Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the development of a new sensitive nested reverse transcription-polymerase chain reaction (RT-PCR) assay, using primers derived from the prostate-specific membrane antigen (PSM) cDNA sequence, to detect an hematogenous spread of prostate adenocarcinoma cells. In 60 patients with a biopsy-proven prostate cancer, PSM and PSA RT-PCR detected circulating prostate cells in 40 and 20 patients, respectively. In pT4 M+ and pT3 M+ disease patients, nested PSM primers detected cells in 28 of 33 patients (85%), whereas nested PSA primers detected cells in 17 of 33 (51%). In patients with organ-confined cancer spread (pT2a and pT2b patients) before radical prostatectomy, nested PSM RT-PCR detected circulating prostatic epithelial cells in 6 of 17 patients (35%), which suggests that an hematogenous spread of prostate cells may occur early in prostate cancer history. Altogether, these results suggest that the detection of PSM-expressing cells in blood may predict the development of cancer in patients without clinically apparent prostate cancer. Nevertheless, the potential application and the clinical significance of detection of hematogenous prostate cells through the use of nested PSM primers need an extensive longitudinal study.
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PMID:Enhanced detection of hematogenous circulating prostatic cells in patients with prostate adenocarcinoma by using nested reverse transcription polymerase chain reaction assay based on prostate-specific membrane antigen. 749 5

On retrospective review of the tumor registry files between 1979 and 1992 at the North Iowa Medical Center, six cases of endometrioid adenocarcinoma of the prostate were identified among 1582 cases of prostatic carcinoma. Along with long-term clinicopathologic follow-up, immunohistochemical studies of the prostatic tumor tissues were performed. All six cases of endometrioid carcinoma, together with control cases of benign prostatic hypertrophy (BPH) and ordinary adenocarcinoma of the prostate had unequivocal diffuse positive staining for PSA and similar reactivity to ER-D5 and PS2. Thus, endometrioid carcinoma is most likely derived from the prostate or prostatic urethral duct rather than the utricle. However, due to its unusual initial clinical manifestations, biological behavior, and distinctive histomorphology, the term "endometrioid adenocarcinoma of the prostate" is worth preserving.
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PMID:Endometrioid adenocarcinoma of the prostate: a clinicopathologic and immunohistochemical study. 751 74

Clinical and immunohistochemical studies were conducted to evaluate prostatic papillary adenocarcinoma and prostatic papillary hyperplasia. Subjects consisted of 5 cases of papillary adenocarcinoma and 2 cases of papillary hyperplasia. There is no conclusive clinical factor for preoperative diagnosis, but we attach importance to endoscopic findings. PSA, PAP, high molecular weight cytokeratin, and PCNA were evaluated immunohistochemically. PSA became positive in every instance but one--a case of papillary adenocarcinoma which became +/-. PAP was + in all cases, except for 1 case of papillary adenocarcinoma. Basal cells were positive for high molecular weight cytokeratin in 2 cases of papillary hyperplasia but were missing in papillary adenocarcinoma. Although PCNA was free from positive nuclei in papillary hyperplasia, positive nuclei were found in all cases of papillary adenocarcinoma. Considering these immunohistochemical results, papillary adenocarcinoma can be said to originate in the glandular epithelium of the prostate, as does ordinary prostatic carcinoma.
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PMID:A clinical and immunohistochemical study of papillary adenocarcinoma of the prostate. 753 25

Great interest has been generated recently in preoperative androgen deprivation for clinical stage B ou C (T2 ou T3) prostate cancer. The influence of neoadjuvant hormonal therapy on down-staging and down-grading is still controversial. To assess the influence of preoperative androgen deprivation on serum PSA levels, we compared pre- and post-treatment serum PSA levels in 54 patients who received complete pre-operative androgen blockade (LHRH agonist + flutamide) 3 months prior to surgery. All patients with a pretreatment PSA > 20 ng/ml had extra-prostatic disease excepted two patients who presented lesions of acute prostatitis with adenocarcinoma. After hormonal deprivation, 51/54 patients experienced a return of PSA to normal values (< 4 ng/ml). Among this patient, 33 had undetectable PSA levels (< 0.25 ng/ml). 90% of the patients with undetectable had tumor confined to the gland (pT2/B). On the other hand, patients who still have PSA > 4 ng/ml after hormonal deprivation, had extra-prostatic cancer (pT3-pT4). Thus, PSA levels after 3 months neo-adjuvant hormonal treatment might have a useful predictive value in patients selection for radical surgery.
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PMID:[Predictive value of the serum PSA level in patients having undergone neo-adjuvant hormone treatment before radical prostatectomy]. 753 12

