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At least 19 recordsLinked to original sources
PubMed1990

201Tl scintigraphy in the staging of lung cancer, breast cancer and lymphoma.

To evaluate 201Tl in the detection of the primary tumour, lymph node involvement and mediastinal spread we have studied a total of 188 patients with histologically proven lung cancer, breast cancer or malignant lymphoma. Ten patients with benign lung disease were also examined. Static images were performed 20 min after intravenous injection of 75 MBq of thallous (201Tl) chloride. The results were compared with those of standard staging procedures including CT scanning and mediastinal exploration. Thallium-201 imaging was highly sensitive in detecting the primary tumour (lung cancer 86%, breast carcinoma 100%, lymphoma 85%), but showed low sensitivity in detecting mediastinal spread or lymph node involvement. Thallium-201 uptake was also observed in active sarcoidosis (one case) and active TB (two cases). We conclude that 201Tl imaging is unlikely to have a clinically useful role in the diagnosis or staging of lung cancer, breast cancer or lymphoma.

Adenocarcinoma↗
PubMed1992

Pre-cancerous breast lesions: implications for breast cancer prevention trials.

The relationship between benign breast disease and breast cancer has become the focus of increased clinical attention as breast cancer prevention becomes a clinical reality. In this setting an understanding of the magnitude of the increase in risk conferred by the various types of benign breast disease assumes increasing importance. When benign breast disease is considered as an aggregate, estimates of the relative risk of breast cancer development range from 0.8 to 4.5. This article describes the risk associated with proliferative and non-proliferative benign breast disease, as well as the rationale for considering lobular carcinoma in situ and ductal carcinoma in situ (in some cases) as risk factors for breast carcinoma rather than actual malignant lesions. Mathematical models can provide a more precise estimate of breast cancer risk, but these efforts may be confounded by the lack of uniformity in the pathologic definition of borderline benign breast lesions. The breast cancer prevention trials offer a unique opportunity to improve our database on the natural history of high risk benign breast lesions, while attempting to reduce the 44,000 deaths occurring annually from breast cancer.

Breast Neoplasms↗
PubMed1985

Non-protein bound oestradiol, sex hormone binding globulin, breast cancer and breast cancer risk.

It has recently been found by various authors that despite a normal serum concentration of oestradiol (E2), the percentage of non-protein-bound or free E2 is abnormally high in breast cancer patients. Since it is the free E2 which is considered to be biologically active, confirmation of this finding would be most relevant to the pathogenesis of breast cancer. Using Hammond's centrifugal ultrafiltration dialysis method we have measured free E2 in heparinized plasma from 68 premenopausal women (a) at high familial risk of breast cancer (n = 18), (b) with benign breast disease (n = 17), (c) cured of T1N0M0 breast cancer at least 6 months previously (n = 17) and (d) normal controls matched for age, parity and Quetelet index (n = 16). Sex hormone binding globulin (SHBG) was measured as [3H]-dihydrotestosterone binding capacity. Free E2 and SHBG were also measured in the serum of (e) postmenopausal patients having breast cancer (n = 38) and (f) matched control cancer patients (n = 67). We confirmed a very good inverse correlation between log free E2 per cent and log SHBG (P less than 0.0001). The regression lines for groups (a)-(d) were not statistically different. The regression lines for groups (e) and (f) were identical and ran nearly parallel to those for groups (a)-(d) though somewhat lower. This small difference may be ascribed to menopausal status. Therefore, we found no difference in free E2 percentage, calculated free E2 concentration or SHBG between premenopausal women at risk, women with benign breast disease, patients cured for early breast cancer or having breast cancer and matched controls. However, postmenopausal breast cancer patients had a significantly higher total serum E2 concentration and, by consequence a higher calculated free E2 concentration compared to the carefully matched control group.

Adult↗
PubMed1992

[A comparative analysis of interval breast cancer with breast cancer detected by mass screening or in outpatient clinics].

To investigate the characteristics and the prognosis of interval breast cancer, 21 interval cases were reviewed and compared with a total of 87 patients with breast cancer detected by mass screening and 266 found in outpatient clinics on the basis of the clinicopathological features. The postoperative cumulative 7-year disease-free rates were 61.1%, 81.4% and 69.0% in the interval cases, mass screening cases and outpatient clinic cases, respectively. The percentage of cases showing frequent mitoses in cancer cells was statistically higher for interval cancer than for the other breast cancers. The average tumor size of the interval cases calculated from the speculated tumor doubling times, was 1.51 cm. It is surmised that interval breast cancer is characterized by a marked proliferation of tumor cells and has a poorer prognosis than the other breast cancers. This might be due to the marked proliferation of interval breast cancer rather than under-counting because there were no malignant findings at the time of the last screening.

Adult↗
PubMed1975

Androgens in breast cancer. III. Breast cancer recurrences years after mastectomy and increased androgenic activity.

