Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases.The term was introduced in the inaugural Editorial,Introducing Oncotarget.

As of January 1, 2022,Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

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Interview with Dr. Felsher from Stanford University

Oncotarget published "BIM mediates oncogene inactivation-induced apoptosis in multiple transgenic mouse models of acute lymphoblastic leukemia " which reported BIM mediates oncogene inactivation-induced apoptosis in multiple transgenic mouse models of acute lymphoblastic leukemia

Dr. Dean W. Felsher fromStanford University, and Founding Editorial Board member ofOncotarget said, "Although cancers evolve through a multistage process with accumulation of both genetic and epigenetic changes, many cancers are dependent on specific driver oncogenes for maintenance of the malignancy "

The inactivation of driver oncogenes in mouse cancer models and human targeted therapy often leads to tumor regression associated with the induction of apoptosis.

The mechanism by which oncogene inactivation induces apoptosis in cancer has not been defined.

More recently, BIM, together with other BCL-2 family proteins, have been implicated in the mechanism of apoptosis and therapeutic sensitivity of BCR-ABL positive cells treated with imatinib,lung adenocarcinoma cells treated with EGFR inhibitors, andbreast cancer cells treated with HER2 inhibitors.

By crossing of E μ-tTA mice with mice carrying different oncogenes controlled by a tetracycline-responsive element, theOncotarget authors are able to regulate oncogene expression in lymphocytes.

Here they have used these transgenic mouse models driven by different oncogenes to investigate the mechanism by which oncogene inactivation induces apoptosis.

The Felsher Research Team concluded in theirOncotargetPriority Research Paper that the activity of BIM seems to be particularly critical in regulating the balance between pro-apoptotic and pro-survival signals.

Even modest changes in BIM activity can significantly influence tumorigenesis and therapeutic responses of cancer.

An intronic deletion polymorphism that produces a less active form of BIM in chronic myeloid leukemia and lung adenocarcinoma patients leads to therapeutic resistance to tyrosine kinase inhibitors.

Thus, BIM is a central mediator of apoptosis associated with therapeutic responses of cancer.

In particular, activation of BIM-mediated apoptosis pathway using BH3 mimetics may synergize with targeted therapeutics to induce sustained tumor regression.

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DOI -https://doi.org/10.18632/oncotarget.8731

Full text -https://www.oncotarget.com/article/8731/text/

Correspondence to - Dean W. Felsher -[email protected]

Keywords -apoptosis,BIM,targeted therapies,oncogene inactivation