PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 9227255

Quality control programme in mammography: second level quality controls.

E Nassivera·L Nardin
View original source ↗Export metadata ↓

Abstract

Mammography is the most reliable method by which to detect lesions in the breast. Since contrast between normal and pathological areas in the breast is extremely low, mammographic image quality should reach high standards without exceeding acceptable exposure levels for the breast. A quality control programme in mammography has been implemented. This programme is subdivided into two levels. The first consists of simple daily checks of image quality and film processing, while the second deals with more complex checks of mammographic unit, screen-film system, darkroom, illuminators, viewing conditions and reference dose determination. The values of all the parameters undergoing measurement are compared with the limiting values given by National and International Protocols. This paper describes the second level controls carried out every 6 months by the medical physicist. The parameters described are only those which have been studied and analysed in detail since the quality control programme in mammography was implemented. Such parameters (kilovoltage, focal spot dimension, half value layer, tube output, automatic exposure control system, screen-film characteristic curve and mean glandular dose) were measured during the period 1991-1995 and the results summarised. The values obtained prove the constant correct functioning of the equipment.

Explore related subjects

BreastBreast NeoplasmsCalibrationFemaleHumansMammographyQuality ControlRadiation DosageX-Ray Intensifying ScreensJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E Nassivera, L Nardin. 1997. Quality control programme in mammography: second level quality controls.. https://doi.org/10.1259/bjr.70.834.9227255

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2000

Smooth estimation of the survival function for interval censored data.

Interval censored data arise naturally in large-scale panel studies where subjects can only be followed periodically and the event of interest can only be observed in some time intervals. To estimate the survival function the non-parametric maximum likelihood estimator (NPMLE) is commonly used, which is a step function having some large jumps. However, in many applications the underlying survival function can be reasonably assumed to be smooth, and then the NPMLE does not efficiently use this information. Two smooth estimators have been f the NPMLE; another is the logspline density model. However, to our knowledge there is no finite sample study yet to assess their performance in the literature. In this paper we first show by simulation that both smooth estimators improve over the NPMLE for smooth survival functions. We then apply these estimators to compare two survival curves. The test statistics based on the maximum difference between two survival functions (Kolmogorov-Smirnov test) and on the integrated weighted difference of two survival functions (IWDB test) are investigated via the bootstrap. From our simulation studies the IWDB test seems particularly promising for some stochastically ordered survival functions that do not satisfy the proportional hazards model. The methods are illustrated by reanalysing the Breast Cosmesis Study data set.

Breast↗
PubMed2000

Apicidin, an inhibitor of histone deacetylase, prevents H-ras-induced invasive phenotype.

Cancer metastasis represents the most important cause of cancer death and agents that may inhibit tumor cell invasion have been extensively pursued. In the present study, we have examined the anti-invasive effect of apicidin [cyclo(N-O-methyl-L-tryptophanyl-L-isoleucinyl-D-pipecolinyl -L-2-amin o-8-oxodecanoyl)], a fungal metabolite that was identified as an antiprotozoal agent known to inhibit parasite histone deacetylase (HDAC). We show that apicidin significantly inhibits H-ras-induced invasive phenotype of MCF10A human breast epithelial cells in parallel with a specific downregulation of matrix metalloproteinase (MMP)-2, but not MMP-9. We also show that apicidin induces a morphological reversal and growth inhibition of H-ras MCF10A cells similar to that induced by other HDAC inhibitors. Taken in conjunction with the fact that uncontrolled ras activation is probably the most common genetic defect in human cancer cells, our data showing the anti-invasive and detransforming activities of apicidin in H-ras-transformed MCF10A cells may suggest a potential use of HDAC inhibitors for treatment of cancer.

Breast↗
PubMed2000

A hypersensitive estrogen receptor-alpha mutation in premalignant breast lesions.

The best current model of breast cancer evolution suggests that most cancers arise from certain premalignant lesions. We have identified a common (34%) somatic mutation in the estrogen receptor (ER)-alpha gene in a series of 59 typical hyperplasias, a type of early premalignant breast lesion. The mutation, which affects the border of the hinge and hormone binding domains of ER-alpha, showed increased sensitivity to estrogen as compared with wild-type ER-alpha in stably transfected breast cancer cells, including markedly increased proliferation at subphysiological levels of estrogen. The mutated ER-alpha exhibits enhanced binding to the TIF-2 coactivator at low levels of hormone, which may partially explain its increased estrogen responsiveness. These data suggest that this mutation may promote or accelerate the development of cancer from premalignant breast lesions.

Breast↗