In the report we refer to our experience as regards the role of transrectal ultrasonography in the early diagnosis of prostatic heteroplasia based on the results obtained by a research led from January 1991 to January 1995 on 1185 dysuria patients who have been subjected also to a rectal exploration and a serous dosage of PSA. Among the 306/1185 (25.8%) of the patients subjected to prostatic echoguided biopsy sec. Hodge in 238 (77.7%) a hypoechogenic zone on behalf of the periphery of the prostatic parenchyma has been reported. The histological result has pointed out the presence of adenocarcinoma in 81 (26.4%) patients; of benign prostatic hypertrophy in 196 (64%); of acute and/or chronic non specific phlogosis in 26 patients (8.4%) and granulomatosis prostatitis in 3 (1%). The sensibility, the specificity and the diagnostic efficiency of the transrectal ultrasonography in the diagnosis of prostatic heteroplasia have resulted equal, respectively to 100%, to 30.2% and to 48.6%. In 122 patients (66%) the hypoechogenic zone was not pathognomonic of prostatic heteroplasia. Definitely, considering the high sensibility in opposition to the insufficient specificity of the echography, it is our future intention not submit to prostatic biopsy those patients who show only a hypoechogenic zone in absence of pathology EDR and PSA but to monitor them through quarterly clinic checks.
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PMID:[Ultrasonography and prostatic adenocarcinoma]. 758 23

"Incidental" cancer refers to predominantly well differentiated cancer that arises in the transition zone and is found by chance in TURP chips. These tumours are frequently small and may be completely resected by TURP, although a significant number have an additional tumour that is unreachable with a resectoscope. These tumours often co-exist with benign prostatic hyperplasia. Putative precursors of incidental carcinoma include high grade PIN and AAH, and these lesions are frequently found in the transition zone in prostatectomies for cancer. The single most significant question in treating incidental adenocarcinoma is how to separate tumours that will progress from those that will not progress during the expected lifetime of the patient. The 1992 revision of the TNM staging system separated non-aggressive (T1a) and aggressive (T1b) incidental cancer according to the number of foci of cancer, using more than three foci as the cutpoint to identify more aggressive cancer. However, 8-37% of patients with T1 a cancer will develop cancer progression within 10 years if untreated, with the risk of progression increasing with additional years of follow-up. Important prognostic factors include the patient's age, tumour location (peripheral zone v. transition zone), tumour grade, tumour volume, serum PSA concentrations and morphometric factors such as nuclear roundness. Studies directed at early detection allow discovery of increasingly smaller cancers.
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PMID:The pathology of incidental carcinoma. 762 75

Prostate cancer with marked neuroendocrine (NE) differentiation belongs to the hormone resistant carcinomas. We report the development of TSH-secreting small cell prostate cancer (SCPC) from high grade adenocarcinoma (Gleason score 8) with an elevated number of chromogranin A positive cells located in benign structures adjacent to the cancer. Conversion to SCPC was followed-up during 4 years. The initial adenocarcinoma exerted a stronger positivity for PAP than for PSA (respective staining indexes, Sls, 2.2 and 1.8, maximum staining 3.0). In the developed SCPC, 2 cell subpopulations that were derived from epithelial cells were found (positive stain for EMA and CEA, respectively) and from one of them originated CEA-positive liver metastases. Blood CEA and NSE levels were elevated in SCPC (284 ng/ml and 24.5 ng/ml). However, blood TPS level which reflects proliferation of epithelial cells was within the normal range. The development of a << pure >> sarcomatoid prostatic tumor from adenocarcinoma with 2 areas of similar differentiation grades (Gleason score 7 and 9-10) that initially differ in staining for PSA and PAP (SIs for PSA were 1.2 and 0.02 and for PAP were 1.6 and 0.02, respectively) was followed-up during 4 years of treatment with Estracyt. Adenocarcinoma tissue specimens was slightly CEA-positive. The disappearance of lower grade adenocarcinoma during treatment was accompanied by the development of sarcomatoid areas that were 100% vimentin positive. In the last year of follow-up the primary tumor was composed only of vimentin positive sarcomatoid cells with a slight positivity for Chromogranin A, NSE and ACTH. In parallel, normal serum PSA and PAP values and elevated CEA and NSE serotests (12.6 ng/ml and 24.7 ng/ml, respectively) were found. Blood TPS level was at the upper limit of the normal range. Scintigraphy revealed extensive liver metastases. The recorded data indicate (i) extremely poor prognoses associated with high grade adenocarcinomas that demonstrate stronger immunohistochemical positivity for PAP than that for PSA (ii), chromogranin A positive cells in benign structures adjacent to the cancer as a possible paracrine promoter of SCPC from poorly differentiated adenocarcinoma, and (iii) a high degree of heterogeneity of both SCPC and sarcomatoid prostatic neoplasms with some evidence for definite links (EMA and CEA) to secretory epithelial cells.
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PMID:Immunohistochemical staining and serotest markers during development of a sarcomatoid and small cell prostate tumor. 784 May 15

