Non-small-cell lung cancer (NSCLC) is a genetically heterogeneous disease. In approximately 2% of NSCLC cases, the primary oncogenic mutation is a chromosomal rearrangement involving ROS1 (ROS proto-oncogene 1), where one of many diverse gene partners fuses to the 3’ kinase domain of ROS1 and results in the constitutive activation of the ROS1 receptor tyrosine kinase. The ROS1-targeted tyrosine kinase inhibitor (TKI) entrectinib is an FDA-approved treatment for patients with these ROS1 fusions (ROS1+ NSCLC) and has dramatically improved patient outcomes.

Endometrial polyps (EMPs) are localized overgrowths of endometrial tissue composed of endometrial glands, stroma, and blood vessels. The reported prevalence of EMPs increases with age and ranges from 8-35%, depending on the population studied. EMPs are considered benign, with a risk of malignancy of around 3%.

Alzheimer’s disease (AD) is the most common form of dementia in older adults. Cerebral amyloid angiopathy (CAA), which is characterized by the deposition of β-amyloid (Aβ) peptides within cerebral blood vessels, co-occurs with AD to some extent in 85-95% of AD cases and is an independent contributor to AD dementia. Indeed, cerebrovascular dysfunction, possibly resulting from Aβ deposits, has been implicated in early AD pathogenesis, preceding neuronal damage.

In the broadest sense, cancer development is spurred by genetic abnormalities that result in oncogene activation and tumor suppressor gene inactivation. In multiple myeloma (MM), a hematological malignancy that affects plasma cells, the amplification of chromosome 1q and the deletion of chromosome 17p have both been shown to be related to disease progression and poor patient outcomes. Chromosome 1q contains several oncogenes including NEK2 (never in mitosis gene A-related kinase 2), which has been shown to promote tumor cell proliferation, metastasis, and drug resistance in MM and other cancer types.

The aggressive basal-like breast cancer (BLBC) subtype, which strongly correlates with triple-negative (ER- PR- HER2-) breast cancers, comprises 15-20% of all breast cancer cases and has a poor prognosis, largely resulting from a lack of a molecularly targeted treatment regimen. Loss of control of signaling pathways frequently triggers tumorigenesis, and molecules involved in these signaling pathways are frequent molecular treatment targets. However, the mechanisms of tumorigenesis in BLBCs have yet to be fully elucidated.

Non-small cell lung cancer (NSCLC) is the most common form of lung cancer and a leading cause of death worldwide. Fortunately, the survival rate for NSCLC patients has been increasing, largely due to advances in targeted molecular and immunotherapies. Somatic mutations

Allogeneic hematopoietic cell transplantation (alloHCT) is used to treat a variety of hematologic malignancies and represents the best chance for cure for many patients with these disorders. The effectiveness of alloHCT relies primarily on graft-versus-tumor (GVT) reactivity facilitated by donor T cells, which

Selectively inhibiting protein function through proteolysis-targeting chimeras (PROTACs) has emerged as a novel cancer therapeutic strategy. PROTACs are small molecules with two active domains that bind to an E3 ubiquitin ligase and a protein of interest, which results in