The DOI matches its Crossref record; 60 of the 60 references it cites were found in a registry or an index; 24 of the 29 sources its claims cite were checked for support.
Chromosomal instability drives metastasis through a cytosolic DNA response
Open accessAbstract
Chromosomal instability is a hallmark of cancer that results from ongoing errors in chromosome segregation during mitosis. Although chromosomal instability is a major driver of tumour evolution, its role in metastasis has not been established. Here we show that chromosomal instability promotes metastasis by sustaining a tumour cell-autonomous response to cytosolic DNA. Errors in chromosome segregation create a preponderance of micronuclei whose rupture spills genomic DNA into the cytosol. This leads to the activation of the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) cytosolic DNA-sensing pathway and downstream noncanonical NF-κB signalling. Genetic suppression of chromosomal instability markedly delays metastasis even in highly aneuploid tumour models, whereas continuous chromosome segregation errors promote cellular invasion and metastasis in a STING-dependent manner. By subverting lethal epithelial responses to cytosolic DNA, chromosomally unstable tumour cells co-opt chronic activation of innate immune pathways to spread to distant organs.
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24 of 29 cited sources checked · 10 supported · 0 flagged · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Chromosomally unstable cells exhibit evidence of chromosome missegregation during anaphase3,4”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Abstract
What the sources say
- Supportedcites [3] Thompson, S. L. & Compton, D. A. Examining the link between chromosomal instability and aneuploidy in human cells. J. Cell Biol. 180, 665–672 (2008) source
The Results and discussion section reports lagging chromatids during anaphase in chromosomally unstable cell lines, identifying them as the most common mitotic defect observed. It also reports more lagging chromatids per anaphase in unstable than in stable cells. Page numbers are not provided in our copy. (LLM, conf=0.94)
- Partly supportedcites [4] Cimini, D. et al. Merotelic kinetochore orientation is a major mechanism of aneuploidy in mitotic mammalian tissue cells. J. Cell Biol. 153, 517–527 (2001) sourceExperimental — accuracy not yet measured
The Results section reports lagging chromosomes and occasional sister-chromatid missegregation during anaphase in PtK1 cells. It does not establish that the cells studied were chromosomally unstable, so the claim’s population qualifier is not supported by this paper. (LLM, conf=0.84)
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“we overexpressed Kif2a, a third member of the kinesin-13 proteins that lacks kinetochore and centromere localization domains13, and observed no effect on CIN despite exhibiting microtubule-depolymerizing activity on interphase microtubules”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
What the sources say
- Partly supportedcites [13] Ems-McClung, S. C. & Walczak, C. E. Kinesin-13s in mitosis: key players in the spatial and temporal organization of spindle microtubules. Semin. Cell Dev. Biol. 21, 276–282 (2010) sourceExperimental — accuracy not yet measured
The citation is attached to the description of Kif2A, not to the citing authors’ own overexpression and CIN results. Section 3.1 identifies Kif2A as a kinesin-13 found mainly at spindle poles, but also reports its association with centromeres; the copy does not establish that it lacks kinetochore and centromere localization domains. The cited review does not report the stated overexpression experiment. (LLM, conf=0.75)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Destabilization of microtubule attachments to chromosomes at the kinetochores, through overexpression of the non-motile microtubule depolymerizing kinesin-13 proteins, Kif2b or MCAK/Kif2c, directly suppresses CIN in otherwise chromosomally unstable cells5–7.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Abstract
What the sources say
- Partly supportedcites [5] Bakhoum, S. F. et al. The mitotic origin of chromosomal instability. Curr. Biol. 24, R148–R149 (2014) sourceExperimental — accuracy not yet measured
In the main text (page unavailable), GFP–Kif2b overexpression reduced karyotypic heterogeneity in two CIN+ cell lines, supporting suppression of CIN. The paper also reports earlier results for kinesin-13 overexpression in two other CIN+ lines, but our copy does not identify MCAK/Kif2c or establish its effect separately. (LLM, conf=0.88)
- Supportedcites [6] Bakhoum, S. F. et al. Numerical chromosomal instability mediates susceptibility to radiation treatment. Nat. Commun. 6, 5990 (2015) source
In Results, “Extra-nuclear DNA damage in irradiated mitotic cells” (page unavailable), the paper reports that Kif2b overexpression reduced chromosome segregation errors in chromosomally unstable U251 cells by destabilizing kinetochore–microtubule attachments. In Results, “w-CIN influences viability of irradiated mitotic cells” (page unavailable), it also identifies MCAK overexpression as suppressing whole-chromosome CIN, albeit in a slightly different manner. (LLM, conf=0.92)
- Supportedcites [7] Bakhoum, S. F., Thompson, S. L., Manning, A. L. & Compton, D. A. Genome stability is ensured by temporal control of kinetochore–microtubule dynamics. Nat. Cell Biol. 11, 27–35 (2009) source
The ‘Suppression of chromosomal instability’ section reports that GFP-Kif2b or GFP-MCAK overexpression reduces chromosome mis-segregation and suppresses CIN in the unstable U2OS and MCF-7 cell lines. It attributes this effect to increased kinetochore–microtubule turnover that releases inappropriate attachments. (LLM, conf=0.95)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“whereas overexpression of a dominant negative MCAK mutant12 (dnMCAK) led to a modest increase in chromosome missegregation in MDA-MB-231 cells.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
What the sources say
- Supportedcites [12] Moore, A. T. et al. MCAK associates with the tips of polymerizing microtubules. J. Cell Biol. 169, 391–397 (2005) source
The citation is attached to the MCAK mutant, rather than to the citing paper’s result in MDA-MB-231 cells. In Results and discussion (Fig. 2; page not given), the source identifies and uses GFP-hypir-MCAK, a motor-domain mutant inactive in microtubule depolymerization. It does not report the chromosome-missegregation result. (LLM, conf=0.86)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“Cells overexpressing Kif2b or MCAK continue to propagate abnormal aneuploid karyotypes albeit in a stable manner7.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Abstract
What the sources say
- Supportedcites [7] Bakhoum, S. F., Thompson, S. L., Manning, A. L. & Compton, D. A. Genome stability is ensured by temporal control of kinetochore–microtubule dynamics. Nat. Cell Biol. 11, 27–35 (2009) source
The ‘Suppression of chromosomal instability’ section reports that U2OS clones overexpressing GFP-Kif2b or GFP-MCAK retained their aneuploid modal chromosome numbers while showing reduced deviations from those numbers. Those reductions persisted for 50 generations, supporting stable propagation of abnormal karyotypes. (LLM, conf=0.93)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Chromosomal instability (CIN) correlates with tumor metastasis1,2”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Abstract
What the sources say
- Partly supportedcites [1] Jamal-Hanjani, M. et al. Tracking the evolution of non-small-cell lung cancer. N. Engl. J. Med. 376, 2109–2121 (2017) sourceExperimental — accuracy not yet measured
The Results passage (page not available in our copy) links a high proportion of subclonal copy-number alterations to a higher risk of recurrence or death in patients with non–small-cell lung cancer. The Discussion describes copy-number heterogeneity in relation to chromosomal instability, but neither passage establishes a correlation with metastasis specifically. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [2] Turajlic, S. & Swanton, C. Metastasis as an evolutionary process. Science 352, 169–175 (2016) source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“We found a striking localization of cGAS to approximately half of all micronuclei as previously observed22,23.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
What the sources say
- Partly supportedcites [22] Harding, S. M. et al. Mitotic progression following DNA damage enables pattern recognition within micronuclei. Nature 548, 466–470 (2017) sourceExperimental — accuracy not yet measured
The section labeled Abstract (page not provided) reports that cGAS localizes to micronuclei, and Extended Data Figure 4 describes measuring cGAS-positive micronuclei. However, the passages do not report that approximately half of all micronuclei are cGAS-positive. The reported majority concerns micronucleated daughter cells in a live-imaging experiment, not all micronuclei. (LLM, conf=0.85)
- Partly supportedcites [23] Mackenzie, K. J. et al. cGAS surveillance of micronuclei links genome instability to innate immunity. Nature 548, 461–465 (2017) sourceExperimental — accuracy not yet measured
The paper reports that cGAS localizes to micronuclei, but its quantified result is 83.3 ± 1.4% GFP-cGAS-positive micronuclei in RNase H2-deficient mouse fibroblasts (Abstract, Fig. 1d), not approximately half. It also describes localization in other settings without establishing a proportion for all micronuclei. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Impeding micronuclear rupture through Lamin B2 overexpression20 significantly diminished the relative fraction of cGAS+ micronuclei (Fig. 6a–b).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
