Extramedullary hematopoiesis (EMH) usually occurs in hematological disease, but more rarely develops in cases of malignant solid tumors. Due to its features on computed tomography (CT) and magnetic resonance imaging (MRI) that are atypical, EMH in tumor patients might easily be misdiagnosed as metastasis leading to the improper TNM staging and inappropriate therapy. Here, we reported the first case of pleural EMH occurring in a patient with esophageal carcinoma whose pleural lesion was first diagnosed as metastasis and confirmed EMH after the needle biopsy. In addition, a retrospective review was conducted by analyzing patients presented with EMH with malignant solid tumors from PubMed and Medline databases. A total of 42 solid tumor patients with EMH were enrolled, and breast cancer was the most common (n=13, 31.0%), followed by renal carcinoma (n=7, 16.7%) and lung cancer (n=6, 14.3%). A wide variety of body sites may be affected by EMH in malignant solid tumor patients, of which the lymph nodes (n=8, 19.0%) and liver (n=7, 16.7%) were the most common, followed by the kidney (n=6, 14.3%). All patients were diagnosed with EMH by excision, biopsy, or autopsy. Treatment strategies for EMH included surgery (n=25, 59.5%), hydroxyurea (n=1, 2.4%), and blood transfusions (n=2, 4.8%); a further 14 patients (33.3%) were subjected to clinical observation without intervention. Of the patients for whom outcome was reported, 10 patients maintained a good performance status (23.8%) and a further six patients died from the malignant tumor. This was the first study to summarize the presentations of EMH in malignant solid tumors, and our findings might provide some useful guidance for clinical practice, especially for treating patients harboring nonresponse lesions during the antitumor treatment.
The incidence of oropharyngeal squamous cell carcinoma (OPSCC) has been rapidly increasing. Disease stage and smoking history are often used in current clinical trials to select patients for deintensification therapy, but these features lack sufficient accuracy for predicting disease relapse. Our purpose was to develop an imaging signature to assess early response and predict outcomes of OPSCC. Methods: We retrospectively analyzed 162 OPSCC patients treated with concurrent chemoradiotherapy, equally divided into separate training and validation cohorts with similar clinical characteristics. A robust consensus clustering approach was used to spatially partition the primary tumor and involved lymph nodes into subregions (i.e., habitats) based on 18 F-FDG PET and contrast CT imaging. We proposed quantitative image features to characterize the temporal volumetric change of the habitats and peritumoral/nodal tissue between baseline and midtreatment. The reproducibility of these features was evaluated. We developed an imaging signature to predict progression-free survival (PFS) by fitting an L1-regularized Cox regression model. Results: We identified 3 phenotypically distinct intratumoral habitats: metabolically active and heterogeneous, enhancing and heterogeneous, and metabolically inactive and homogeneous. The final Cox model consisted of 4 habitat evolution-based features. In both cohorts, this imaging signature significantly outperformed traditional imaging metrics, including midtreatment metabolic tumor volume for predicting PFS, with a C-index of 0.72 versus 0.67 (training) and 0.66 versus 0.56 (validation). The imaging signature stratified patients into high-risk versus low-risk groups with 2-y PFS rates of 59.1% versus 89.4% (hazard ratio, 4.4; 95% confidence interval, 1.4-13.4 [training]) and 61.4% versus 87.8% (hazard ratio, 4.6; 95% confidence interval, 1.7-12.1 [validation]). The imaging signature remained an independent predictor of PFS in multivariable analysis adjusting for stage, human papillomavirus status, and smoking history. Conclusion: The proposed imaging signature allows more accurate prediction of disease progression and, if prospectively validated, may refine OPSCC patient selection for risk-adaptive therapy.
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