Society of Breast Imaging residency and fellowship training curriculum

A recently developed Society of Breast Imaging curriculum for residency training is intended to provide guidance to residents and their mentors, and to practicing radiologists who want to keep up to date in screening, diagnosis, and interventional procedures. The curriculum contains lists of key concepts in 14 subject areas: epidemiology; anatomy; pathology, and physiology; equipment and technique; quality control; interpretation; problem-solving mammography; ultrasound; interventional procedures; reporting and medicolegal aspects; screening; MR imaging; therapeutic considerations; and patient management principles. The curriculum also makes recommendations about residency training, including the number of examinations the resident should interpret, and the time the resident should spend in breast imaging. Recommendations for fellowship training are also discussed.     

The enigma of arsenic carcinogenesis: role of metabolism

Inorganic arsenic is considered a high-priority hazard, particularly because of its potential to be a human carcinogen. In exposed human populations, arsenic is associated with tumors of the lung, skin, bladder, and liver. While it is known to be a human carcinogen, carcinogenesis in laboratory animals by this metalloid has never been convincingly demonstrated. Therefore, no animal models exist for studying molecular mechanisms of arsenic carcinogenesis. The apparent human sensitivity, combined with our incomplete understanding about mechanisms of carcinogenic action, create important public health concerns and challenges in risk assessment, which could be met by understanding the role of metabolism in arsenic toxicity and carcinogenesis. This symposium summary covers three critical major areas involving arsenic metabolism: its biodiversity, the role of arsenic metabolism in molecular mechanisms of carcinogenesis, and the impact of arsenic metabolism on human risk assessment. In mammals, arsenic is metabolized to mono- and dimethylated species by methyltransferase enzymes in reactions that require S-adenosyl- methionine (SAM) as the methyl donating cofactor. A remarkable species diversity in arsenic methyltransferase activity may account for the wide variability in sensitivity of humans and animals to arsenic toxicity. Arsenic interferes with DNA methyltransferases, resulting in inactivation of tumor suppressor genes through DNA hypermethylation. Other studies suggest that arsenic-induced malignant transformation is linked to DNA hypomethylation subsequent to depletion of SAM, which results in aberrant gene activation, including oncogenes. Urinary profiles of arsenic metabolites may be a valuable tool for assessing human susceptibility to arsenic carcinogenesis. While controversial, the idea that unique arsenic metabolic properties may explain the apparent non-linear threshold response for arsenic carcinogenesis in humans. In order to address these outstanding issues, further efforts are required to identify an appropriate animal model to elucidate carcinogenic mechanisms of action, and to define dose-response relationships.      

Rothmund-Thomson syndrome and tolerance of chemoradiotherapy

Rothmund-Thomson syndrome (RTS) is a rare disorder with a predisposition for cutaneous and non-cutaneous malignancy. It is speculated that ultraviolet (UV) sensitivity and deficient DNA repair may account for this predisposition and influence the tolerance of chemoradiotherapeutic management. A case is reported of the management of an RTS patient with squamous cell carcinoma of the tongue who demonstrated increased radiosensitivity and tissue intolerance to chemotherapy.     

The effects of X-ray contrast media on bacterial growth

Six widely used X-ray contrast media (XRC) were tested against nine commonly isolated organisms to determine the practicality of using XRC to outline body spaces prior to obtaining specimens for culture and to assess the feasibility of using XRC in divided doses to reduce cost. Preparations of Escherichia coli, Klebsiella pneumoniae, Enterococcus faecalis, Staphylococcus aureus, Staphylococcus epidermidis, Pseudomonas aeruginosa, Candida albicans, Streptococcus pyogenes and Streptococcus milleri in two approximate concentrations of 10⁴ and 10⁸ colony forming units/mL (cfu/mL) were inoculated into the following XRC: Conray 280, Hexabrix 320, lopamiro 370, Omnipaque 350, Ultravist 300 and Optiray 320 each in two concentrations. Sampling was performed in triplicate at 0, 2, 4 and 20 h with the 20 h counts made after exposure at both 22°C and 4°C. There were 16 significant interactions, predominantly with the Gram-negative organisms. Conray 280 produced the greatest number of effects. Most effects were bacteriostatic. Organisms were most susceptible at low concentration and after prolonged contact with XRC. No effect was seen with dilute XRC. All weekly sterility checks were negative. Non-ionic XRC have no significant effect on the growth of Gram-positive organisms and little effect on Gram-negative organisms if processing is performed promptly. Using standard aseptic technique, no contamination of XRC occurred, suggesting multi-dosing may be a safe and cost-effective method of XRC utilization.     

Novel translational model for breast cancer chemoprevention study: accrual to a presurgical intervention with tamoxifen and N-[4-hydroxyphenyl] retinamide.

Surrogate end point biomarkers for risk assessment and efficacy of potential chemopreventive agents are needed to improve the efficiency and reduce the cost of chemoprevention trials. It is imperative to develop the best clinical breast model for translational surrogate end point biomarker studies, especially with respect to accrual feasibility. We have initiated a prospective study to develop biomarkers for tamoxifen and N-[4-hydroxyphenyl] retinamide by administering either a placebo or both drugs for 2-4 weeks to women with ductal carcinoma in situ or early invasive cancers in the interval between the initial diagnostic core biopsy and definitive surgery. The principle end point is pretreatment versus posttreatment tumor levels of Ki-67; a number of other exploratory markers will also be examined. The planned target sample size is 100 patients. Between February 1997 and February 2000, 4514 women who had either an abnormal mammogram or a diagnosed breast cancer were screened for the study. Of these 4514 screened patients, 52 (1%) were registered on the study. Major factors of nonparticipation in the remaining 4462 women were as follows: (a) no evidence of malignancy (2081 patients; 46%); (b) ineligible per protocol criteria (575 patients; 13%); (c) preoperative chemotherapy/tamoxifen (520 patients; 11%); (d) surgery scheduling conflict (360 patients; 8%); (e) outside needle biopsy (221 patients; 5%); (f) no residual disease after excisional biopsy (345 patients; 8%); and (g) second opinion only (123 patients; 3%). Other nonparticipation factors included fine needle aspiration only, refusal, tumor size > 2 cm, and estrogen replacement therapy (35 patients each; 2% each). The protocol was amended in midstudy to allow outside needle biopsy, tumor > 2 cm, and estrogen replacement therapy. Accrual to biomarker (nontherapeutic) protocols with delay in definitive cancer surgery is challenging but feasible. Although some accrual problems remain, we have nonetheless succeeded in recruiting 50% of our target sample size in a 3-year period.     

Periodontal disease and systemic health: current status

The relationship between poor oral health and systemic diseases has been increasingly recognized over the past two decades. Indeed, the clichés "You cannot have good general health without good oral health", "The mouth is part of the body" and "Floss or die", are gaining an increasing momentum. A large number of epidemiological studies have now linked poor oral health with cardiovascular diseases, poor glycaemic control in diabetics, low birthweight preterm babies and a variety of other conditions. The majority have shown an association, although not always strong. As a result, a number of meta-analyses have been conducted and have confirmed the associations and at the same time cautioned that further studies are required, particularly with regard to the effect of periodontal treatment in reducing risk. A number of biologically plausible mechanisms have been put forward to explain the association and there is accumulating evidence in support of them, although at this stage, insufficient to establish causality. Nevertheless, the relationship between poor oral health and systemic diseases has become a significant issue, such that adult oral health can no longer be ignored in overall health strategies. This review provides an update on current understanding of the contribution of poor oral health to systemic diseases, the possible mechanisms involved and the relevance of this for general dental practitioners.