What the sources say
- Supportedcites [20] Hatch, E. M., Fischer, A. H., Deerinck, T. J. & Hetzer, M. W. Catastrophic nuclear envelope collapse in cancer cell micronuclei. Cell 154, 47–60 (2013) source
The Results section (“NE collapse is triggered by lamin disorganization”) reports significantly more intact micronuclei after Lamin B2 overexpression and concludes that increased lamin B can prevent micronuclear disruption. Citation 20 is attached to that intervention; the decrease in cGAS-positive micronuclei is presented as the citing paper’s own Figure 6a–b result. (LLM, conf=0.92)
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The top 23 differentially expressed genes in CIN-high cells (referred to as CIN signature) predicted distant-metastasis-free survival (DMFS) in a meta-analysis16 as well as a validation cohort17 of patients with breast cancer, irrespective of tumor subtype, grade, or lymph node status”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN enriches for mesenchymal traits
What the sources say
- Partly supportedcites [16] Györffy, B. et al. An online survival analysis tool to rapidly assess the effect of 22,277 genes on breast cancer prognosis using microarray data of 1,809 patients. Breast Cancer Res. Treat. 123, 725–731 (2010) sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
- Could not verifycites [17] Hatzis, C. et al. A genomic predictor of response and survival following taxane–anthracycline chemotherapy for invasive breast cancer. J. Am. Med. Assoc. 305, 1873–1881 (2011) sourceExperimental — accuracy not yet measured
The Methods describe predictors using 33 and 27 probe sets for early relapse, not a 23-gene CIN signature. The Results report distant-relapse-free survival in an independent validation cohort, but our copy does not say that the CIN signature was tested there or that it predicted survival irrespective of subtype, grade, or lymph-node status. Searches for the CIN signature and those validation claims found no supporting passage; page numbers were unavailable. (LLM, conf=0.76)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These two mutually exclusive states, which were recently observed in a pan-cancer genomic analysis of metastatic tumors41, likely account for the reversibility in chromosome missegregation rates seen in primary tumors and metastases”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > DISCUSSION
What the sources say
- Supportedcites [41] Robinson, D. R. et al. Integrative clinical genomics of metastatic cancer. Nature 548, 297–303 (2017) source
The citation is attached to the observation of two mutually exclusive states, not to the citing authors’ proposed explanation for reversible chromosome missegregation rates. In “Transcriptional signatures of metastatic disease,” the source identifies two metastatic-tumor subtypes and reports mutual exclusivity between their proliferative and EMT gene sets. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
- It may state two separate claims as one. 32
- Probably not a substantial claim. 13
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Overexpression of the spindle assembly checkpoint protein, Mad2 in MCAK-expressing cells partially rescued chromosome missegregation15, and correspondingly augmented metastasis”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
What the sources say
- Could not verifycites [15] Sotillo, R. et al. Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Cancer Cell 11, 9–23 (2007) sourceExperimental — accuracy not yet measured
The Summary (p. 1) and the chromosomal-instability results (p. 5) describe Mad2 overexpression in mice and fibroblasts, not in MCAK-expressing cells. Searches for MCAK, rescue of missegregation, and metastasis found no passage addressing those claimed outcomes. The reported increase in segregation defects without MCAK does not establish what happens when MCAK is expressed. (LLM, conf=0.75)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Suppressing micronuclear envelope rupture through mCherry-Lamin B2 overexpression20 reduced cytosolic dsDNA staining without influencing chromosome segregation errors.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN generates cytosolic DNA
What the sources say
- Partly supportedcites [20] Hatch, E. M., Fischer, A. H., Deerinck, T. J. & Hetzer, M. W. Catastrophic nuclear envelope collapse in cancer cell micronuclei. Cell 154, 47–60 (2013) sourceExperimental — accuracy not yet measured
The Results section, “NE collapse is triggered by lamin disorganization” (page unavailable), reports that LmnB2 expression increased the proportion of intact micronuclei. It does not report reduced cytosolic dsDNA staining or test whether LmnB2 overexpression affects chromosome segregation errors. A separate Results passage finds no significant effect of micronuclear disruption on micronucleus formation after a second mitosis, but that is not the stated overexpression comparison. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“We found evidence for noncanonical NF-κB activation in CIN-high cells as revealed by lower levels of the precursor protein, p100, a trend toward higher ratios of p52 and phosphorylated p100 relative to total p100, as well as lower levels of the noncanonical NF-κB pathway inhibitor, TRAF231”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
What the sources say
- Supportedcites [31] Sun, S.-C. Controlling the fate of NIK: a central stage in noncanonical NF-κB signaling. Sci. Signal. 3, pe18 (2010) source
The cited paper supplies the mechanistic basis for interpreting the citing authors’ measurements: it describes p100 as the precursor of p52, phosphorylation and processing of p100 during noncanonical NF-κB activation, and TRAF2-dependent restraint of that pathway (passages 1, 2, and 6). The CIN-high measurements are presented as the citing authors’ own findings, not as findings attributed to this source. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These findings are in line with reported roles for the noncanonical NF-κB pathway in EMT, cellular invasion, and metastasis33–35.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
What the sources say
- Partly supportedcites [33] Wang, X. et al. Oestrogen signalling inhibits invasive phenotype by repressing RelB and its target BCL2. Nat. Cell Biol. 9, 470–478 (2007) sourceExperimental — accuracy not yet measured
The Abstract reports that RelB promotes EMT and an invasive phenotype in breast cancer cells. It discusses metastasis through prior findings about NF-κB and Bcl-2, and calls for future studies of RelB in metastatic breast disease; it does not establish a role for the RelB pathway in metastasis. (LLM, conf=0.84)
- Partly supportedcites [34] Wang, J., Yi, S., Zhou, J., Zhang, Y. & Guo, F. The NF-κB subunit RelB regulates the migration and invasion abilities and the radio-sensitivity of prostate cancer cells. Int. J. Oncol. 49, 381–392 (2016) sourceExperimental — accuracy not yet measured
The Discussion (p. 10) reports a role for RelB, a noncanonical NF-κB subunit, in EMT in breast cancer cells and shows that RelB knockdown reduced invasion in prostate cancer cells. It discusses links to metastasis, but does not establish that RelB itself promotes metastasis; the authors say in vivo studies remain for future work (Discussion, p. 11). (LLM, conf=0.86)
- Partly supportedcites [35] Yang, C. et al. Antagonism of inhibitor of apoptosis proteins increases bone metastasis via unexpected osteoclast activation. Cancer Discov. 3, 212–223 (2013) sourceExperimental — accuracy not yet measured
The Results section ('Osteoclast expression of constitutively active NIK promotes tumor growth in bone'; page unavailable) links activation of the alternative NF-κB pathway in osteoclasts to increased tumor burden in bone. The Discussion likewise describes promotion of metastatic growth through osteoclast activity. These passages support a role in bone metastatic growth, but do not establish roles in EMT or cellular invasion. (LLM, conf=0.85)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Kinesin-13 overexpression did not alter cellular proliferation or the number of centrosomes per cell (Fig. 2a–b, Extended Data Figs. 1f–h and 3a).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Importantly, CIN-low cells maintained highly aneuploid karyotypes, yet they faithfully propagated them in a stable manner.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“whereas metastases from CIN-high cells involved multiple organs and rapidly progressed leading to death.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“as evidenced by reduction in metastatic dissemination, lifespan extension, and reduction in in vitro and in vivo invasion in CIN-high cells depleted of STING, RelB, or p100 (NFKB2).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“whereas the addition of cGAMP or overexpression of Mad2 increased nuclear RelB in MCAK-expressing cells (Fig. 6d, Extended Data Figs. 4e and 9c–e).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Karyotype analysis revealed that the injected cell lines and most metastases had three copies of chromosome 1, whereas primary tumors consistently had 2 copies.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN enriches for mesenchymal traits
