastases (>6 "hot" spots). In conclusion, our findings demonstrate that the prognostic value of GS (P=0.043), TNM staging (P=0.1410), serum PSA levels (P=0.002) and BS (P=0.0135) when used alone, not always improve the prognosis to hormone indepentent but when combined (P<0.001) increase the prognosis in patients with advanced PCa under hormonal palliative treatment.
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PMID:Four prognostic indices in advanced prostate cancer patients, under palliative androgen deprivation treatment. 1839 22

The decrease of the level of serum prostate specific antigen (PSA) after discontinuation of estramustine phosphate (EMP) has rarely been reported. We report 2 cases in whom EMP withdrawal syndrome was encountered. Case 1 was a 68-year-old man with a complaint of paresis of lower limbs. He was diagnosed with prostate cancer with multiple bone metastases. The serum PSA level was 9,300 ng/ml. He was treated with luteinizing hormone-releasing hormone agonist (LH-RHa) and bicalutamide (BCL). Six months later, EMP was started against PSA failure. During the 3-year treatment with EMP, PSA decreased to the nadir of 0.7 ng/ml and gradually increased to 14 ng/ml. After withdrawal of EMP, PSA decreased to 0.3 ng/ml (97.9% decline) and remained at this level for 4 months. Case 2 was a 61-year-old man who visited our hospital with gross hematuria. Transurethral bladder biopsy and transrectal prostate biopsy were performed. The diagnosis was moderately differentiated adenocarcinoma of the prostate that invaded to the bladder. Computed tomography (CT) showed a lymph node metastasis. He was treated with LH-RHa and BCL. The treatment was changed to EMP after PSA failure. EMP was withdrawn when PSA was 30 ng/ml. Then PSA decreased to less than 0.2 ng/ml (99% decline) and remained at this level for 9 months. We consider that in patients with EMP-resistant progression, EMP withdrawal syndrome should be checked.
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PMID:[Estramustine phosphate withdrawal syndrome in relapsed prostate cancer: two case reports]. 1863 39

Spontaneous development of osteoblastic lesions of prostate cancer (PCa) in mice is modeled by orthotopic (intraprostatic) deposition of neoplastic cells followed by an extremely long latency associated with low incidence of spontaneous bone metastasis. Intracardial injection results in overt bone metastases only with osteoclastic PCa cells (i.e., PC-3). Herein, we report that androgen independent osteoblastic PCa cells readily colonize bone when in a high remodeling state. SCID/Beige mice were subjected to periods of intermittent human parathyroid hormone 1-34 (hPTH) exposure, followed by an intracardiac infusion of osteoblastic C4-2 PCa cells. At the time of PCa infusion, analysis of bone turnover markers from mice treated with hPTH revealed significant increases in osteocalcin (55.06 +/- 7.5 vs. 74.01 +/- 18.5 ng/ml) and TRAcP-5b (3.3 +/- 0.6 vs. 4.81 +/- 0.8 U/l), but no change in type I collagen C-terminal teleopeptide levels relative to control mice. Analysis of femoral cancellous bone architecture revealed significant increases in bone mineral density, trabecular thickness (0.056 +/- 0.002 vs. 0.062 +/- 0.001 mm) and porosity, but significant decreases in connectivity density and trabecular number in hPTH treated mice relative to controls. By 8 weeks post-infusion, 70% of mice pre-treated with hPTH demonstrated detectable serum prostate specific antigen (PSAs) ranging between 2 and 18.8 ng/ml. Immuno-histochemical labeling of femurs for PSA and pan-Cytokeratin revealed the presence of significant tumor cell nests in marrow and trabecular spaces. These results suggest that: (1) local bone physiology is an important factor for developing osteoblastic/sclerotic PCa bone metastases in murine hosts; (2) the establishment of osteosclerotic PCa bone metastases in mice is enhanced by alterations that drive bone formation.
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PMID:Osteosclerotic prostate cancer metastasis to murine bone are enhanced with increased bone formation. 1942 79

Renal cell carcinoma accounts for 2% of all cancers. Metastases to bone occur 35% to 40% of the time, second in prevalence of metastases only to the lungs. These metastases are highly destructive, hypervascular tumors known to be difficult to manage. This article reports a unique case in which a patient was disease free for 33 years from initial nephrectomy for treatment of primary renal cell carcinoma to discovery of metastatic disease to the pelvis. Search for an unknown primary was performed, consisting of a complete blood count, chemistry, alkaline phosphatase, calcium, serum and urine protein electrophoresis, immunoglobulin levels, prostate specific antigen, liver function tests, bone scan, and chest, abdomen, and pelvis computed tomography scans. This workup was negative for any other primary source of malignancy, and the patient's remaining kidney was found to be free from any tumor burden. The patient successfully underwent excisional biopsy of the lesion, which proved to be vascular in nature, consistent with the final pathology of renal cell carcinoma. The longest amount of time from completion of treatment for the primary renal cell carcinoma to discovery of the first metastatic disease has previously been reported at 22.3 years. Mean interval between primary treatment and discovery of metastases has been defined as 3.0+/-5.4 years. This article highlights the need for advanced medical workup as well as maintaining a high clinical suspicion in patients with remote histories of primary malignancies who present with bony lesions.
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PMID:Renal cell carcinoma metastases to bone after a 33-year remission. 1963 12

