Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biologic properties of breast cancer in men that might reflect alterations in pathogenesis from the disease in women were examined. We studied 22 tumors from males, 18 invasive carcinomas, three of which were papillary, and three in situ tumors of which one was papillary, and one papilloma. Our data support the previously reported high incidence of papillary carcinoma in men. Estrogen receptor status and the expression of cancer-associated antigens recognized by antibodies DF3, B73.2, SP-1, and c-erbB-2 were compared to matched tumors from females. Immunocytochemistry was performed on formalin-fixed, paraffin-embedded sections using standard avidin-biotin techniques; anti-PSA was used to exclude the possibility of metatastic prostate cancer, and 12 cases of gynecomastia were included as nonmalignant controls. The incidence of estrogen receptor positivity was higher in tumors from males (73%) than from females (54%), as has been reported previously. The range of expression of all breast cancer antigens tested in male tumors was similar to that observed in females, but some interesting differences were noted. With the exception of the anti-mucin DF3, all the antibodies reacted only with neoplastic tissues. Expression of the oncoprotein c-erbB-2 was lower (17%) in males than in females (33%), despite the preponderance in men of the large-cell type carcinomas that have been associated with c-erbB-2 expression. Unexpectedly, the pregnancy-associated hormone detected by SP-1 was expressed in 33% of tumors from males and, in contrast to females, was found in less differentiated tumors.
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PMID:Immunocytochemical characterization of male breast cancer. 136 97

Bone alkaline phosphatase (b-ALP) and tartrate resistant acid phosphatase (tr-ACP) are markers of the activity of osteoblasts and osteoclasts, respectively. We have already shown that the serum activity of these isoenzymes was elevated in breast cancer patients with bone metastasis (BM); we show here that the serum activity of b-ALP and tr-ACP were also elevated in prostate cancer patients with BM. Specificity and sensitivity of b-ALP for BM were 0.90 and 0.75, respectively; and for tr-ACP, 0.60 and 0.60, respectively. The accuracy of b-ALP as a BM marker was higher than the accuracy of usual markers of prostatic carcinoma (tartrate labile ACP [tl-ACP], prostatic acid phosphatase [PAP] and prostate specific antigen [PSA]). The highest value predictive of a positive bone scan was obtained with b-ALP (0.88); this increased to 0.97 when b-ALP was coupled with PAP.
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PMID:Phosphatase isoenzymes as bone metastasis markers in prostatic carcinoma. 176 Aug 84

Serum activities of bone alkaline phosphatase (b-ALP) and of tartrate resistant acid phosphatase (tr-ACP) were evaluated in 271 cancer patients; 120 of them had bone metastases (BM) and 151 had none. Correlation coefficients, specificities, sensitivities, negative and positive predicting values were computed. They showed the important contribution that these isoenzymes can bring to the diagnosis of BM in 80 patients with prostate cancer, and to the followup of 191 patients with breast cancer. The assay results were analysed in parallel with bone scan and radiography. They were also compared to those of serum antigens: PSA and PAP for prostate cancer, and CEA and CA15.3 for breast cancer. These results clearly indicate that both isoenzymes are better correlated with BM than antigens, these antigens being markers of the whole tumor burden--primary tumor, metastases, recurrence--whereas b-ALP and tr-ACP are specific markers of bone metabolism.
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PMID:[Evaluation of two serum isoenzyme phosphatases as bone metastasis markers]. 208 Dec 81

A number of biological markers have been recently introduced in clinical use as an aid for diagnosis and monitoring of malignant tumors. Some of them are relatively tumor-specific, i.e. CA 125 for non-mucinous ovarian cancer, CA 15.3 for breast cancer, PSA for prostate cancer, CA 19.9 for colo-rectal and pancreatic cancers. The clinical usefulness, the sensitivity and specificity of these tumor markers and of a few others (CA 50, SCC and TPA) are commented in this review.
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PMID:[Critical study of current tumoral markers]. 245 33

Tumour markers are often circulating tumour-associated indicators of tumour development. As such they are not suitable for tumour screening and localization, but valuable as adjuncts for medical follow-up care of tumour patients, where their serum level alterations may anticipate the clinical detection of tumour behaviour by a lead time of 1 to 6 months before other methods. The following tumour may be controlled by established markers: endocrine tumours by NSE, calcitonin, parathormone, 5-HIAA, catecholamines/metabolites etc.; head-neck tumours: SCC, CEA; thyroid carcinoma: TG, calcitonin; lung cancer: CEA, NSE, SCC; liver cancer: AFP (PLC), CA 19-9 (cholangiocell.), CEA (secondary): biliary tract and pancreatic cancer: CA 19-9; colorectal carcinoma: CEA, CA 19-9; squamous cell carcinoma (ENT, oesophagus, anal): SCC; breast cancer: CEA and CA 15-3; ovarian cancer: CA 125 (epithelial), CA 19-9 (mucinous); germ cell tumours (ovary including trophoblastic tumours/testes): AFP and HCG; prostatic cancer: PAP and PSA; bladder cancer: TPA.
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PMID:[Clinical relevance of tumor markers]. 267 6