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Indeed, induced missegregation of the Y chromosome led to the upregulation of OAS2, an ISG, and increased interferon-β production by DLD-1 cells (Extended Data Fig. 9f–g).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Conversely, mice injected with CIN-low cells exhibited lower metastatic burden and a median survival of 207 days.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“STING depletion reduced RelB nuclear localization and led to downregulation of EMT and inflammatory pathways”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The dsDNA signal, which was distinct from mitochondrial staining, disappeared after treatment with double-strand-specific – but not single-strand-specific – nuclease and after overexpression of Dnase2, confirming the specificity of these antibodies”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN generates cytosolic DNA
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Suppression of CIN had no effect on primary tumor implantation efficiency and even enhanced primary tumor growth in the 4T1 model.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Strikingly, Y chromosome-specific fragments were found dispersed within the cytosol 2–3 days after Dox/IAA addition, whereas the control autosome remained confined to the nucleus (Fig. 5h), demonstrating that cytosolic DNA is generated from chromosomes undergoing high rates of missegregation”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN generates cytosolic DNA
Load-bearingStrength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Yet, in both models, suppression of CIN significantly reduced spontaneous metastasis and prolonged survival (Extended Data Fig. 3d–e).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we performed a gene-gene Pearson correlation analysis using scRNA-seq data and identified two large gene modules: module 1 was characterized by proliferative and metabolic pathways, whereas module 2 comprised EMT and inflammation gene sets”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN generates cytosolic DNA
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“We ruled out a direct role for kinesin-13-mediated microtubule depolymerization in activating small GTPases14 by performing RhoA and Rac1 pull-down assays, which revealed low basal levels of activity and no correlation with kinesin-13 overexpression”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN is a driver of metastasis
What the sources say
- Not checked — no full text of the sourcecites [14] Waterman-Storer, C. M., Worthylake, R. A., Liu, B. P., Burridge, K. & Salmon, E. D. Microtubule growth activates Rac1 to promote lamellipodial protrusion in fibroblasts. Nat. Cell Biol. 1, 45–50 (1999) source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Principle component analysis (PCA) and unsupervised clustering accurately separated samples according to their CIN status.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN enriches for mesenchymal traits
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There was a robust correlation between the CIN signature, STING, and the CIN-responsive NC-NF-κB genes in scRNA-seq data, in contrast to a weaker correlation between CIN and type I interferon targets”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Conversely, increased canonical NF-κB or type I interferon regulatory factors were associated with an improved prognosis (Extended Data Fig. 10a).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Metastasis from cytosolic DNA response
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we stained cells using two different anti-dsDNA antibodies after selective plasma membrane permeabilization and found increased cytosolic dsDNA and single-stranded DNA (ssDNA) in CIN-high cells.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN generates cytosolic DNA
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CIN-high cells and those derived from metastases exhibited a higher preponderance of micronuclei compared with CIN-low or primary tumor-derived cells, respectively”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN generates cytosolic DNA
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and displayed evidence of actin cytoskeletal reorganization, diffuse vimentin staining, and increased cytoplasmic and nuclear localization of β-catenin (Extended Data Figs. 6c–d and 7a–d).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN enriches for mesenchymal traits
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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In the paper
“Yet, metastases contained a large number of differentially upregulated EMT and inflammation-related genes that were disproportionately clustered on chromosome 1, signifying chromosome 1-specific selection.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > CIN enriches for mesenchymal traits
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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In the paper
“Changes in β-catenin are seen upon alteration of CIN; enriched at cell-to-cell junctions in MCAK expressing cells but cytoplasmic and nuclear in dnMCAK expressing cells”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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In the paper
“This leads to the activation of the cGAS-STING cytosolic DNA-sensing pathway and downstream noncanonical NF-κB signaling.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Abstract
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CIN generates micronuclei and cytosolic DNA”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
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In the paper
“There was no need to randomize animals.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Animal studies
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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In the paper
“Diploid controls were used to determine false positive rate of the centromeric probes.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
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In the paper
“Investigators were not blinded to group allocation.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Animal studies
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“All cells tested negative for mycoplasma.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Cell culture
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“ongoing chromosome missegregation is required to replenish cytosolic DNA pools and to maintain cells in a pro-metastatic state.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > DISCUSSION
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In the paper
“For each probe, three normal peripheral blood samples (GM07535, GM06875 and GM00558), obtained from Coriell Institute (Camden, New Jersey) were also analyzed to derive cut-off values (false-positive).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Fluorescence in situ hybridization (FISH) analysis
Strength:plain· not yet calibratedn = 3Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CIN promotes formation and maintenance of metastasis”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
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In the paper
“For each sample a minimum of 20 inverted DAPI-stained metaphases were fully karyotyped and analyzed according to the International System of Human Cytogenetic Nomenclature (ISCN) 2013.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Single-cell karyotyping
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In the paper
“Our analysis was robust to imputation and we obtained similar results without imputed data (not shown).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Single-cell RNA sequencing
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“For the 4T1 experiments, Power analysis indicates that 10 mice per group will be sufficient to detect a difference at relative hazard ratios of <0.25 or >4.0 with 80% power and 95% confidence, given a median survival of 58 days in the control group and a total follow up period of 180 days.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Animal studies
Strength:hedged· not yet calibratedn = 10Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, to minimize the effects of experimental artifacts on the analysis, data was pre-processed to filter out cells with low total molecule counts (library size), low complexity and high mitochondrial content, identified by a bimodal fit.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Single-cell RNA sequencing
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The evolutionary benefits of the noncanonical pathway would justify the scarcity of inactivating mutations in cGAS and STING among breast and lung cancers (Extended Data Fig. 10e).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > DISCUSSION
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“For disease-specific survival in MDA-MB-231 experiments, power analysis indicated that 10 mice per group will be sufficient to detect a difference at relative hazard ratios of <0.2 or >5 with 80% power and 95% confidence, given a median disease-specific survival of 3 months in the control group and a total follow up period of 250 days.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Animal studies
Strength:hedged· not yet calibratedn = 10Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Mitochondria were purified at 12,000xg to minimize their contamination in the cytosolic fraction.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Quantification of cytosolic DNA
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CIN promotes in vitro invasion and migration”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
The role of CIN in metastasis has not been established.
