Dr. Thomas L Rothstein M.D.
Hematologist-Oncologist | Hematology & Oncology
Boston Medical Center 650 Albany St-Ebr C Boston MA, 02118About
Dr. Thomas Rothstein is a hematologist oncologist practicing in Boston, MA. Dr. Rothstein specializes in the diagnosis, treatment and prevention of blood diseases such as anemia, hemophilia, sickle-cell disease, leukemia and lymphoma. Hematologist Oncologists are also trained in the study of cancer and its attack on other organs.
Board Certification
Internal MedicineAmerican Board of Internal MedicineABIM
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Expert Publications
Data provided by the National Library of Medicine- BCR engagement induces Fas resistance in primary B cells in the absence of functional Bruton's tyrosine kinase.
- B cell activation leads to upregulated expression of the murine Sik-similar protein gene.
- Cutting edge commentary: two B-1 or not to be one.
- Interleukin-4-mediated protection of primary B cells from apoptosis through
- Cutting edge: CD40 engagement eliminates the need for Bruton's tyrosine kinase in B cell receptor signaling for NF-kappa B.
- NF-kappa B is required for surface Ig-induced Fas resistance in B cells.
- Cell cycle control mechanisms in B-1 and B-2 lymphoid subsets.
- Phosphatidylinositol 3-kinase-dependent mitogen-activated protein/extracellular signal-regulated kinase kinase 1/2 and NF-kappa B signaling pathways are required for B cell antigen receptor-mediated cyclin D2 induction in mature B cells.
- Suppression of expression and function of negative immune regulator PD-1 by certain pattern recognition and cytokine receptor signals associated with immune system danger.
- Peritoneal and splenic B-1 cells are separable by phenotypic, functional, and transcriptomic characteristics.
- Spontaneously Ig-secreting B-1 cells violate the accepted paradigm for expression of differentiation-associated transcription factors.
- B cell receptor (BCR) cross-talk: CD40 engagement enhances BCR-induced ERK activation.
- Interleukin-4 produces a breakdown of tolerance in vivo with autoantibody formation and tissue damage.
- B cell receptor (BCR) cross-talk: IL-4 creates an alternate pathway for BCR-induced ERK activation that is phosphatidylinositol 3-kinase independent.
- B cell receptor (BCR) cross-talk: CD40 engagement creates an alternate pathway for BCR signaling that activates I kappa B kinase/I kappa B alpha/NF-kappa B without the need for PI3K and phospholipase C gamma.
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