March 1, 2018

Models for non-small cell lung carcinoma - part 2

Because lung cancer is so prevalent, there are numerous opportunities for new human lines to be acquired and characterized. Scientists have become highly skilled in distinguishing the mutations that drive increased proliferation from those that suppress tumor growth. This information is key to developing novel therapies to treat lung cancer.

November 1, 2019

Modeling liver cancer with syngeneic hepa 1-6: an update

Depending on the stage of disease, HCC can be treated with surgery, chemotherapy, targeted therapies, and radiation.[4] Current clinical trials are tackling unresectable or advanced stage HCC with mono or combination immunotherapy, monoclonal antibodies or oncolytic virus therapy.[1-4] These approaches have demonstrated

February 1, 2020

Modeling immuno-oncology in a humanized mouse

NOD-scid IL2R?null (NSG) mice engrafted with human peripheral blood mononuclear cells (hPBMCs) have been utilized in xenograft models with success to evaluate efficacy and pharmacodynamics of immune checkpoint inhibitors targeting epitopes on human T-Lymphocytes1.

May 1, 2016

A549 – A model for non-small cell lung cancer

Lung cancer is the leading cause of cancer-related deaths in the world with non-small cell lung cancer (NSCLC) making up about 85% of all lung cancer cases. With the identification of particular tyrosine kinase mutations, such as EGFR and ALK, targeted therapies shifted the paradigm of drug discovery for NSCLC.

December 1, 2016

MV(4;11): A model of human AML (acute myeloid leukemia)

In an effort to more effectively evaluate treatments preclinically, Labcorp offers a human AML model, MV(4;11) (FUW-Luc-mCherry-puro), that has been modified to include both luciferase and mCherry reporter constructs.  Through expression of luciferase, bioluminescent imaging (BLI) can be used to quantitatively measure and track in vivo

May 1, 2017

MM.1S: A model for multiple myeloma

Multiple myeloma is a clonal B cell malignancy characterized by the accumulation of terminally differentiated, antibody-producing plasma cells in the bone marrow. Genetic mutations within the myeloma cells and their interaction with various cytokines and growth factors contribute to the invasiveness of the disease and enhanced drug resistance.