“its role in metastasis has not been established.”
The paper relies on this without support.
The mouse xenograft and orthotopic models recapitulate human metastatic progression sufficiently to infer CIN's role in human metastasis.
“We injected MDA-MB-231 cells into the left cardiac ventricles of athymic mice to enable systemic dissemination while tracking metastatic colonization using a bioluminescence reporter.”
The paper relies on this without support.
The human tumor cohorts analyzed are representative of human metastatic disease generally.
“we applied the weighted-genomic integrity index (wGII) as a proxy for CIN8 on 79 primary tumor-brain metastases matched pairs from a recently published cohort9.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“While MN have been proposed to activate as tumor suppressor pathways, MN also play a critical pathogenic role in the evolution of cancer genomes and metastasis by driving genomic instability through chromothripsis (Bakhoum et al., 2018; Umbreit et al., 2020; Ye et al., 2019; Zhang et al., 2015).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Bakhoum et al., 2018
In the citing paper
“Moreover, STING-dependent activation of noncanonical NF-κB signaling, due to ruptured MN, promotes metastasis (Bakhoum et al., 2018).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Bakhoum et al., 2018
In the citing paper
“For example, in breast and lung cancers, suppression of chromosomal instability and associated cytoDNA decreases metastasis (Bakhoum et al., 2018).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Bakhoum et al., 2018
In the citing paper
“Researchers have observed differences in the expression of essential genes in the cGAS‐STING signaling mechanism between normal and malignant tissues, along with MB21D1‐encoding cGAS, transmembrane protein 173 (TMEM‐173)‐encoding STING, TANK‐binding kinase 1 (TBK‐1) and interferon regulatory factor 3 (IRF‐3).”
From Tumor microenvironment signaling and therapeutics in cancer progression (2023) · cites this paper as [253]
In the citing paper
“Comprehensive research and recent evidence proved that these four genes were significantly elevated in almost all cancer models, suggesting that cGAS‐STING signal transduction might be stimulated in all cancer types [252, 253].”
From Tumor microenvironment signaling and therapeutics in cancer progression (2023) · cites this paper as [253]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Noncanonical NF-κB protein ratios differ between the text and figure caption
MinorThe text describes ratios of p52 and phosphorylated p100 to total p100. The Extended Data Figure 8 caption instead names phosphorylated p52-to-p100 and p100-to-total p100 ratios.
“a trend toward higher ratios of p52 and phosphorylated p100 relative to total p100”
“Normalized ratio of phosphorylated p52-to-p100 (left) and p100-to-total p100 (right) protein levels.”
PCR indexing step is described as both 10 and 14 cycles
MinorThe methods give two different cycle counts for the same sample-index PCR amplification.
“A unique sample index for each library was introduced through 10 cycles of PCR amplification”
“(98°C for 45 s; 98°C for 20s, 60°C for 30s, and 72°C for 20 s x 14 cycles; 72°C for 1min; held at 4°C).”
Citations
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Items 501–600 of 1,551
The Role of STING-Mediated Activation of Dendritic Cells in Cancer Immunotherapy
Ribeiro, A. R. S., Neuper, T., & Horejs‐Hoeck, J. (2024) · International Journal of Nanomedicine · doi:10.2147/ijn.s477320 · Cited by 33
“119,120 In fact, chronic activation of the cGAS-STING pathway, even at low levels, can sustain immunoregulatory gene expression such as IDO in DCs, thereby supporting tumor outgrowth and metastasis.”
BackgroundShitara, K., Janjigian, Y. Y., Ajani, J. A., Moehler, M. H., Yao, J. G., Wang, X., Chhibber, A., Pandya, D., Shen, L., Marcelo Garrido, S., et al. (2025) · Nature Medicine · doi:10.1038/s41591-025-03575-0 · Cited by 36
“One of the CIN-driven mechanisms to evade the immune system is the chronic activation of the cGAS–STING pathway, which increases resistance to anti-PD-1/PD-L1 treatment 35–37 .”
Cen, Y., Zhu, T., Zhang, Y., Zhao, L., Zhu, J., Wang, L., Xu, J., Ding, T., Xie, X., Wang, X., et al. (2021) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2021.11.020 · Cited by 31
“Various mechanisms associated with tumor metastasis have been demonstrated, such as the epithelial-to-mesenchymal transition (EMT),(6) the cancer stem cell theory,(7,8) a remodeled tumor microenvironment,(9) and others.(10,11) Recently, the involvement of circular RNAs (circRNAs) in tumor metastasis has attracted cons…”
BackgroundNajaflou, M., Shahgolzari, M., Khosroushahi, A. Y., & Fiering, S. (2022) · Cancers · doi:10.3390/cancers15010082 · Cited by 31
Analysis of the role of GSK3 in the mitotic checkpoint
Rashid, M. S., Mazur, T. M., Ji, W., Liu, S. T., & Taylor, W. R. (2018) · Scientific Reports · doi:10.1038/s41598-018-32435-w · Cited by 30
Identification of NUF2 and FAM83D as potential biomarkers in triple-negative breast cancer
Zhai, X., Yang, Z., Liu, X., et al. (2020) · PeerJ · doi:10.7717/peerj.9975 · Cited by 29
The pleiotropic roles of cGAS–STING signaling in the tumor microenvironment
Li, J., & Bakhoum, S. F. W. (2022) · Journal of Molecular Cell Biology · doi:10.1093/jmcb/mjac019 · Cited by 30
Self-citationAlterations of Cytoskeleton Networks in Cell Fate Determination and Cancer Development
Wang, E. J.-Y., Chen, I., Kuo, B. Y.-T., Yu, C., Lai, M., Lin, J., Lin, L. Y.-T., Chen, C., Hwang, T., & Sheu, J. J. (2022) · Biomolecules · doi:10.3390/biom12121862 · Cited by 33
Cancer cell-autonomous cGAS-STING response confers drug resistance
Lv, Q.-M., Lei, H.-M., Wang, S., Zhang, K., Tang, Y., Shen, Y. H., Lu, L., Chen, H., & Zhu, L. (2023) · Cell chemical biology · doi:10.1016/j.chembiol.2023.05.005 · Cited by 31
Coll, R. P., Bright, S. J., Martinus, D. K. J., Georgiou, D. K., Sawakuchi, G. O., & Manning, H. C. (2023) · Molecular Imaging and Biology · doi:10.1007/s11307-023-01857-y · Cited by 30
Lü, X., Wang, S., Hua, X., Chen, X., Zhan, M., Hu, Q., Cao, L., Wu, Z., Zhang, W., Zuo, X., et al. (2023) · Advanced Science · doi:10.1002/advs.202306092 · Cited by 29