The vast majority of patients with metastatic prostate cancer present with bone metastases and high prostate specific antigen (PSA) level. Rarely, prostate cancer can develop in patients with normal PSA level. Here, we report a patient who presented with a periureteral tumor of unknown primary site that was confirmed as prostate adenocarcinoma after three years with using specific immunohistochemical examination. A 64-year old man was admitted to our hospital with left flank pain associated with masses on the left pelvic cavity with left hydronephrosis. All tumor markers including CEA, CA19-9, and PSA were within the normal range. After an exploratory mass excision and left nephrectomy, the pelvic mass was diagnosed as poorly differentiated carcinoma without specific positive immunohistochemical markers. At that time, we treated him as having a cancer of unknown primary site. After approximately three years later, he revisited the hospital with a complaint of right shoulder pain. A right scapular mass was newly detected with a high serum PSA level (101.7 ng/ml). Tissues from the scapular mass and prostate revealed prostate cancer with positive immunoreactivity for P504S, a new prostate cancer-specific gene. The histological findings were the same as the previous pelvic mass; however, positive staining for PSA was observed only in the prostate mass. This case demonstrates a patient with prostate cancer and negative serological test and tissue staining that turned out to be positive during progression. We suggest the usefulness of newly developed immunohistochemical markers such as P504S to determine the specific primary site of metastatic poorly differentiated adenocarcinoma in men.
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PMID:Cancer of unknown primary finally revealed to be a metastatic prostate cancer: a case report. 1968 71

Prostate adenocarcinomas (PAC) consist mainly of tumour cells of luminal immunophenotype and scattered neuroendocrine (NE) cells. NE cells are defined by chromogranin A (CgA) immunoreactivity. T he aim of this study is the evaluation of CgA serum levels in monitoring prostate cancer (PC) patients under complete androgen deprivation (CAD) in comparison with the prostate specific antigen (PSA) as a prognostic marker of androgen resistance and bone metastases. Ninety-two patients with newly diagnosed PAC and 30 healthy blood donors serving as the control group were enrolled in the study. Serum CgA and PSA values were measured. All patients had locally advanced or metastatic disease and received CAD treatment. In the group of PAC patients bone scanning with 925MBq (99m)Tc-MDP revealed the presence of bone metastatic lesions in 50 patients (29 with more than 3 lesions and 21 with less than 3 lesions). The other 42 patients had no bone metastases. The patients and the control group were re-evaluated after 1 year. Our results showed that serum CgA positively correlated with multiple bone metastases and higher Gleason score, serum levels of CgA and PSA. Levels of PSA were significantly higher in patients with PAC and bone metastases compared with those with no bone metastases (P<0.001). In patients with multiple bone metastases and Gleason Score >7 elevated serum levels of CgA higher than those of PSA were found. In conclusion, serum CgA levels is a valuable marker for predicting the presence of multiple bone metastases in PAC patients. Combined with PSA, CgA can predict disease progression in patients with advanced PAC under CAND treatment and is correlated with poor prognosis.
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PMID:The prognostic value of serum chromogranin A and prostate specific antigen in prostate cancer patients for progression to the hormone resistance state. 1993 34

Tissues of prostatic origin representing variable phenotypes were tested for reactivity to the prostate cancer specific mouse monoclonal antibody PD-41. Avidin biotin immunoperoxidase was applied on formalin-fixed, paraffin-embedded tissue sections of 15 benign prostatic hyperplasia (BPH), 23 prostatic intraepithelial neoplasia (PIN), 14 untreated primary adenocarcinoma, 35 diethylstilbestrol (DES) treated tumors, 50 lymph node and 11 bone metastases. Specimens were stratified according to the percentage of tumor cells expressing PD-41 antigen and degree of staining intensity, and correlated with PIN grade, Gleason score, flow cytometry (FCM) measured DNA ploidy, and reactivity to other antibodies. In PIN, 4 specimens (17.4%) showed reactivity in a significant number of cells while a few cells were reactive in most cases. PD-41 was significantly reactive (>5% of tumor cells) in 88% of nodal metastases and in 73% of bone metastases in contrast to 49% reactivity in primary tumors (p=0.0003). There was a tendency of increased antigen expression in hormonally treated primary tumors. In addition, involutional and metaplastic changes in hormonally treated cases were reactive in many instances. Semi-quantitative evaluation of PD-41 reactivity showed a statistically significant correlation with Gleason score in primary tumors (p=0.007) and in lymph node metastases (p=0.009). Moreover, the PD-41 antibody reacted in metastatic lesions that failed to express both prostatic acid phosphatase and prostate specific antigen. These data suggest that monoclonal antibody PD-41 merits further investigation to evaluate its potential diagnostic, prognostic and therapeutic role in prostate cancer.
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PMID:Monoclonal-antibody pd-41 recognizes a prostate-cancer associated antigen whose expression increases in metastases and following hormonal-therapy. 2155 82


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