Cancer Heterogeneity and Plasticity — A new journal dedicated to understanding cancer cell states and interactions with the tumor microenvironment
Year: 2024
Type: article
Abstract: Cancer claims a high mortality worldwide.The American Cancer Society estimates more than 2 million new cancer cases in the U.S. in 2024 [1].Despite significant advances in oncology drug development and clinical approval in the past 25 years, especially in targeted therapeutics such as inhibitors of receptor tyrosine kinases (RTKs) and mutated oncogenes (e.g., K-Ras) and immuno-oncology (IO) drugs [2], >600,000 cancer-related deaths are projected for 2024 in the U.S. alone [1].In addition, there are currently >18 million cancer survivors in the States, who would always have the worriment of cancer recurrence in the back of their mind.Why is cancer such a lethal and recalcitrant disease?As cancer is an extraordinarily complex ecosystem and represents an abnormally developed organ [3] and most cancer drugs target specific deregulated signaling drivers or pathways that operate in cancer cells, our failure in controlling and curing cancer is intimately related to cancer cell heterogeneity and plasticity, the scientific premise that has motivated us to launch the journal Cancer Heterogeneity and Plasticity (CHP).Cancer cell heterogeneity, observed for many decades in both experimental and patient tumors, is manifested as variegated subpopulations of cancer cells that possess distinct phenotypic and functional properties, heterogeneously express the therapeutic target, and exhibit differential responses to anticancer drugs.For example, most cancers harbor the bulk 'differentiated' cancer cells (that express high levels of differentiation markers of the normal cells in the organ) as well as less mature cancer cells with many stem/progenitor cell properties called cancer stem cells (CSCs).There is substantial evidence, in multiple cancers, that advanced, metastatic and therapy-resistant tumors have higher cancer stemness that is associated with increased aggressiveness and CSC abundance and/or state [4].Most CSCs may lack or under-express the differentiation molecules targeted by the mainstay cancer drugs used in the clinic, e.g., androgen receptor (targeted by ADT/enzalutamide) in prostate cancer, estrogen receptor (targeted by tamoxifen and fulvestrant) in breast cancer, RTKs (targeted by tyrosine kinase inhibitors (TKIs)) in multiple epithelial cancers, and PD-L1 (targeted by immune checkpoint inhibitors or ICIs such as Atezolizumab, Avelumab and Durvalumab) in solid tumors.Cancer cell heterogeneity is also reflected, prominently,
Author: Dean G. Tang
Institution: Roswell Park Comprehensive Cancer Center
Language: English
Topic: Cancer Cells and Metastasis
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Funder: National Cancer Institute
Awards: G1337400203, G3655562096
OpenAlex ID: W4400773200