Activation and regulation of cGAS-STING signaling in cancer cells
Shim, A., Chen, Y., & Maciejowski, J. (2025) · Molecular Cell · doi:10.1016/j.molcel.2025.08.030 · Cited by 37
The DNA damage response in immunotherapy and radiation
Samstein, R. M., & Riaz, N. (2018) · Advances in Radiation Oncology · doi:10.1016/j.adro.2018.08.017 · Cited by 30
“In the setting of chromosomal instability, chronic activation of the cGAS/STING pathway and perhaps an adapted response (without interferon production) can facilitate tumor invasion and metastasis and may be an important prognostic factor across cancer types.(86,96) Thus activation of these pathways in some tumors may…”
BackgroundConsequences of Genomic Diversification Induced by Segregation Errors
Soto, M., Raaijmakers, J. A., & Medema, R. H. (2019) · Trends in Genetics · doi:10.1016/j.tig.2019.01.003 · Cited by 28
Pereira, S. M., Ribeiro, R., & Logarinho, E. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20040938 · Cited by 31
“The presence of cytosolic double-stranded DNA (dsDNA) activates the innate immune signaling, which elicits a pro-inflammatory response through the activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) anti-viral pathway and the downstream interferon type I and NF-κB signaling pathways […”
BackgroundWang, H., Zang, C., Ren, M., Shang, M., Wang, Z., Peng, X., Zhang, Q., Wen, X., Xi, Z., & Zhou, C. (2020) · Scientific Reports · doi:10.1038/s41598-020-72393-w · Cited by 29
The In Vivo Selection Method in Breast Cancer Metastasis
Nakayama, J., Han, Y., Kuroiwa, Y., Azuma, K., Yamamoto, Y., & Semba, K. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22041886 · Cited by 30
Nanotechnology‐Based Strategies to Evaluate and Counteract Cancer Metastasis and Neoangiogenesis
Şen, Ö., Emanet, M., & Ciofani, G. (2021) · Advanced Healthcare Materials · doi:10.1002/adhm.202002163 · Cited by 29
Martín, A. L., Epifano, C., Vilaplana‐Martí, B., Hernández, I., Macı́as, R. I. R., Martínez‐Ramírez, Á., Cerezo, A., Cabezas‐Sainz, P., Garranzo‐Asensio, M., Amarilla‐Quintana, S., et al. (2022) · Cell Death and Differentiation · doi:10.1038/s41418-022-01044-6 · Cited by 29
Misaligned Chromosomes are a Major Source of Chromosomal Instability in Breast Cancer
Tucker, J. B., Bonema, S. C., García‐Varela, R., Denu, R. A., Hu, Y., McGregor, S. M., Burkard, M. E., & Weaver, B. A. A. (2022) · Cancer Research Communications · doi:10.1158/2767-9764.crc-22-0302 · Cited by 27
“Metastatic cancers have previously been reported to have higher levels of genomic instability than unmatched primary tumors based on bulk analysis of tumor cells (42, 43).”
Xu, Y., Nowsheen, S., & Deng, M. (2023) · Cancers · doi:10.3390/cancers15051619 · Cited by 31
“Meanwhile, chromosomal instability leads to a preponderance of MN [107,108], which also results in the persistence of unrepaired DSBs during mitosis [91].”
BackgroundCancer cell-specific cGAS/STING Signaling pathway in the era of advancing cancer cell biology
Kumar, V., Bauer, C., & Stewart, J. H. (2023) · European Journal of Cell Biology · doi:10.1016/j.ejcb.2023.151338 · Cited by 33
Andrade, J., Gallagher, A., Maharaj, J., & McClelland, S. E. (2023) · Chromosome Research · doi:10.1007/s10577-023-09737-5 · Cited by 35
“The presence of cytosolic DNA activates the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) pathway which induces the transcriptional upregulation of epithelial-to-mesenchymal transition (EMT)related genes, promoting migratory and invasive cellular properties, via non-canonical activation of NF-κB…”
BackgroundInfluentialTargeting TREX1 Induces Innate Immune Response in Drug-Resistant Small-Cell Lung Cancer
Murayama, T., Mahadevan, N. R., Meador, C. B., Ivanova, E. V., Pan, Y., Knelson, E. H., Tani, T., Nakayama, J., Ma, X., Thai, T. C., et al. (2024) · Cancer Research Communications · doi:10.1158/2767-9764.crc-24-0360 · Cited by 29
“This might be because mesenchymal and EMT markers, which are expressed in H69M cells, are tightly correlated with STING expression (27).”
Oh, K.-S., Nam, A., Bang, J., Jeong, Y., Choo, S. Y., Kim, H. J., Lee, S. I., Kim, J., Yoon, J., Kim, T.-Y., et al. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01893-3 · Cited by 35
“Previous studies have shown that cGAS-STING can promote metastasis and tumor progression in certain contexts, likely through chronic inflammation and recruitment of myeloid-derived suppressor cells [50, 51].”
BackgroundTargeting chromosomally unstable tumors with a selective KIF18A inhibitor
Phillips, A. F., Zhang, R., Jaffe, M., Schulz, R., Carty, M. C., Verma, A., Feinberg, T. Y., Arensman, M. D., Chiu, A., Letso, R. R., et al. (2025) · Nature Communications · doi:10.1038/s41467-024-55300-z · Cited by 28
“CIN can drive metastatic progression through cytosolic DNA activation of a cGAS/ STING/non-canonicalNF-κ Bpathway 9 .”
Luke, J. J., Sweis, R. F., Hecht, J. R., Schneider, R., Stein, M. N., Golan, T., Yap, T. A., Khilnani, A. D., Huang, M. C., Zhao, R., et al. (2025) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-24-2824 · Cited by 31
The oncogenic neurotrophin receptor tropomyosin-related kinase variant, TrkAIII
Farina, A. R., Cappabianca, L. A., Ruggeri, P., Gneo, L., Pellegrini, C., Fargnoli, M. C., & Mackay, A. R. (2018) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-018-0786-3 · Cited by 30
“DNA response [62], suggesting that TrkAIII activity at”
BackgroundThe three-dimensional organization of the genome in cellular senescence and age-associated diseases
Evans, S. A., Horrell, J., & Neretti, N. (2018) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2018.07.022 · Cited by 30
“formation of cytosolic DNA in senescence and in cancer have been linked to increased cell metastasis potential, and that cytoplasmic DNA results in cell intrinsic and extrinsic pro inflammatory responses [43,49,65].”
BackgroundInfluentialRao, C. V., Farooqui, M., Madhavaram, A., Zhang, Y., Asch, A. S., & Yamada, H. Y. (2020) · Aging Cell · doi:10.1111/acel.13221 · Cited by 29
“The cGAS-STING pathway can be activated with genomic instability and generation of fragmented DNA in cytoplasm (Bakhoum et al., 2018), and thus was suspected to be activated in the model.”
