Intratumor heterogeneity has attracted more and more attention in recent years. Heterogeneity is the driving force of tumor clone evolution. Chromosomal instability, somatic mutation, epigenetic modification and extrachromosomal DNA (ecDNA) contribute to tumor heterogeneity. The degree of such heterogeneity is extremely high.

Background: Endoscopic ultrasound-guided tissue acquisition (EUS-TA) is a well-established diagnostic tool to obtain tissue from solid pancreatic masses, gastrointestinal subepithelial lesions, lymph nodes, liver as well as other neighboring organs. EUS-TA has proven to have a major clinical impact in diagnosis and staging, decreasing the need for invasive diagnostic procedures, such as thoracoscopy, mediastinoscopy, laparoscopy and open surgery.

A key feature of chronic inflammatory disease is heterogeneity. For clinicians, this poses problems not only in disease diagnosis and assessment, but also in providing personalized disease management for the patients. There are at least two explanations for disease heterogeneity: First, different patient subgroups have different etiologies and subsequent pathways involvement, leading to a similar clinical outcome. Secondly, patients have similar etiologies but with different pathway modulations in patient subgroups, resulting in different degree of clinical outcome.

In breast cancer, the status of the axillary lymph node decides the prognosis of the disease. Axillary lymph node dissection (ALND) was the traditional method to address the lymph node. Final histopathological examination is the confirmatory method to detect metastasis in axillary lymph node. As the tumor stage advances, the rate of metastasis in axillary lymph nodes increases, simultaneously. 

In resource limited settings (RLS), the resources and capacity to perform standard genotype resistance testing for the management of antiretroviral therapy (ART) drug resistance in People Living With HIV/AIDS (PLHIV) are limited. Therefore, in most instances, ART drug switches are based on unreliable clinical and laboratory data. Thus, such switching may occur unnecessarily or individuals may be switched to sub-optimal treatment, leading to the accumulation of drug resistance mutations (DRMs).