To test the hypothesis that increased androgenic activity is involved in breast cancer, the urinary testosterone was assayed in 19 clinically cured breast cancer patients and in 22 patients developing metastases from breast cancer during the same period of observation (5 to 15 years after mastectomy). The levels in the clinically cured patients were near normal whereas those in patients with metastases were significantly above normal.

Age Factors↗
PubMed1992

Randomized trial of adjuvant tamoxifen in node negative postmenopausal breast cancer. Stockholm Breast Cancer Study Group.

The paper presents long-term results of a randomized trial of adjuvant tamoxifen (40 mg daily for 2 or 5 years) versus surgery alone including 1,347 postmenopausal patients with histologically negative axillary nodes and a tumour diameter less than or equal to 30 mm. Data on the estrogen receptor status of the primary tumour were available in 1,136 patients (84%). At a median follow-up of 7 years (range 1.7-13.0 years) there was a significant prolongation of the recurrence-free survival among those allocated to tamoxifen (p less than 0.01), significantly fewer deaths due to breast cancer (p = 0.02) and a trend towards improved overall survival (p = 0.11). The treatment benefit was restricted to patients with ER-positive tumours. There was no significant reduction of breast cancer recurrences in the tamoxifen group among patients whose tumours were classified as ER-negative. The results support and extend previous studies in showing a long-term benefit of tamoxifen in postmenopausal breast cancer patients with node-negative, estrogen receptor positive disease.

Breast Neoplasms↗
PubMed1992

Chemotherapy with or without high-dose medroxyprogesterone acetate in oestrogen-receptor-negative advanced breast cancer. Norwegian Breast Cancer Group.

In a randomised study 142 patients with advanced oestrogen-receptor-negative breast cancer in the tumour tissue received chemotherapy alone or chemotherapy combined with high doses (1000 mg daily) of oral medroxyprogesterone acetate (HD-MPA). Of the 126 fully evaluable for response, the response rates were 46% for chemotherapy alone and 73% for chemotherapy with HD-MPA (P = 0.005). There was no significant difference with regard to duration of response. Of the 138 patients evaluable for survival and toxicity, survival was shorter in the combined treatment group; median survival of 9 versus 13 months (P less than 0.05). Considerable toxicity was seen from HD-MPA, especially weight gain and fluid retention. The present study provides evidence that in concordance with preclinical studies an interaction between chemotherapy and HD-MPA may exist in breast cancer normally resistant to hormone therapy. The side-effects from MPA were substantial, however, and the survival data are of great concern.

Antineoplastic Agents↗
PubMed1992

Genetic predisposition to breast cancer.

Breast cancer is the most common cancer among American women. Because metastatic breast cancer is an incurable disease, efforts to decrease breast cancer mortality have focused on early detection and improved treatment. Identification and analysis of a specific genetic susceptibility could permit detection of susceptible women and greatly increase the understanding of the initial step that eventually leads to cancer. Because susceptibility loci have been recognized as sites that often are altered during tumor progression, the identification and cloning of such loci could be important in developing cancer therapies. In this article, the progress being made in segregation analysis, linkage analysis, and cloning of breast cancer susceptibility loci is reviewed. The evidence for genetic inheritance is most consistent with dominant inheritance for at least three major susceptibility loci. Proliferative breast disease has been hypothesized to be an inherited lesion in breast cancer kindreds with both premenopausal and postmenopausal probands. Currently, there are many genetic markers for mapping the human genome. Technologic advances have progressed from restriction fragment length polymorphisms to highly polymorphic markers. Using this technology, breast cancer susceptibility in some kindreds with an early onset has been shown to be linked to chromosome 17q. Gene isolation eventually will follow with an increased understanding of the percentage of breast cancer cases that are a result of this genetic locus. Li-Fraumeni syndrome, which often is expressed as breast cancer, is due to mutations in the p53 gene. Characterization of the syndrome and its relationship to the altered gene should proceed rapidly. There is also a group of families exhibiting a genetic susceptibility that is not due to either of these loci. Together, these findings indicate that there are at least three separate major loci segregating for breast cancer susceptibility. With the current initiative to map and sequence the entire human genome and the advances that recently have been reported, a detailed molecular understanding of breast cancer predisposition can be envisaged.

Age Factors↗
PubMed1986

[Heterogeneity of breast cancer].

Breast cancer is in many aspects a heterogeneous disease. This becomes also evident in family studies. The families of 116 women with breast cancer with 50 years and less at diagnosis were compared to than of 161 breast cancer patients with 51 years and more with respect to breast cancer in the relatives. Younger breast cancer patients had more second degree relatives with breast cancer. Probands with a positive family history were on the average 10 years younger than probands with a negative family history. A positive family history increases breast cancer risk by 4.3 times for first degree relatives and by 2.3 times for second degree relatives in comparison to the general population. These results point to an etiological heterogeneity of breast cancer.

