Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five tumor markers can be simultaneously determined in the serum by radioimmunoassay: carcinoembryonal antigen (CEA), alpha-fetoprotein (alpha-FP), human chorionic gonadotropin (HCG), beta-subunit of HCG (beta-HCG) and kappa-casein. In a series of 935 healthy subjects, these antigens remain detectable or are detected within very precise limits. At the start of the clinical evolution of breast cancer, the incidence of pathological concentrations is increased as compared with the highest level observed in normal subjects. This high incidence is mainly due to a concomitant determination of CEA, kappa-casein, HCG and beta-HCG. The alpha-FP test is never positive, while the kappa-casein concentration is particularly high in the first clinical stages of breast cancer and with metastases. The concomitant determination of these tumor markers may be a biological element contributing to the diagnosis of neoplasia, although it is neither an absolute nor a specific criterium. Indeed, a pathological concentration of at least one antigen was observed in 5.5% of the subjects presenting with benign mastopathy. When metastases occur (25 patients), the incidence of pathological concentrations of at least one antigen increases: 88%, the absolute values of these levels increasing simultaneously. The determination of the antigen concentration therefore allows an evaluation of the extension of the disease. Surgical removal reduces the incidence of positivity of these antigens to 34%. Persistence of pathological levels seems to be related to a possibility of relapse or metastatic spreading. Finally, chemotherapy and radiotherapy applied on a tumor which is not excised, does not decrease the incidence of positivity of the tumoral markers, although their levels seem to fluctuate with the clinical evolution.
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PMID:Casein and other tumor markers in relation to cancer of the breast. 7 72

The doubling time (DT) was estimated quantitatively for 16 carcinomas of the breast according to the method described by Collins and co-workers in 1956. This is based on the concept of constant and exponential growth. Observation interval for these mammographically confirmed tumors was between 83 and 1,034 days. The DT was calculated to vary from 45 to 260 days; in order to reach a diameter of 1 cm. after 30 divisions would require a period of 3.7 to 21.4 years. Mammography frequently demonstrates small, clinically occult, tumours. Axillary lymph node metastases are relatively rare from small tumours; growth rate of 70% of breast carcinomas in such that an annual clinical and radiological check-up will prove to be the best means of reducing mortality from carcinoma of the breast. The risk inherent in the radiation resulting from annual mammography is acceptable in women over 35 years. This leaves the problem of rapidly growing carcinomas which would escape early diagnosis by early examinations. Half-yearly examinations of women in high risk groups (1. Previous mastectomy for carcinoma, 2. Biopsy-proven mastopathy with atypical proliferation) comprising about 30% of carcinomas with a short doubling time would appear to be reasonable.
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PMID:[The diagnosis of carcinoma of the breast in relation to growth rate (author's transl)]. 17 78

The estrogen receptor (ER) status is an important factor for prognosis and endocrine therapy of breast cancer. Therefore 16-alpha-123I-iodoestradiol-17-beta (123I-E2) as a receptor-specific radiopharmacon was used for scintigraphic tumor detection in 62 patients suspected of breast cancer. The studies were performed as a multicenter trial (5 university hospitals) to validate the method and to overcome methodical problems. A fast tracer elimination from the blood pool into the liver was seen, followed by biliary excretion allowing early imaging of the thorax due to low background activity but resulting in difficult imaging conditions of the abdomen. In 42 patients (30 carcinomas, 12 benign lesions) the overall sensitivity was 66% (ER status cut-off: 10 fmol/mg). Some patients with breast cancer showed focal or diffuse uptake in the area of primary lymph drainage (parasternal, axillary) without any clinical correlation, demanding follow-up investigations. There was only one false-positive result in a receptor-negative primary carcinoma; thus, the non-invasive determination of the ER status seems to be feasible. The sensitivity of 123I-E2 in the detection of primary breast cancer or metastases and recurrences is low compared to mammography and other methods; therefore, 123I-E2 scintigraphy cannot be used as a screening method. Differentiation of malignant and benign tissue is even more difficult as both may have a positive ER status, for example in mastopathy. Nevertheless, 123I-E2 scintigraphy is an in vivo imaging technique for the detection of breast cancer depending on the ER status and provides information about tumor localisation. It may become a specific method for the non-invasive diagnosis of the ER status and may be helpful in follow-up studies. As a receptor-specific agent 123I-E2 may give answers to questions of tumor heterogeneity and changes of the ER status during therapy.
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PMID:[Tumor scintigraphy using 123I-labeled estradiol in breast cancer--receptor scintigraphy]. 187 Oct 7