The response of advanced prostatic cancer with metastatic chest wall tumor to high-dose diethylstilbestrol diphosphate (DESP) therapy was monitored by in vivo 31P magnetic resonance spectroscopy (31P MRS) study. A eighty-three year old man with Stage D2 prostatic cancer had been treated with chlormadinone acetate and cyclophosphamide since 1984. He was admitted to our hospital with a chest wall tumor and anemia on May 9, 1992. The elevated PAP, PSA and gamma-Sm levels were also observed. Needle biopsy of the tumor revealed poorly differentiated adenocarcinoma metastatic from the prostatic cancer. The patient received 500 mg of DESP by DIV daily for 10 days, and the tumor was reduced by 54% clinically. The abnormal PAP, PSA and gamma-Sm levels returned to almost normal range by three weeks after the initiation of high-dose DESP therapy, and regression of the tumor was confirmed by the MRI. After the first administration of DESP, the MR spectra of the chest wall tumor showed elevated peaks of phosphomonoesters and phosphodiesters. These substances are related to the membrane metabolism and their increase represents the membranous degeneration of tumor cells. The same changes continued consecuitively for three weeks, and corresponded with the regression of the tumor. In conclusion, these results suggest that in vivo 31P MRS of malignant tumors can be useful for evaluating early response to therapy prior to other clinical examinations.
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PMID:[Monitoring tumor response to therapy by means of 31P magnetic resonance spectroscopy. A case of advanced prostatic cancer with metastatic chest wall tumor]. 802 47

Metastatic prostate adenocarcinoma is a leading cause of cancer-related deaths among men. First line treatment is primarily aimed at blocking the synthesis and action of androgens. As primary endocrine treatment, androgen deprivation is usually achieved by orchidectomy or LHRH analogues, frequently combined with androgen receptor antagonists in order to block the residual adrenal androgens. However, nearly all the patients will eventually relapse. Available or potential second line therapies include, among others, alternative endocrine manipulations and chemotherapy. Cytochrome P450-dependent enzymes are involved in the synthesis and/or degradation of many endogenous compounds, such as steroids and retinoic acid. Some of these enzymes represent suitable targets for the treatment of prostate cancer. In first line therapy, inhibitors of the P450-dependent 17,20-lyase may achieve a maximal androgen ablation with a single drug treatment. Ketoconazole at high dose blocks both testicular and adrenal androgen biosynthesis but its side-effects, mainly gastric discomfort, limit its widespread use. A series of newly synthesized, more selective, steroidal 17,20-lyase inhibitors related to 17-(3-pyridyl)androsta-5,16-dien-3beta-ol, may open new perspectives in this field. In prostate cancer patients who relapse after surgical or medical castration, therapies aiming at suppressing the remaining adrenal androgen biosynthesis (ketoconazole) or producing a medical adrenalectomy (aminoglutethimide+hydrocortisone) have been used, but are becoming obsolete with the generalization of maximal androgen blockade in first line treatment. The role of inhibition of aromatase in prostate cancer therapy, which was postulated for aminoglutethimide, could not be confirmed by the use of more selective aromatase inhibitors, such as formestane. An alternative approach is represented by liarozole fumarate (LIA), a compound that blocks the P450-dependent catabolism of retinoic acid (RA). In vitro, it enhances the antiproliferative and differentiation effects of RA in cell lines that express RA metabolism, such as F9 teratocarcinoma and MCF-7 breast carcinoma cells. In vivo, monotherapy with LIA increases RA plasma levels and, to a greater extent, endogenous tissue RA levels leading to retinoid-mimetic effects. In the rat Dunning prostate cancer models, it inhibits the growth of androgen-independent as well as androgen-dependent carcinomas relapsing after castration. Concurrently, changes in the pattern of cytokeratins characteristic of increased differentiation were observed. Early clinical trials show that LIA, in second or third line therapy in metastatic prostate cancer, induces PSA responses in about 30% of unselected patients. In some patients regression of soft tissue metastasis ha been observed. In a subgroup of patients, an important relief of metastatic bone pain was also noted.
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PMID:P450-dependent enzymes as targets for prostate cancer therapy. 860 34

To determine whether long-term oral administration of UFT, a combination of 5-fluorouracil and uracil, in addition to conventional estrogen therapy improved the response and survival of the patients with advanced stage D2 prostate adenocarcinoma, a randomized prospective study was performed with either estrogen alone (Honvan 200 mg/day or presexol 1 mg/day: group A) or estrogen plus UFT (400 mg/day:group B). This study comprises 34 newly diagnosed patients with poorly differentiated prostatic adenocarcinoma (18 patients in group A and 16 in group B). Survival from all causes of death or cancer-specific death were compared using Kaplan-Meier actual methods among the patients separated by histological composition of tumors analyzed WHO histologic patterns, score of extent of disease (EOD), and with or without normalization of serum PSA or PAP levels after treatment. Although combination therapy with UFT against overall survival was effective without statistical significance, better survival in this group than the patients treatment with estrogen alone assessed among the patients whose tumor contained more than 70% of medullary and/or column-cord histological components. The survivals among the patients with EOD score 3 and whose serum PSA or PAP levels did not lead to decrease within normal levels after treatment were also better in group B than in group A. These findings suggest the validity of the combination therapy with UFT in addition to estrogen against highly advanced prostatic cancer patients whose tumor composed of abundant non-hormone-refractor histological components.
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PMID:[Combination therapy with estrogen and UFT in newly diagnosed prostatic cancer (poorly differentiated, stage D2)]. 861 89


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