Absence Of Histological Features Research Articles

PATH-32. COMPARISON OF CLINICAL, RADIOGRAPHIC AND TUMOR GENOMIC ALTERATIONS BETWEEN CLASSIC AND MOLECULAR GLIOBLASTOMA (IDH WILDTYPE)

Abstract INTRODUCTION Prior to 2021, (classic) glioblastoma (GBM) required absence of IDH mutation and histologic features of hypercellularity, nuclear atypia, microvascular proliferation (MVP), and necrosis. Absence of histologic features can be a result of undersampling, with molecular, radiologic, and clinical features consistent with GBM. Accordingly, WHO 2021 defined molecular glioblastoma as diffuse glioma IDHwt, H3wt, with one or more of MVP, necrosis, TERT promoter mutation, EGFR gene amplification (EGFRamp), and/or +7/−10. We hypothesized that there is clinical and radiographic heterogeneity among tumors defined as molecular GBM. METHODS We identified 121 patients that met the criteria for molecular GBM. 121 Classic GBM, defined as IDHwt with hypercellularity, MVP or necrosis, were matched to molecular GBM cases by age, sex, and diagnosis date. All cases were reviewed for relevant histologic features and molecular features. Examined clinical variables included: first symptom, time from first symptom to date of pathological diagnosis, date of first MRI, tumor location, radiographic features of enhancement, diffusion or mass effect, time to progression and overall survival. Clinical, radiologic, and molecular features were compared between classic and molecular GBM. RESULTS Currently,160 cases have been reviewed. Preliminary results show that there is a longer time from first symptom to diagnosis for molecular GBM. Molecular GBM is significantly more likely to be discovered coincidentally, and without enhancement or radiographic necrosis. Classic GBM is significantly more likely to present with focal neurologic deficit as first symptom, regional mass effect on index imaging and have monosomy 10. CONCLUSION While pathologic undersampling accounts for a significant proportion of molecular GBM, our data suggest that there are significant clinical, radiographic, and outcome differences between classical and molecular GBM. Final analysis of the entire cohort will help better define this clinical spectrum.

Update on the Diagnosis and Treatment of Barrett Esophagus and Related Neoplastic Precursor Lesions

At present, Barrett esophagus is the most common cause of esophageal adenocarcinoma. In the past 20 years, the incidence of esophageal adenocarcinoma in white males has exceeded that of tumors of the colorectum, lung, prostate, and skin. To (1) provide an evidence-based review of the diagnosis, classification, and histologic differentiation of Barrett esophagus from gastric carditis, (2) provide a summary of the key pathologic features of precursor lesions, such as dysplasia, and (3) evaluate adjunctive markers of dysplasia and predictive markers for the development of cancer. The natural history and risk of cancer in patients with Barrett esophagus is also reviewed. For this review, selected published peer reviewed articles were chosen from a search through PubMed between the years 1970 and 2007. The current definition of Barrett esophagus is partially flawed because not all cases are endoscopically recognizable, nongoblet epithelium is biologically intestinalized, and determination of the presence or absence of goblet cells is susceptible to sampling error. Differentiation of ultrashort segment Barrett esophagus from chronic gastric carditis can be accomplished, in a minority of cases, by evaluating for the presence or absence of histologic features that are known to be associated with Barrett esophagus. Dysplasia in Barrett esophagus begins in the crypt bases and then extends more superficially to include the upper portions of the crypts and surface epithelium. Low- and high-grade dysplasia are distinguished by the presence of marked cytologic and/or architectural abnormalities in the latter compared with the former. There are few, if any, reliable adjunctive diagnostic techniques that can help differentiate nondysplastic from dysplastic epithelium. However, alpha-methylacyl coenzyme A racemase staining has been shown to be useful in 2 separate studies. Both low- and high-grade dysplasia are progressive lesions, and in general, the extent of dysplasia, particularly low grade, is a strong risk factor for progression to carcinoma. Of all the biologic and genetic biomarkers studied to date, evaluation of DNA content is the most reliable and specific. The management of patients with dysplasia is variable among institutions and ranges from aggressive surveillance, endoscopic mucosal resection, mucosal ablation, or total esophagectomy.

“Benign,” Metastasizing Adenomyoepithelioma of the Breast: A Report of 2 Cases

Adenomyoepitheliomas of the breast are rare tumors composed of a proliferation of 2 cell populations. For the most part, they are considered to be benign, but they locally recur. Those neoplasms that metastasize are deemed to have come from a histologically malignant primary tumor. Herein, we describe 2 cases of metastases of histologically "benign" adenomyoepitheliomas of the breast to the lung. In both cases, the primary neoplasms and the metastases did not show histologic features of malignancy. These unique cases represent another example of neoplasms that can metastasize in the absence of histologic features that would suggest malignant behavior. Establishing the diagnosis, determining optimal therapy, and predicting outcome are problematic because of the rarity of this entity. Perhaps, classification of adenomyoepitheliomas should be changed to recognize those neoplasms with malignant behavior.

"Benign," metastasizing adenomyoepithelioma of the breast: a report of 2 cases.

Adenomyoepitheliomas of the breast are rare tumors composed of a proliferation of 2 cell populations. For the most part, they are considered to be benign, but they locally recur. Those neoplasms that metastasize are deemed to have come from a histologically malignant primary tumor. Herein, we describe 2 cases of metastases of histologically benign adenomyoepitheliomas of the breast to the lung. In both cases, the primary neoplasms and the metastases did not show histologic features of malignancy. These unique cases represent another example of neoplasms that can metastasize in the absence of histologic features that would suggest malignant behavior. Establishing the diagnosis, determining optimal therapy, and predicting outcome are problematic because of the rarity of this entity. Perhaps, classification of adenomyoepitheliomas should be changed to recognize those neoplasms with malignant behavior.