Breast cancer will affect 1 out of 10 women in the United States and cause 27 deaths per 100,000 women per year. The etiology remains unknown, but the incidence correlates with genetic as well as environmental factors. Screening programs have been shown to prolong the survival by early detection compared with control populations but remain underutilized by physicians and patients. Breast disease can be evaluated by physical examination and mammography and a definitive diagnosis made by needle aspiration, needle biopsy, or excisional biopsy. This allows the patient to participate in the decision regarding mastectomy vs. conservative surgery plus radiation therapy. These two approaches have equivalent survival in selected patients. Patients with locally advanced, nonmetastatic disease benefit from a multidisciplinary approach using preoperative chemotherapy and postoperative radiation therapy. This approach has allowed less disfiguring surgery and improved survival. Preinvasive carcinoma is diagnosed more frequently with the increased use of screening mammography. Local therapy options include simple mastectomy, local excision plus radiation, or local excision alone. The natural history and results of therapy in preinvasive disease are evolving as more data are accumulated. Systemic adjuvant therapy is recommended for all node-positive patients and most node-negative patients with invasive cancer. The specific modality (hormonal or cytotoxic) varies with the subgroup involved. Treatment of metastatic disease to palliate symptoms and prolong survival includes the use of local therapies (surgery and radiation) and hormonal and cytotoxic agents. Most patients benefit, but cure has been unobtainable. Newer approaches utilizing high-dose chemotherapy and bone marrow support with growth factors or autologous transplantation are currently being explored.
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PMID:Breast cancer. 240 15

Elevated plasma levels of glutamate (GLU) have been reported to occur in patients with malignancies and other immunodeficiency syndromes (IDS). To evaluate, whether GLU is useful as prognostic indicator, the plasma concentrations were determined in patients with colorectal carcinoma (CRC), with breast cancer (BRC), and with HIV-infection (HIV). The results were correlated with the disease-stages, and compared with data obtained from patients with benign diseases of the same organ, as well as from sex-matched healthy volunteers. GLU concentrations (volunteers: 27.4 +/- 17.6 mumol/l) were elevated in all BRC patients (range of mean values: 53.5-83.2 mumol/l), in CRC patients with T2-T4-tumours (means: 46.8-85.9), and in HIV+ patients of stage WR 5, 6 (means: 53.9-69.7 mumol/l). All CRC- and BRC-patients with metastases showed highly significant elevations of GLU concentrations (p less than 0.001), but there were no direct correlations between disease stages and GLU levels. Pre-operative patients with benign diseases (diverticulitis, adenoma = GID; and mastopathy = MTP) showed increased GLU levels, which were comparable to those of the tumour patients. The glutamine/GLU ratios (volunteers: 19.3 +/- 15.0) were decreased only in HIV-WR 6 (7.6 +/- 2.1), and BRC-stage 4 (8.0 +/- 1.7). From these results we deduce that the plasma GLU concentrations do not allow a discrimination either between patients with malignancies and without, and between persons of different disease stages.
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PMID:Plasma glutamate--a prognostic marker of cancer and of other immunodeficiency syndromes? 257 87

Serum melatonin was determined over 24 hours in 35 patients with breast cancer with either a fresh primary tumor (n = 23) or a secondary tumor (n = 12) and in 28 patients with untreated benign breast disease (controls) having a fibroadenoma (n = 10), fibrocystic mastopathy (n = 14), or other breast diseases (n = 4). Circadian rhythms existed in all groups with acrophases at 2 a.m. A 50% depression of peak and amplitude occurred in the group of patients with primary breast cancer compared with age-matched controls (P less than 0.001, P less than 0.01). The peak declined with increasing tumor size: 27% at Stage T1, 53% at T2 (P less than 0.001), and 73% at T3 (P less than 0.05). In contrast, patients with secondary breast cancer, particularly those receiving antiestrogen therapy, had a melatonin peak similar to controls. These results demonstrated a transient depression of pineal melatonin secretion in primary breast cancer and indicated a dynamic role of the pineal gland in malignancy. To investigate some endocrine effects of a depressed melatonin peak, the 24-hour rhythms of prolactin (PRL) and thyroid stimulating hormone (TSH) were determined in patients with primary breast cancer and compared with patients with secondary breast cancer. The PRL had significant circadian rhythms in both groups; but acrophases occurred at midnight in patients with secondary breast cancer, and there were unusually high concentrations at noon in patients with primary breast cancer. Circadian rhythms were not seen for TSH, but the 24-hour average secretion was depressed by 45% (P less than 0.01) in patients with primary breast cancer. The abnormal concentrations of PRL and TSH in these patients could be due to a depressed melatonin peak normally serving as a central circadian synchronizer and modulator of the secretion of adenohypophysial hormones. Additionally, a positive correlation existed between the nocturnal melatonin peak and progesterone and androgen receptor concentrations in primary tumors indicating a direct involvement of melatonin in the growth control of breast cancer.
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PMID:Stage-dependent depression of melatonin in patients with primary breast cancer. Correlation with prolactin, thyroid stimulating hormone, and steroid receptors. 273 89

