Justin Balko on JAK2 Amplification in TNBC

Justin M. Balko, PharmD, PhD
Published: Thursday, Feb 28, 2013

Justin M. Balko, PharmD, PhD, a research faculty member who works in the lab of Carlos Arteaga, MD, at the Vanderbilt-Ingram Cancer Center in Nashville, Tennessee, describes a study that discovered JAK2 alterations in patients with treatment-refractory triple-negative breast cancer (TNBC).

In the study, 81 tumor samples were interrogated for the presence of multiple tumor suppressor and oncogenes in patients with treatment-refractory residual TNBC following neoadjuvant chemotherapy. In addition to other findings, the trial discovered that approximately 10% of patients had a copy number alteration in JAK2.

A confirmatory analysis of these findings is still needed but other indicators support their authenticity. For instance, Balko notes, the analysis found increased levels of the cytokine interleukin 6, which is known to activate the JAK-STAT pathway. Additionally, the rapidity of recurrence following treatment may be consistent with the connection between the JAK-STAT pathway and stem cell activity.

These findings are particularly encouraging, since JAK2 inhibitors are currently in clinical trials and FDA approved. Larger randomized trials investigating a JAK2 inhibitor in TNBC still need to be undertaken, Balko believes.

Justin M. Balko, PharmD, PhD, a research faculty member who works in the lab of Carlos Arteaga, MD, at the Vanderbilt-Ingram Cancer Center in Nashville, Tennessee, describes a study that discovered JAK2 alterations in patients with treatment-refractory triple-negative breast cancer (TNBC).

In the study, 81 tumor samples were interrogated for the presence of multiple tumor suppressor and oncogenes in patients with treatment-refractory residual TNBC following neoadjuvant chemotherapy. In addition to other findings, the trial discovered that approximately 10% of patients had a copy number alteration in JAK2.

A confirmatory analysis of these findings is still needed but other indicators support their authenticity. For instance, Balko notes, the analysis found increased levels of the cytokine interleukin 6, which is known to activate the JAK-STAT pathway. Additionally, the rapidity of recurrence following treatment may be consistent with the connection between the JAK-STAT pathway and stem cell activity.

These findings are particularly encouraging, since JAK2 inhibitors are currently in clinical trials and FDA approved. Larger randomized trials investigating a JAK2 inhibitor in TNBC still need to be undertaken, Balko believes.


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