Adult↗
PubMed1989

Sequential versus alternating regimens in the treatment of advanced breast cancer. Argentine Breast Cancer Cooperative Group.

With the object of proving whether sequential or alternate forms of chemotherapy would be advantageous one over the other in treating advanced breast cancer and with the purpose of evaluating two different anthracyclines at equimolecular doses in the above-mentioned alternating regimens, 250 patients who had received no prior chemo- or hormonotherapy were entered in a prospective randomized trial. Group A was administered 4-epiadriamycin and cyclophosphamide for 8 courses, followed by 6 cycles of CMF, and medroxyprogesterone acetate (MPA) from the beginning of therapy until progression. In group B, adriamycin + cyclophosphamide were alternated with CMF every two courses until 14 cycles were completed. Group C received 4'-epiadriamycin + cyclophosphamide alternated with CMF for 14 courses. In groups B and C, MPA was administered as in group A. Two hundred and twenty-four patients were evaluated. CR + PR were observed in 55.8% of group A, 43.4% of group B, and 46.4% of group C. Median duration of responses was 16 months (m) in group A, 13 m in group B and 20 m in group C, and median survival (CR + PR) was 16.5 m in group A, 16 m in group B and 24 m in group C. There were no statistically significant differences among the three groups in terms of response rate, duration of response and survival; furthermore, toxicity was moderate in all groups. At equimolecular doses there were no differences between adriamycin and epirubicin in the alternating schedules.

Adult↗
PubMed1991

Adjuvant therapy of breast cancer. International Breast Cancer Study Group.

Adjuvant systemic therapy has been shown to reduce relapses in treated women and to prolong their survival. This is true for all studied subpopulations. Multidrug chemotherapy for the duration of 6 months for the premenopausal patients, and tamoxifen or short-term chemotherapy with long-term tamoxifen for the postmenopausal patients represent the treatments of choice to reduce the risk of relapse. Some of the high priority questions relate to i) the definition of a population for which the risk of relapse is low enough to avoid the use of systemic adjuvant therapy, and ii) the definition of an optimal way of using available adjuvant therapies. These might find answers from ongoing research. The modest but real improvement of the prognosis in operable breast cancer was exclusively obtained only by means of clinical trials, and it is mandatory that participation in programs of clinical research becomes medically and socially the treatment of choice.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1992

Electric power, pineal function, and the risk of breast cancer.

Breast cancer is the leading cause of cancer death in women in the industrialized world, and the rates of breast cancer incidence are rising. Although risk is high in industrialized societies, it is low in nonindustrialized areas. The search for the causes of breast cancer has not yet yielded a convincing explanation for the geographic and temporal patterns in the occurrence of breast cancer. Generation of electric power is a hallmark of industrialization, and two products of electric power, light-at-night (LAN) and electromagnetic fields (EMF), may affect breast cancer risk. Exposure to either LAN or EMF can decrease production of melatonin by the pineal gland. Melatonin, in turn, has been shown to suppress mammary tumorigenesis in experimental animals. Moreover, recent epidemiological findings indicate an increased risk of breast cancer in workers occupationally exposed to EMF. On the basis of these considerations, it is proposed that the use of electrical power accounts, in part, for the higher risks of breast cancer in industrialized societies.

Animals↗
PubMed1992

Aspects of breast cancers.

Breast cancer is the commonest killing malignant disease of women in the European Community. The average annual age standardised mortality rate among the 12 EEC countries ranges from 28.5 to 13.7 per 100,000 females. In Ireland, breast cancer is treated primarily by general surgeons. At our Breast Institute at St. Vincent's Hospital where we see 100 patients with breast diseases weekly it is policy to recommend quadrantectomy, total axillary dissection and radiotherapy (QU.A.R.T.) for patients with T1 and T2 tumours if they are peripherally placed within the breast. Complete axillary dissection in early breast cancer provides accurate staging and virtually eliminates axillary recurrence and the dissection is standardised and audited in our unit. Audit of axillary dissection improves the lymph node yield and enhances the completeness of the procedure. Sophisticated mammography improves the detection of small tumours but even excellent mammography may fail to identify malignant disease. Screening programmes for early breast cancer detection should be based on clinical examination in addition to mammography and some 15% of our patients with palpable breast cancer had falsely negative mammograms. Before operation, extensive scintigraphy and sonography is carried out before primary treatment is undertaken. After treatment, clinical and biochemical surveillance is carried out. We have found the lysosomal protease, Cathepsin D to be a useful marker of progressive disease and prognosis in patients with breast cancer. Routine postoperative CEA and CA15.3 are also valuable markers and a high or rising CA15.3 often precedes clinical or investigative evidence of recurrence. In addition, assay of c-erB-2 protein by ELISA is also a simple, rapid quantitative prognostic guide in patients with breast cancer.

Biomarkers, Tumor↗