BackgroundGenome instability from nuclear catastrophe and DNA damage
Mammel, A., & Hatch, E. M. (2021) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2021.03.021 · Cited by 28
Pharmacological Targeting of STING-Dependent IL-6 Production in Cancer Cells
Al-Asmari, S. S., Rajapakse, A., Ullah, T. R., Pépin, G., Croft, L. V., & Gantier, M. P. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.709618 · Cited by 28
“Accordingly, since cancer cells have deregulated cell cycle checkpoints they frequently harbor cytoplasmic DNA, which is increased further upon genotoxic damage and radiotherapy exposure, and can lead to cGAS-STING activation (Chen et al., 2017; Dou et al., 2017; Harding et al., 2017; Mackenzie et al., 2017; Bakhoum e…”
BackgroundThe Genetic Evolution of Metastasis
Rogiers, A., Lobón, I., Spain, L. A., & Turajlic, S. (2022) · Cancer Research · doi:10.1158/0008-5472.can-21-3863 · Cited by 29
Huang, K., Chandra, D., McGrath, S. M., Dixit, V. S., Zhang, C., Wu, J., TenDyke, K., Yao, H., Hukkanen, R. R., Taylor, N., et al. (2022) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-21-0780 · Cited by 29
Roles of ubiquitination in the crosstalk between tumors and the tumor microenvironment (Review)
Zhang, X., Meng, T., Cui, S., Liu, D., Pang, Q., & Wang, P. (2022) · International Journal of Oncology · doi:10.3892/ijo.2022.5374 · Cited by 30
“Aberrant DNA fragmentation is common in cancer cells due to abnormal chromosome structure and genome instability (68).”
BackgroundThe cGAS-STING pathway: a therapeutic target in chromosomally unstable cancers
Yan, H., Lü, W., & Wang, F. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01328-4 · Cited by 35
Regulation of cGAS-STING signalling in cancer: Approach for combination therapy
Vasiyani, H., Wadhwa, B., & Singh, R. K. (2023) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2023.188896 · Cited by 29
Molecular markers of metastatic disease in KRAS-mutant lung adenocarcinoma
Boiarsky, D., Lydon, C., Chambers, E. S., Sholl, L. M., Nishino, M., Skoulidis, F., Heymach, J. V., Luo, J., Awad, M. M., Janne, P. A., et al. (2023) · Annals of Oncology · doi:10.1016/j.annonc.2023.04.514 · Cited by 32
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Inflammation and tumor immune escape in response to DNA damage
Nihira, N. T., Kudo, R., & Ohta, T. (2025) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2025.02.005 · Cited by 27
Bioengineering strategies to optimize STING agonist therapy
Dosta, P., Cryer, A. M., Prado, M., & Artzi, N. (2025) · Nature Reviews Bioengineering · doi:10.1038/s44222-025-00337-y · Cited by 31
“3a–c).”
Wang, H., Yu, Y., Li, R., Zhang, H., Chen, Z., Sun, C., & Zhuang, J. (2025) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2025.07.022 · Cited by 36
“Activation of cGAS — STING drives a robust immune response by stimulating the production of IFN-I and inflammatory signaling cascades 126,127 .”
Chromosomal instability in untreated primary prostate cancer as an indicator of metastatic potential
Miller, E. T., You, S., Cadaneanu, R. M., Kim, M., Yoon, J., Liu, S. T., Li, X., Kwan, L. C., Hodge, J. C., Quist, M. J., et al. (2020) · BMC Cancer · doi:10.1186/s12885-020-06817-1 · Cited by 25
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“CIN is defined as the ongoing acquisition of structural (mutations, translocations, deletions) and numerical (aneuploidy) chromosomal aberrations as a result of errors in chromosome segregation during mitosis, and it has been shown to drive metastatic dissemination (5, 6) and correlate with poor prognosis (7).”
BackgroundCrosstalk between cGAS-STING pathway and autophagy in cancer immunity
Lu, Q., Chen, Y., Li, J., Zhu, F., & Zheng, Z. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1139595 · Cited by 28
“In metastatic breast cancer, cGAS-STING signaling can activate atypical NF-kB pathways, which can promote metastasis due to epithelial- Frontiers in Immunology 03 mesenchymal transition (EMT) (46).”
BackgroundInfluentialExosome DNA: An untold story of cancer
Bhattacharya, B., Dhar, R., Mukherjee, S., Gorai, S., Devi, A., Anand, K., Alexiou, A. T., & Papadakis, M. (2023) · Clinical and Translational Discovery · doi:10.1002/ctd2.218 · Cited by 27
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“The CGAS/STING pathway is emerging as a key regulator of cancer development and therapeutic response with roles in tumor development, metastasis, immunomodulation, senescence, viral defense, and autophagy (42–48).”
A STAT3–STING–IFN axis controls the metastatic spread of small cell lung cancer
Guanizo, A. C., Luong, Q., Jayasekara, W. S. N., de Geus, E. D., Inampudi, C., Xue, V. S., Chen, J., de Weerd, N. A., Matthews, A. Y., Gantier, M. P., et al. (2024) · Nature Immunology · doi:10.1038/s41590-024-02014-5 · Cited by 28
“Activation of the cGAS–STING pathway has complex outcomes in the context of cancer, with some reports showing antitumor properties 32–34 and others showing that it favors invasion and metastasis 35,36 .”
Genomic instability and cancer: lessons from Drosophila
Gerlach, S. U., & Herranz, H. (2020) · Open Biology · doi:10.1098/rsob.200060 · Cited by 27
“Conversely, providing cGAMP to cancer cells with inhibited CIN results in an increased invasive behaviour and metastasis [105].”
BackgroundSingle-cell imaging of human cancer xenografts using adult immunodeficient zebrafish
Yan, C., Do, D., Yang, Q., Brunson, D. C., Rawls, J. F., & Langenau, D. M. (2020) · Nature Protocols · doi:10.1038/s41596-020-0372-y · Cited by 25
A Bibliometric Analysis of the Innate Immune DNA Sensing cGAS-STING Pathway from 2013 to 2021
Shi, X., Wang, S., Wu, Y., Li, Q., Zhang, T., Min, K., Feng, D., Liu, M., Wei, J., Zhu, L., et al. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.916383 · Cited by 26
“Inhibition of cGAS and STING in tomor cells can prevent tumor metastasis (50, 51).”
BackgroundDhital, B., Santasusagna, S., Kirthika, P., Xu, M. Y., Li, P., Carceles‐Cordon, M., Soni, R. K., Li, Z., Hendrickson, R. C., Schiewer, M. J., et al. (2023) · Cell Reports Medicine · doi:10.1016/j.xcrm.2023.100937 · Cited by 25
Rogava, M., Aprati, T. J., Chi, W.-Y., Melms, J. C., Hug, C. B., Davis, S. H., Earlie, E. M., Chung, C., Deshmukh, S. K., Wu, S. K., et al. (2024) · Nature Cancer · doi:10.1038/s43018-023-00704-x · Cited by 27
“We identified 80 sgRNAs that meet one (65), two (17) or all (2) of these criteria (Supplementary Table 3).”
BackgroundSelf-citationCell-Free eccDNAs: A New Type of Nucleic Acid Component for Liquid Biopsy?
Zhu, J., Chen, S., Zhang, F., et al. (2018) · Molecular Diagnosis & Therapy · doi:10.1007/s40291-018-0348-6 · Cited by 26
“A recent study showed that chromosome instability from errors during chromosome segregation may create micronuclei whose rupture released DNA into the cytosol (cytosolic DNA) and activated the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) cytosolic DNA-sensing pathway to drive their metastasis [5…”
Calcitriol Prevents RAD51 Loss and cGAS‐STING‐IFN Response Triggered by Progerin
Coll-Bonfill, N., de Faria, R. C., Bhoopatiraju, S., & Gonzalo, S. (2019) · PROTEOMICS · doi:10.1002/pmic.201800406 · Cited by 26
DNA sensing in cancer: Pro-tumour and anti-tumour functions of cGAS–STING signalling
Wheeler, O. P. G., & Unterholzner, L. (2023) · Essays in Biochemistry · doi:10.1042/ebc20220241 · Cited by 26
“As an additional immune evasion strategy, tumour cells can also re-wire cGAS-mediated STING signalling towards increased non-canonical NF-κ B activation in cancer cells through the NF-κ B subunits p52 and RelB [118,140].”
BackgroundcGAS-STING at the crossroads in cancer therapy
Wang, R., Hussain, A., Guo, Q., & Ma, M. (2023) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2023.104194 · Cited by 27
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A dual-STING-activating nanosystem expands cancer immunotherapeutic temporal window
Wang, J., Wang, X., Xiong, Q., Gao, S., Wang, S., Zhu, S., Xiang, S., Li, M., Xie, H., & Li, S. (2024) · Cell Reports Medicine · doi:10.1016/j.xcrm.2024.101797 · Cited by 31
“21,23,50,51 This has motivated the need for a deeper understanding of how cells read and respond to STING signals and for developing novel pharmaceutical strategies to unleash the full strength of STING-based therapy.”
Mao, W., Wen, Y., Lei, H., Lu, R., Wang, S., Wang, Y., Chen, R., Gu, Y., Zhu, L., Abhange, K. K., et al. (2019) · Analytical Chemistry · doi:10.1021/acs.analchem.9b03064 · Cited by 25
Kong, E., Kim, H. D., & Kim, J. (2020) · Cell Death and Differentiation · doi:10.1038/s41418-020-0519-y · Cited by 24
Hu, Q., Zhou, Q., Xia, X., Shao, L., Wang, M., Lu, X., Liu, S., & Guan, W. (2021) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-021-01850-9 · Cited by 25
The Role of Human Centromeric RNA in Chromosome Stability
Leclerc, S., & Kitagawa, K. (2021) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2021.642732 · Cited by 25
Bufe, A., del Arco, A. G., Hennecke, M., Jaime-Soguero, A. D., Ostermaier, M., Lin, Y., Ciprianidis, A., Hattemer, J., Engel, U., Beli, P., et al. (2021) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2108145118 · Cited by 25
Hannes, S., Karlowitz, R., & van Wijk, S. J. L. (2021) · Cell Death and Disease · doi:10.1038/s41419-021-04014-x · Cited by 26
“The carcinogenic influence of STING signaling is cancer-type specific and context-dependent [19, 20], and a dual role of STING in antitumor immunity and tumor promotion has been reported [17, 19, 21, 22].”
BackgroundCytosolic Self-DNA—A Potential Source of Chronic Inflammation in Aging
Akbari, M., Shanley, D. P., Bohr, V. A., & Rasmussen, L. J. (2021) · Cells · doi:10.3390/cells10123544 · Cited by 25
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“Normally, exoDNA was DNA fragments originating from either normal physiologic tissues or unnormal pathological tissues as a result of DNA accumulation.(10) The”
BackgroundInterplay of cGAS with micronuclei: Regulation and diseases
Guo, X., Hintzsche, H., Xu, W., Ni, J., Xue, J., & Wang, X. (2022) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2022.108440 · Cited by 25
Planas‐Paz, L., Pliego‐Mendieta, A., Hagedorn, C., Aguilera‐Garcia, D., Haberecker, M., Arnold, F. M., Herzog, M., Bankel, L., Guggenberger, R., Steiner, S., et al. (2023) · EMBO Molecular Medicine · doi:10.15252/emmm.202216863 · Cited by 26
“Most solid tumors have a form of genomic instability termed CIN that is commonly associated with cancer recurrence and multi-drug resistance (Negrini et al, 2010; Bakhoum et al, 2018).”
BackgroundSelf-citationMoore, J. A., Chen, K., Madison, R. W., Newberg, J. Y., Fleischmann, Z., Wang, S., Sharaf, R., Murugesan, K., Fendler, B. J., Hughes, J. D., et al. (2023) · JCO Precision Oncology · doi:10.1200/po.23.00093 · Cited by 31
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Application of PARP inhibitors combined with immune checkpoint inhibitors in ovarian cancer
Xiao, F., Wang, Z., Liu, Q., Zhang, X., Wu, N., Wang, J., & Xing, Y. (2024) · Journal of Translational Medicine · doi:10.1186/s12967-024-05583-z · Cited by 32
“This activation leads to a range of immunogenic effects and associated immune responses [96–98].”
BackgroundKim, S., Gwon, D., Kim, J., Choi, H., & Jang, C. (2019) · Toxicology in Vitro · doi:10.1016/j.tiv.2019.04.009 · Cited by 25
Chromosomal instability and pro-inflammatory response in aging
Barroso‐Vilares, M., & Logarinho, E. (2019) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2019.111118 · Cited by 26
Jiang, Y., Liu, Y., Tan, X., et al. (2019) · Clinical Breast Cancer · doi:10.1016/j.clbc.2019.05.012 · Cited by 25
Détection de l’ADN cytosolique par la voie cGAS-STING
Chanut, R., & Pétrilli, V. (2019) · médecine/sciences · doi:10.1051/medsci/2019095 · Cited by 28
Exploiting aneuploidy-imposed stresses and coping mechanisms to battle cancer
Zhou, L., Jilderda, L. J., & Foijer, F. (2020) · Open Biology · doi:10.1098/rsob.200148 · Cited by 30
“Furthermore, active cGAS-STING signalling promotes metastasis of human triple-negative breast cancer cells in athymic mice [103].”
BackgroundBrain metastasis models: What should we aim to achieve better treatments?
Masmudi‐Martín, M., Zhu, L., Sánchez‐Navarro, M., Priego, N., Casanova-Acebes, M., Ruiz‐Rodado, V., Giralt, E., & Valiente, M. (2020) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2020.12.002 · Cited by 27
cGAS, an innate dsDNA sensor with multifaceted functions
Liu, Y., & Xu, P. (2025) · Cell Insight · doi:10.1016/j.cellin.2025.100249 · Cited by 26
“Intriguingly, cGAS can be enriched within micronuclei due to micronucleus membrane rupture(Bakhoum et al., 2018; Heijink et al., 2019; Joo et al., 2023; MacDonald et al., 2023; Mackenzie et al., 2017; Takaki et al., 2024).”
Maddipati, R. (2025) · Journal of Clinical Investigation · doi:10.1172/jci191943 · Cited by 31
“While early disseminated cells might undergo parallel genomic evolution at distant sites, the chances of eventually converging on similar genomic alterations and transcriptional states would seem low (15, 16).”
How does an RNA selfie work? EV‐associated RNA in innate immunity as self or danger
Xiao, Y., Driedonks, T. A. P., Witwer, K. W., et al. (2020) · Journal of Extracellular Vesicles · doi:10.1080/20013078.2020.1793515 · Cited by 24
“For example, chromosomal instability in cancer cells and errors in chromosomal segregation lead to cytosolic DNA accumulation and subsequent cGAS-STING activation, promoting tumour cell invasion and metastasis [3].”
BackgroundRNF19A-mediated ubiquitination of BARD1 prevents BRCA1/BARD1-dependent homologous recombination
Zhu, Q., Huang, J., Huang, H., Li, H., Yi, P., Kloeber, J. A., Yuan, J., Chen, Y., Deng, M., Luo, K., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-27048-3 · Cited by 24
“Alexa Fluor 488-labeled Donkey anti-Rabbit IgG (H+ L, 715-585-150,1:3000), Alexa Fluor 594-labeled Donkey anti-Rabbit IgG (H+ L, 711-585-152, 1:3000), Alexa Fluor 488-labeled Donkey anti-Mouse IgG (H+ L, 715-545-150, 1:3000), Alexa Fluor 594-labeled Donkey anti-Mouse IgG (H+ L, 715-585-150, 1:3000), Donkey anti-Mouse…”
MethodChetty, V. K., Ghanam, J., Anchan, S., Reinhardt, K., Brenzel, A., Gelléri, M., Cremer, C. G., Grueso-Navarro, E., Schneider, M., Neuhoff, N. V., et al. (2022) · Cancers · doi:10.3390/cancers14092068 · Cited by 27
“release of free DNA in the cytoplasm for the activation of cytosolic DNA sensing pathways and metastasis [29].”
BackgroundInfluentialThe STING pathway: Therapeutic vulnerabilities in ovarian cancer
Shakfa, N. E., Li, D., Nersesian, S., Wilson‐Sanchez, J., & Koti, M. (2022) · British Journal of Cancer · doi:10.1038/s41416-022-01797-4 · Cited by 26
Telomere Maintenance and the cGAS-STING Pathway in Cancer
Ebata, H., Loo, T. M., & Takahashi, A. (2022) · Cells · doi:10.3390/cells11121958 · Cited by 25
“Along with this context, genome instability, a hallmark of cancer cells, generates cytosolic dsDNA that activates the cGAS-STING pathway and induces chronic inflammation [13,14].”
BackgroundExosomal MicroRNAs as Novel Cell-Free Therapeutics in Tissue Engineering and Regenerative Medicine
Zeng, E. Z., Chen, I., Chen, X., & Yuan, X. (2022) · Biomedicines · doi:10.3390/biomedicines10102485 · Cited by 25
Zhang, X., Li, X., Wang, W., Zhang, Y., Gong, Z., Peng, Y., Wu, J., & You, X. (2022) · Cancers · doi:10.3390/cancers14215188 · Cited by 25
“As a result of unstable chromosomes and mitochondrial dysfunction in tumor cells, genomes and mitochondrial DNA can be segregated and released into the cytosol [60].”
BackgroundLi, J., Zhao, J., Gan, X., Wang, Y., Jiang, D., Chen, L., Wang, F., Xu, J., Pei, H., Huang, J., et al. (2023) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2303479120 · Cited by 25
Role of chromosomal cohesion and separation in aneuploidy and tumorigenesis
Pati, D. (2024) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-024-05122-5 · Cited by 23
“These include DNA damage, activation of the cytosolic DNA-sensing pathway involving cyclic GMP–AMP synthase (cGAS) and stimulator of interferon genes (STING), and chromothripsis, a phenomenon where one or more chromosomes shatter and are incorrectly reassembled [163–167].”
BackgroundReplication stress: Driver and therapeutic target in genomically instable cancers
Schoonen, P. M., Llobet, S. G., & van Vugt, M. A. T. M. (2018) · Advances in protein chemistry and structural biology · doi:10.1016/bs.apcsb.2018.10.006 · Cited by 26
Kirsch‐Volders, M., Pacchierotti, F., Parry, E. M., Russo, A., Eichenlaub-Ritter, U., & Adler, I. ‐. (2018) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2018.11.002 · Cited by 25
Persistent DNA damage signaling and DNA polymerase theta promote broken chromosome segregation
Clay, D. E., Bretscher, H. S., Jezuit, E. A., Bush, K. B., & Fox, D. T. (2021) · The Journal of Cell Biology · doi:10.1083/jcb.202106116 · Cited by 26
“, 2020) and an inflammatory response linked to tumor formation and metastasis (Bakhoum et al., 2018; Harding et al., 2017; Mackenzie et al., 2017).”
BackgroundPP6 regulation of Aurora A–TPX2 limits NDC80 phosphorylation and mitotic spindle size
Sobajima, T., Kowalczyk, K. M., Skylakakis, S., Hayward, D., Fulcher, L. J., Neary, C., Batley, C., Kurlekar, S., Roberts, E., Grüneberg, U., et al. (2023) · The Journal of Cell Biology · doi:10.1083/jcb.202205117 · Cited by 23
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Targeting ENPP1 for cancer immunotherapy: Killing two birds with one stone
Huang, R., Ning, Q., Zhao, J., Zhao, X., Zeng, L., Yi, Y., & Tang, S. (2023) · Biochemical Pharmacology · doi:10.1016/j.bcp.2023.116006 · Cited by 25
The multiple faces of cGAS-STING in antitumor immunity: prospects and challenges
Zhou, Z., Huang, S., Fan, F., Xu, Y., Moore, C., Li, S., & Han, C. (2024) · Medical Review · doi:10.1515/mr-2023-0061 · Cited by 25
“Moreover, CIN chronically activates STING-dependent noncanonical NF-κ B signaling to drive secretion of proin fl ammatory cytokines and metastasis formation, thereby contributing to CIN maintenance [49].”
BackgroundSTING in cancer immunoediting: Modeling tumor-immune dynamics throughout cancer development
Zhang, X., Chen, Y., Liu, X., Li, G., Zhang, S., Zhang, Q., Cui, Z., Qin, M., Simon, H., Terzić, J., et al. (2025) · Cancer Letters · doi:10.1016/j.canlet.2024.217410 · Cited by 28
Obesity–cancer axis crosstalk: Molecular insights and therapeutic approaches
Rakib, A., Mamun, M. A. A., Mandal, M., Sinha, P., & Singh, U. P. (2025) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2025.04.029 · Cited by 25
“The chromosomal instability of cancer cells affects the segregation of chromosomes during the mitotic phase of the cell cycle 144 .”
Predicting resistance to chemotherapy using chromosomal instability signatures
Thompson, J. S., Madrid, L., Hernando, B., Sauer, C. M., Vias, M., Escobar-Rey, M., Leung, W., Garcia-Lopez, D., Huckstep, J., Sekowska, M., et al. (2025) · Nature Genetics · doi:10.1038/s41588-025-02233-y · Cited by 29
“When micronuclei rupture and release their contents into the cytoplasm, this can trigger the activation of cGAS– STING signaling, resulting in proinflammatory signaling through type I interferon 18 .”
Attenuation of cGAS/STING activity during mitosis
Uhlorn, B. L., Gamez, E. R., Li, S., & Campos, S. K. (2020) · Life Science Alliance · doi:10.26508/lsa.201900636 · Cited by 22
“In addition to innate defense against microbial infections, cGAS/STING is involved in cellular responses to DNA damage and replicative/mitotic stress (5, 30, 31, 32, 33, 34, 35, 36).”
Background
Metadata
- Authors
- Bakhoum, S. F., Ngo, B., Laughney, A. M., Cavallo, J.-A., Murphy, C. J., Ly, P., Shah, P., Sriram, R. K., Watkins, T. B. K., Taunk, N. K., Duran, M., Pauli, C., Shaw, C., Chadalavada, K., Rajasekhar, V. K., Genovese, G., Venkatesan, S., Birkbak, N. J., McGranahan, N., Lundquist, M., LaPlant, Q., Healey, J. H., Elemento, O., Chung, C. H., Lee, N. Y., Imielenski, M., