Increased AID results in mutations at the CRLF2 locus implicated in Latin American ALL health disparities.

Activation-induced cytidine deaminase (AID) is a B cell-specific mutator required for antibody diversification. However, it is also implicated in the etiology of several B cell malignancies. Evaluating the AID-induced mutation load in patients at-risk for certain blood cancers is critical in assessing disease severity and treatment options.

The NUTRIENT Trial (NUTRitional Intervention among myEloproliferative Neoplasms): Results from a Randomized Phase I Pilot Study for Feasibility and Adherence.

Purpose: Chronic inflammation is integral to myeloproliferative neoplasm (MPN) pathogenesis. JAK inhibitors reduce cytokine levels, but not without significant side effects. Nutrition is a low-risk approach to reduce inflammation and ameliorate symptoms in MPN.

Increased AID Results in Mutations at the CRLF2 Locus Implicated in Latin American ALL Health Disparities.

Activation-induced cytidine deaminase (AID) is a B cell-specific base editor required during class switch recombination and somatic hypermutation for B cell maturation and antibody diversification. However, it has also been implicated as a factor in the etiology of several B cell malignancies. Evaluating the AID-induced mutation load in patients at-risk for certain types of blood cancers is critical in assessing disease severity and treatment options.

The Continued Rise of Syphilis: A Case Report to Aid in Identification of the Great Imitator.

Unlabelled: Syphilis is a progressive sexually transmitted infection that has a wide variety of presentations depending on the disease stage. These variable presentations can make it difficult to differentiate syphilis from other diseases. While tertiary syphilis is less common in the United States compared to primary or secondary syphilis, recognition of the varied manifestations of advanced syphilis can help providers accurately diagnose this disease to help prevent continued spread.

Myeloproliferative neoplasms - blurring the lines between cancer and chronic inflammatory disorder.

Myeloproliferative Neoplasm (MPN) is a group of chronic blood cancers that arise from a hematopoietic stem cell (HSC) clone with somatic mutations causing constitutive activation of myeloid cytokine receptor signaling. In addition to elevated blood cell counts, MPN typically presents with increased inflammatory signaling and inflammation symptoms. Therefore, while being a clonally derived neoplasm, MPN has much in common with chronic non-cancerous inflammatory conditions, such as rheumatoid arthritis, lupus, and many more.

The NUTRIENT Trial (NUTRitional Intervention among myEloproliferative Neoplasms): Feasibility Phase.

Purpose: Chronic inflammation is integral to Myeloproliferative Neoplasm (MPN) pathogenesis. JAK inhibitors reduce cytokine levels, but not without significant side effects. Nutrition is a low-risk approach to reduce inflammation and ameliorate symptoms in MPN.

Inflammation in Myeloid Malignancies: From Bench to Bedside.

Myeloid malignancies, stemming from a somatically mutated hematopoietic clone, can cause a wide variety of clinical consequences, including pancytopenia in myelodysplastic syndrome, overproduction of three myeloid lineages in myeloproliferative neoplasm, and the rapid growth of immature hematopoietic cells in acute myeloid leukemia (AML). It is becoming clear that inflammation is a hallmark feature of clonal myeloid conditions, ranging from clonal hematopoiesis of indeterminate potential to AML. Fundamental findings from laboratory research on inflammation in myeloid malignancies has potential implications for diagnosis, prognostication, and treatment in these diseases.