To study the production and significance of prostacyclin (PGI2) and thromboxane A2 (TxA2) in breast cancer, tissue fragments of breast cancer (n=23) and mastopathy (n=10) were superfused in vitro and the release of 6-keto-PGF1 alpha (a metabolite of PG12) and TxB2 (a metabolite of TxA2) measured by radioimmunoassay. Breast cancer formed more 6-keto-PGF1 alpha (4.5 +/- 0.9 ng min-1 g-1 of tissue dry weight, mean +/- s.e.) and TxB2 (2.5 +/- 0.6 ng min-1 g-1) (P less than 0.01) than did mastopathic breast (1.4 +/- 0.5 and 0.4 +/- 0.1 ng min-1 g-1, respectively). These productions were similar in steroid receptor positive and negative tumours. Breast cancer metastasized in 15 patients during the follow-up time of 3.7 +/- 0.7 years, but the initial prostanoid productions in these patients were not different from those in nonmetastatic patients. Two patients died from metastases, but their initial mammary production of prostanoids was not profoundly different from those in the survivors. In 8 patients (4 with steroid receptor positive and 4 with negative tumour), the cancer tissue was superfused in the presence or absence of medroxyprogesterone acetate (100-5000 ng ml-1), which is commonly used for treatment of breast cancer. This hormone had no effect on mammary PGI2 and TxA2 production. We thus conclude that the PGI2 and TxA2 productions are increased in mammary cancer but that this may not be of primary significance for metastastic spread.
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PMID:Prostacyclin and thromboxane in breast cancer: relationship between steroid receptor status and medroxyprogesterone acetate. 298 66

A rare case of mammary signet-cell carcinoma which was not diagnosed at life is described. In a woman of 28, an enlargement of the right uterine appendages with pleural and lung metastasis were clinically noted and this was interpreted as ovarian carcinoma with pleural and lung metastasis. Histological examination of ovarian tumour performed during the necropsy allowed one to suggest the metastatic signet-cell carcinoma. No tumours were found macroscopically or histologically in the organs of the alimentary canal. Fibro-cystic mastopathy and no nodes were found macroscopically in the mammary glands. Lobular invasive carcinoma consisting of signet-cell elements containing mucus and carcinomatous lymphangoitis were found histologically. Metastasis to the left axillary, perigastral and pancreatic lymph nodes, lungs, carcinomatosis of pleura were revealed. It is suggested, due to its clinical course and histological structure, to distinguish this form of carcinoma as a separate variety of the lobular invasive carcinoma of the mammary gland.
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PMID:[Signet ring cell cancer of the breast]. 298 87

A proliferating mastopathy with severe epithelial atypia as well as with so-called radial scars, intraductal papillomatosis, and findings of so-called lobular cancerisation are regarded as possible precursors of mammary carcinoma. The histological differential diagnosis can be difficult between atypical epithelial proliferations in mastopathy and noninvasive intraductal carcinoma, between tubular formations in radial scars and tubular carcinoma, papilloma and papillary carcinoma as well as between primary and secondary lobular cancerisation. Noninvasive and invasive breast carcinomas can be diagnosed according to the WHO classification (12) with a relatively good reproduceability. Besides the histological type, other macroscopic (tumour size, number of metastatically involved lymph nodes, distant metastases), microscopic (tumour grading) as well as biochemical findings (receptor status) are also important for treatment and prognosis of breast carcinoma.
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PMID:[Histologic classification of breast cancer and its precancerous stages]. 303 49

Two properties seem fundamental to cancer; heterogeneity and progression (Foulds (1975) Academic Press, New York; Heppner et al. (1979) Commentaries on Research in Breast Disease, Vol. 1 (Bulbrook, R. and Taylor, D.J., eds.), pp. 177-191, Plenum Press, New York). Relatively little is understood about the premalignant stages of human breast disease in vivo. When the disease manifests as invasive carcinoma, its behavior exhibits great diversity, sometimes metastasizing rapidly, while in other cases 10-30 years pass before metastases proliferate. Here we review various aspects of breast cancer in vivo and consider how they predict properties of breast cancer found in culture. All of the experiments are consistent with the hypothesis proposed by Nowell (1976) Science 194, 23-28, that a fundamental aspect of malignancy is an increased genetic instability and that many of the cells within tumors are nonviable results of genetic instability. We suggest that most of the viable cells within primary breast carcinomas are diploid and are not yet capable of aspects of metastatic spread. What these cells have attained is an increased propensity for genetic instability which enables them to generate randomly aneuploid but frequently lethal genetic configurations. Occasionally one of these altered genomes is associated with the ability to proliferate at a metastatic site. This hypothesis implies that metastases from various patients may have arisen by divergent pathways and may also be divergent in many other aspects of their physiology, unrelated to malignancy. Such extreme heterogeneity may hamper attempts to understand fundamental aspects of malignancy. Hence we suggest that the less anaplastic and less divergent diploid cells within the primary carcinomas might be an important resource to gain insights into the critical alterations that are responsible for initiating frankly malignant behavior.
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PMID:The biology of breast cancer at the cellular level. 639 45


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