Several common misconceptions have fueled the debate over the early detection and treatment of prostate cancer. While prostate cancer is often described as a common cancer that older men die with rather than of, the reality is that the incidence, mortality, and mean age and stage at diagnosis of prostate cancer are very similar to those of breast cancer, which is rarely the subject of similar concerns. Many studies have confirmed that given enough time, all clinically detected prostate cancers will inexorably progress locally and eventually metastasize to regional lymph nodes as well as to distant sites. The relatively slow doubling time compared to that of other cancers and the wide spectrum of biologic activity of prostate cancer have made retrospective studies reporting the long-term survival of conservatively treated patients highly suspect due to selection bias and inadequate follow-up. While it is accepted that a large number of men harbor clinically insignificant cancers in their prostate glands, these estimates have been based on careful pathologic step-sectioning studies of prostates obtained either at autopsy or after cystoprostatectomy for bladder cancer. Several studies have now demonstrated that currently available diagnostic modalities for detecting prostate cancer, DRE, PSA, and TRUS, are not able to detect a significant proportion of small, clinically unimportant cancers. Rather, studies have shown that while the traditional DRE has been largely unsuccessful in detecting prostate cancers at a sufficiently early stage for effective treatment with either radical prostatectomy or radiation therapy, a combination of the DRE and PSA followed by TRUS and ultrasound-guided biopsy in those with abnormal results can detect an increased proportion of clinically significant prostate cancers while they are still confined to the prostate gland and thus more likely to be eradicated by treatment. Several randomized trials are now under way in this country and in Europe that may settle many of these issues over the next decade. However, currently available data suggest that prostate cancer screening holds the promise of decreasing the considerable morbidity and mortality caused by this disease.
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PMID:Screening for prostate cancer: an analysis of the early experience. 753 41

Clinical and epidemiological research on prostate cancer is faced with some unusual methodological challenges. The very high prevalence of latent cancer, much of which never becomes clinically manifest, complicates the approach to screening and the conduct of epidemiological studies. Cost-effectiveness issues are especially relevant regarding screening policies, and these trade-offs are complicated by the absence of definitive results on the effectiveness of the various treatment options. The presentation of advanced disease is also unusual, in that the vast majority of patients do not have measurable disease suitable for traditional studies of new chemotherapy agents. These problems necessitate creative approaches to the design and analysis of research studies in this disease: cost-effectiveness analysis is crucial to the evaluation of screening policies; opportunistic designs will be essential to the valid study of cancer etiology, eg, the use of cystoprostatectomy series for studies of epidemiologic risk factors; and posttreatment changes in PSA levels may be valuable as a criterion for screening new agents in advanced disease. Regardless of these new methods, traditional methodological approaches are essential to the valid study of prostate cancer. Randomization is required for valid comparison of treatments and screening strategies. Statistical analysis should observe the intent-to-treat principle whereby patient groups are analyzed with respect to the planned, rather than the delivered therapy, and studies should have sufficiently large sample sizes to reliably distinguish the true effects of the interventions from random statistical fluctuation. Recently, meta-analysis has become popular as a tool for synthesizing the information from available studies on a specific clinical problem. Its most conspicuous success has been in showing the efficacy of adjuvant therapy in breast cancer, for which many individual studies appeared to give conflicting results.64 In this setting there was a large number of published randomized trials, many of which had large sample sizes and long follow-up, and so the meta-analysis was able to show convincingly a small but clinically meaningful treatment effect on long-term disease recurrence and survival. This is similar to the situation in localized prostate cancer in all respects except for the availability of randomized trials. Unfortunately there is no free lunch. This technique can only be applied if the high quality data are available. One must be similarly cautious in applying decision analytic techniques (and also cost-effectiveness analysis) to try to resolve clinical dilemmas.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Methodological issues in studies of the treatment, diagnosis, and etiology of prostate cancer. 793 48

