Automating Scoliosis Measurements in Radiographic Studies with Machine Learning: Comparing Artificial Intelligence and Clinical Reports

Journal of Digital Imaging - Scoliosis is a condition of abnormal lateral spinal curvature affecting an estimated 2 to 3% of the US population, or seven million people. The Cobb angle is the...     

Rising Cancer Incidence and Role of the Evolving Diet in Kenya

Kenya has experienced an increase in the incidence of various types of cancers in the last few decades. This article highlights dietary factors as major contributors to this rising trend of cancer incidence in Kenya at the backdrop of an evolving diet. Literature search revealed that diet plays a major role in the etiology of various cancers with highest incidence rates in various categories of people in Kenya. Other than among children (≤15 years) and HIV/AIDs patients, diet-related cancers such as esophageal, colorectal, stomach, prostate and breast appear to predominate among Kenyans in various categories, i.e., young people (15?≤?30 years), adults (31?≤?65 years), and older people (>65 years). In the past few decades, Kenya has been undergoing nutritional transition characterized by departure from potentially cancer-protective traditional diets (mostly rich in dietary fiber, fruits, and vegetables) to “western diet” (rich in charred red/organ meats, fat, cholesterol, sugar, and salt) that poses elevated cancer risks. Other potentially carcinogenic factors that characterize the evolving Kenyan diet include; drinking of illicit and/or excess alcohol, traditional soot-laced sour milk, reuse of frying fats/oils, kerosene-laced meals, aflatoxin and agrochemical contaminated foods. The various plausible mechanisms of carcinogenesis of these dietary factors are discussed.     

The prognostic and predictive role of 21-gene recurrence scores in hormone receptor-positive early-stage breast cancer

Over the past two decades, gene expression profiling of breast cancer has emerged as an important tool in early-stage breast cancer management. The approach provides important information on underlying biological mechanisms, breast cancer classification, future risk potential of developing recurrent metastatic disease, and provides beneficial clues for adjuvant chemotherapy in hormone receptor (HR) positive breast cancer. Of the commercially available genomic tests for breast cancer, the prognostic and predictive value of 21-gene recurrence score tests have been validated using both retrospective data and prospective clinical trials. In this paper, we reviewed the current evidence on 21-gene expression profiles for HR-positive HER2-negative early-stage breast cancer management. We show that current evidence supports endocrine therapy alone as an appropriate adjuvant systemic therapy for approximately 70% of women with HR-positive, HER2-negative, node-negative breast cancer. Evolving evidence also suggests that 21-gene recurrence scores have predictive values for node-positive breast cancer and that chemotherapy can be avoided in more than half of women with nodes 1 to 3 positive HR-positive breast cancer. Furthermore, retrospective data also supports the predictive role of 21-gene recurrence scores for adjuvant radiation therapy. A prospective trial in this area is ongoing.     

Cervicofacial actinomycosis

Cervicofacial actinomycosis is an uncommon, chronic, suppurative, and granulomatous bacterial infection. It is often of dental origin and tends to mimic other dental infections, granulomatous disorders, and cancers. The initial diagnostic workup, predicated upon imaging and tissue biopsies, is frequently nonspecific. A definitive diagnosis is usually rendered only after surgical excision and histologic examination of the cervicofacial mass. We propose a classification of three stages: localized infection without sinus involvement, localized infection with sinus involvement, and disseminated infection, to facilitate recognition, diagnosis, and early aggressive treatment. Untreated infection may be life-threatening. Therapy may require long-term antibiotics; however, many cases may also necessitate complete surgical excision.     

Increased N7‐methyldeoxyguanosine DNA adducts after occupational exposure to pesticides and influence of genetic polymorphisms of paraoxonase‐1 and glutathione S‐transferase M1 and T1

There are concerns about genetic risks associated with long‐term exposure to pesticides as these compounds may damage DNA, resulting in mutations that eventually lead to cancer, neurological, and reproductive adverse health effects. This study assessed DNA damage in intensive agricultural workers exposed to pesticides by determining the levels of N7‐methyldeoxyguanosine (N7‐MedG), an adduct known to be a robust biomarker of recent exposure to chemical methylating agents. A cohort of 39 plastic greenhouse workers was assessed for changes in lymphocyte DNA N7‐MedG levels between low level and high level exposures during the course of a spraying season. The contributions of genetic polymorphisms of the pesticide‐metabolizing enzymes paraoxonase‐1 (PON1) and the glutathione S‐transferases, GSTM1 and GSTT1, on N7‐MedG levels and other potential confounders were also assessed. N7‐MedG increased in the period of high pesticide exposure as compared to the low exposure period (0.23 and 0.18 µmol N7‐MedG/mol dG for the unadjusted and adjusted linear mixed models, P = 0.02 and 0.08, respectively). Significant decreased levels of erythrocyte acetylcholinesterase and plasma cholinesterase were observed in the high versus low exposure period in both the unadjusted (2.85 U/g hemoglobin and 213.13 U/L, respectively) and adjusted linear mixed models (2.99 U/g hemoglobin and 230.77 U/L, respectively), indicating pesticide intake. In intensive agriculture workers, higher pesticide exposure increased DNA alkylation levels, further demonstrating the genotoxicity of pesticides in man. In addition, pesticide‐exposed individuals with inherited susceptible metabolic genotypes (particularly, null genotype for GSTM1 and the PON1 192R allele) appear to have an increased risk of genotoxic DNA damage. Environ. Mol. Mutagen. 56:437–445, 2015. © 2014 Wiley Periodicals, Inc.