1. DNA Damage in Stem Cells
Ilio Vitale, Gwenola Manic, Ruggero De Maria, Guido Kroemer, Lorenzo Galluzzi 
Molecular Cell 
Volume 66, Issue 3, Pages (May 2017)
DOI: /j.molcel
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2. Figure 1 Main Molecular Pathways Underlying DNA Repair and the DDR
(A) Genetic defects as different as abasic sites (a), mildly distorting lesions (b), SSBs (c), deaminations (d), T-T dimers (e), distorting lesions (f), insertion/deletion loops (IDLs) (g), base-base mispairs (h), DSBs (i), end-resected DSBs (j), and ssDNA stretches adjacent to dsDNA (k) can be efficiently repaired by specialized mechanisms encompassing base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), non-homologous end joining (NHEJ), and homologous recombination (HR). Alternatively, multiple DNA lesions can be tolerated upon translesion synthesis (TLS). Please refer to the main text for the official and common names of the proteins and multiprotein complexes involved in these pathways.
(B) In response to ssDNA stretches adjacent to dsDNA or DSBs, ATR and ATM, respectively, activate signal transduction pathways that are involved in the maintenance of nuclear, cellular, or organismal homeostasis, including regulated cell death (RCD).
EPE, end-processing enzyme; Gly, glycosydase; MRN, MRE11-RAD50-NBS1; POLδ, polymerase δ; POLζ, polymerase ζ; Y-POL, Y-family polymerase.
Molecular Cell  , DOI: ( /j.molcel )
Copyright © 2017 Elsevier Inc. Terms and Conditions

3. Figure 2 Targeting DNA Repair in Cancer Stem Cells
In physiological conditions, chemo- and radioresistant CSCs self-renew as they generate relatively more chemo- and radiosensitive malignant cells with limited stemness. Multiple components of the DDR can be directly or indirectly targeted as a standalone strategy for the preferential eradication of CSCs or as a means to boost their chemo- and radiosensitivity, via differentiation, regulated cell death (RCD), or cellular senescence.
Molecular Cell  , DOI: ( /j.molcel )
Copyright © 2017 Elsevier Inc. Terms and Conditions