The dynamic evaluation of tumor markers is a promising area of investigation which is expected to provide clinical information when serial samples are available from the same patient. This is feasible in the post-operatory evaluation, during the follow-up after the treatment for to the primary tumor and in the monitoring of the treatment for metastatic disease. Variations among serial samples may be assessed using both empirical and mathematical approaches. Empirical approaches rely on overcoming a given percentage usually chosen on the base of arbitrary decisions. Mathematical approaches include the actual half-life, the doubling time, a dose/time regression analysis and the calculation of the critical difference. The two former are currently used in clinical practice whereas the two latter are still matter of investigation. As concerns the assessment of the radicality of the surgery for the primary tumor, the serum markers are used in germ cell tumors and in prostate cancer. The half-life of the markers is the decision criteria used in germ cell cancers, while in prostate cancer PSA is expected to be undetectable more than 30 days after the radical prostatectomy. Tumor markers are currently used during the follow-up of several malignancies after the treatment for primary tumor. Although several samples are available, decision criteria are still based on positive/negative cut-off values in several instances. Promising dynamic approaches are under investigation and are expected to lead to earlier and probably more accurate information concerning the disease progression. A critical point still under debate is the actual impact of tumor markers on patients' survival in malignancies incurable when metastatic, such as colorectal cancer and breast cancer. This matter urgently demands perspective clinical studies. Finally, the dynamic use of tumor markers is now commonly applied in the monitoring of the therapy for metastatic malignancies. In this clinical setting mathematical criteria are used for ovarian and and germ cell tumors with promising results. Nevertheless, the use of empirical criteria, namely the percentage of variation between two consecutive samples, is successfully used for the monitoring of the therapy of metastatic breast cancer. In conclusion, when several samples are available from an individual patient they may be evaluated according to dynamic criteria instead of referring to a conventional positive/negative cut-off point. Although mathematical decision criteria are expected to provide more reliable data, empirical approaches are used as well and provide useful information in decision making.
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PMID:Dynamic use of tumor markers, rationale-clinical applications and pitfalls. 869 56

Expression of a truncated or extracellular form (p105erbB-2) of p185erbB-2 has been demonstrated in the sera of breast cancer patients. We examined the levels of p105erbB-2 in the sera of patients with various stages of prostatic adenocarcinoma, in patients with benign prostatic hyperplasia (BPH) and in a series of control male patients hospitalized for illnesses unrelated to the prostate. p105erbB-2 levels did not differ between the controls and BPH patients or between these groups and patients with stage A, B or C adenocarcinomas. In contrast, serum p105erbB-2 levels of patients with stage D adenocarcinomas were significantly elevated when compared with either control or BPH patients. There was no correlation between PSA and p105erbB-2 levels among controls, patients with BPH or patients with prostate cancer. Patients with poorly differentiated tumors (combined Gleason score >7) or moderately differentiated tumors (combined Gleason score 5-7) had higher p105erbB-2 levels as compared to patients with well-differentiated tumors (combined Gleason score <5), though this difference was not statistically significant. There was no correlation between serum p105erbB-2 levels and p185erbB-2 expression in malignant tissue, as determined by immunohistochemistry. However, patients with moderate to strong expression of p185erbB-2 within the adenocarcinomas were approximately 4 times more likely to demonstrate elevated serum p105erbB-2 levels as compared with patients with low expression of p185erbB-2.
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PMID:Elevated serum levels of p105(erbB-2) in patients with advanced-stage prostatic adenocarcinoma. 890 Mar 74

The name prostate-specific antigen has been given to a protein that now is known not to be prostate-specific; however, prostatic tissue does produces extremely high levels of PSA and secrets it into the seminal plasma. Seminal plasma contains about 1 million micrograms/L of PSA and is the richest source of PSA reported. The biologic fluid with the second highest PSA concentration, however, is nipple aspirate fluid from the female breast (up to about 5000 micrograms/L), and the third is milk from lactating women (up to 300 micrograms/L). Male serum PSA is usually less than 4 micrograms/L. In nonprostatic tissues, PSA exists mainly in its free molecular form, but PSA-ACT complex is also present in most of the fluids that contain PSA, such as breast secretions and amniotic fluid. The gene expression and protein production of PSA in nonprostatic tissues are under the regulation of steroid hormones via their receptors. Androgens, glucocorticoids, and progestins up-regulate the PSA gene expression, resulting in an increase of protein production. Estrogen by itself seems to have no effect on PSA regulation, but it can impair PSA production induced by androgen. It remains unknown whether PSA is enzymatically active and what is the physiologic role of PSA in nonprostatic tissues. It is speculated that PSA may be involved in the regulation of growth factors. Measuring PSA in breast cancer cytosol, breast-nipple aspirate fluid, and female serum may have potential clinical utilities, including breast cancer prognosis, breast cancer risk assessment, and evaluation of androgen excess. Further studies are needed to identify the exact function and regulation of PSA in nonprostatic tissues and to explore the clinical application of this protein.
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PMID:Nonprostatic sources of prostate-specific antigen. 912 24


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