Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Dec;1506(1):142-163.
doi: 10.1111/nyas.14719. Epub 2021 Nov 30.

Cancer stem cells: advances in biology and clinical translation-a Keystone Symposia report

Jennifer Cable  1 , Duanqing Pei  2   3   4 , Lola M Reid  5 , Xin Wei Wang  6 , Sonam Bhatia  7 , Panagiotis Karras  8 , Jan Joseph Melenhorst  9 , Markus Grompe  10 , Justin D Lathia  11 , Erwei Song  12   13 , Calvin J Kuo  14 , Ning Zhang  15 , Richard M White  16 , Stephanie Ky Ma  17 , Lichun Ma  18 , Y Rebecca Chin  19 , Michael M Shen  20 , Irene Oi Lin Ng  21 , Klaus H Kaestner  22 , Lei Zhou  23 , Shaheen Sikandar  24 , Clemens A Schmitt  25 , Wei Guo  26 , Carmen Chak-Lui Wong  21 , Junfang Ji  27 , Dean G Tang  28 , Anna Dubrovska  29   30   31   32 , Chunzhang Yang  33 , Wolf R Wiedemeyer  34 , Irving L Weissman  35
Affiliations
Review

Cancer stem cells: advances in biology and clinical translation-a Keystone Symposia report

Jennifer Cable et al. Ann N Y Acad Sci. 2021 Dec.

Abstract

The test for the cancer stem cell (CSC) hypothesis is to find a target expressed on all, and only CSCs in a patient tumor, then eliminate all cells with that target that eliminates the cancer. That test has not yet been achieved, but CSC diagnostics and targets found on CSCs and some other cells have resulted in a few clinically relevant therapies. However, it has become apparent that eliminating the subset of tumor cells characterized by self-renewal properties is essential for long-term tumor control. CSCs are able to regenerate and initiate tumor growth, recapitulating the heterogeneity present in the tumor before treatment. As great progress has been made in identifying and elucidating the biology of CSCs as well as their interactions with the tumor microenvironment, the time seems ripe for novel therapeutic strategies that target CSCs to find clinical applicability. On May 19-21, 2021, researchers in cancer stem cells met virtually for the Keystone eSymposium "Cancer Stem Cells: Advances in Biology and Clinical Translation" to discuss recent advances in the understanding of CSCs as well as clinical efforts to target these populations.

Keywords: cancer stem cell; hepatocellular carcinoma; organoids; pluripotent; progenitors; stemness; tumor heterogeneity; tumorigenesis.

PubMed Disclaimer

Figures

Figure_1.
Figure_1.
Comparison of transplantation methods for epithelia.
Figure_2.
Figure_2.
Liver section from RGBow+/– mouse labeled with Cre-recombinase and chronically injured with TAA. The dotted line delineates a GFP+mOrange+ (yellow) polyploid-derived HCC containing monocolored portions (red and green), which are the result of ploidy reversal in the tumor. Scale bar = 1mm
Figure_3.
Figure_3.
Sex differences in MDSC subsets; model depicting findings from Bayik et al. showing m-MDSCs are elevated in the male GBM microenvironment while g-MDSCs are elevated in the female GBM circulation. Results based on mouse GBM models and validation in human GBM samples.
Figure_4.
Figure_4.
L. ScRNA-seq of 17,000 malignant and 40,000 nonmalignant cells in patients with liver cancer that led to development an algorithm to define tumor cell states based on functional clonality.
Figure_5.
Figure_5.
Heterogeneity of luminal epithelial cells in the mouse prostate. (A) Single-cell RNA sequencing of normal mouse prostate reveals multiple luminal epithelial cell populations. t-distributed stochastic neighbor embedding (tSNE) plot of 5,288 cells from an aggregated dataset of two adult mouse prostates. (B) Schematic model of prostate lobes, with the distribution of luminal epithelial populations as indicated.
Figure_6.
Figure_6.
Therapy-induced reprogramming into senescence-associated stemness. Anticancer therapy debulks the initial tumor burden and evokes cellular senescence, characterized by histone H3 lysine 9 trimethylation (H3K9me3)-governed repression of S-phase genes and a senescence-associated secretory phenotype (SASP). Chromatin remodeling accounts for transcriptional activation of stem cell pathways such as Wnt signaling. Occasional loss of the H3K9me3 mark lifts the G1 block, licensing cell-cycle re-entry of de novo cancer stem cells, which drive aggressive tumor relapses. https://doi.org/10.1038/nature25167; https://doi.org/10.1016/j.ccell.2018.01.002
Figure_7.
Figure_7.
The activities of miRNAs in hepatic CSC populations.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Berger MF & Mardis ER. 2018. The emerging clinical relevance of genomics in cancer medicine. Nat. Rev. Clin. Oncol. 15: 353–365. - PMC - PubMed
    1. Miyamoto T, Weissman IL & Akashi K. 2000. AML1/ETO-expressing nonleukemic stem cells in acute myelogenous leukemia with 8;21 chromosomal translocation. Proc. Natl. Acad. Sci. U. S. A. 97: 7521–7526. - PMC - PubMed
    1. Reya T, Morrison SJ, Clarke MF, et al. 2001. Stem cells, cancer, and cancer stem cells. Nature 414: 105–111. - PubMed
    1. Jan M, Snyder TM, Corces-Zimmerman MR, et al. 2012. Clonal evolution of preleukemic hematopoietic stem cells precedes human acute myeloid leukemia. Sci. Transl. Med. 4: 149ra118. - PMC - PubMed
    1. Pang WW, Pluvinage JV, Price EA, et al. 2013. Hematopoietic stem cell and progenitor cell mechanisms in myelodysplastic syndromes. Proc. Natl. Acad. Sci. U. S. A. 110: 3011–3016. - PMC - PubMed

Publication types

MeSH terms

Substances