Ann Killary and colleagues describe a new gene that is genetically altered in breast tumors, and that may provide a new breast cancer prognostic marker.

We report the first evidence that CVNM may cause serious patient harm. This novel approach is invasive and threatens patient safety. Although it may occasionally provide meaningful information, the risk-benefit ratio does not favor widespread adoption.

Objectives To define characteristics that influence patient perceptions of thyroidectomy scar cosmesis. Study Design Prospective cohort study. Setting Tertiary endocrine surgery practice in an academic medical center. Subjects and Methods Institutional review board-approved trial in which 136 subjects were recruited from a population of patients being seen for either thyroid or sinus surgery and evaluated standardized photographs, superimposed with computer-generated thyroidectomy scars of varying lengths (2, 4, and 6 cm) and widths (1 and 2 mm), and graded their perception of the scars using the observer scar assessment scale (OSAS) domains of the patient and observer scar assessment scale. Results There were 69 subjects in the thyroid group and 67 in the nonthyroid group. Controlling for width, longer scars were perceived as worse than shorter scars; controlling for length, thicker scars were perceived as worse than thinner scars ( P < .01). Beyond 2 cm, thick scars were judged to be worse than thin scars, even when they were shorter. There was no difference in the mean overall OSAS scores between surgery, sex, or age groups. Nonwhites tended to judge scars as being worse than whites did ( P < .01). Conclusion As expected, patients of all demographics prefer shorter scars compared with longer scars and thinner scars over thick scars. Ethnic differences in scar perception were identified and deserve additional study. Surgeons should endeavor to perform thyroid surgery through the smallest incision that allows the operation to be performed safely to minimize the cosmetic impact of the operation.

Glutathione S-transferases (GST) detoxify carcinogens in tobacco smoke, which plays a major role in development of not only squamous cell carcinoma of the head and neck (SCCHN) but also second primary malignancy (SPM) after index SCCHN.We hypothesized that GSTM1 null, GSTT1 null, GSTP1 Ile 105 Val, and GSTP1 Ala 114 Val polymorphisms would individually and, more likely, collectively show an association with risk of SPM after index SCCHN. One thousand three hundred seventy-six incident SCCHN patients were prospectively recruited between May 1996 and December 2006, genotyped, and followed for SPM development.One hundred ten patients (8%) developed SPM: 43 (39%) second SCCHN, 38 (35%) other tobacco-associated sites, and 29 (26%) other non-tobacco-associated sites. Patients with GSTP1 Ile 105 Val polymorphism had a statistically significant association with risk of SPM development (adjusted hazard ratio, 1.7; 95% confidence interval, 1.1-2.5). However, no statistically significant associations were observed with GSTM1, GSTT1, or GSTP1 Ala 114 Val polymorphisms. After combining risk genotypes for all four polymorphisms, rates of SPM development with 0 to 1, 2, 3, and 4 risk genotypes were 6.4%, 8.4%, 10.9%, and 15.1%, respectively, and a stepwise increase in SPM risk was observed with increasing number of risk genotypes (P = 0.004 for trend). Patients with 3 to 4 risk genotypes had a 1.7-fold increased risk for SPM compared with patients with 0 to 2 risk genotypes (hazard ratio, 1.70; 95% confidence interval, 1.2-2.5).This large prospective cohort study supports a modestly increased risk of SPM after index SCCHN with GSTP1 Ile 105 Val polymorphism and an even greater risk of SPM with multiple combined GST risk genotypes.Approximately 80% to 90% of squamous cell carcinoma of the head and neck (SCCHN) in the United States has historically been attributed to tobacco and alcohol (1). Cigarette smokers are estimated to be at a 10-fold increased risk over never smokers of developing SCCHN, and alcohol has been suggested both to be an independent risk factor for SCCHN and to enhance the risk associated with smoking (2). However, most smokers and drinkers never develop SCCHN, suggesting that genetic susceptibility also contributes to SCCHN etiology. Surgery, radiotherapy, and chemotherapy cure many SCCHN, but a significant cause of posttreatment morbidity and mortality is the development of second primary malignancies (SPM), estimated to occur in ∼15% of SCCHN patients (3).Enzymes in carcinogen detoxification, nucleotide excision repair, cell cycle control, and apoptosis pathways have all been suggested to interact with tobacco-associated carcinogens to modulate interindividual susceptibility to SCCHN (4, 5). Glutathione S-transferases (GST) are a family of seven phase II metabolizing enzymes that play a central role in catalyzing the conjugation of electrophilic compounds such as environmental carcinogens to glutathione, converting them to hydrophilic compounds that are less reactive and more easily excreted (6). Th...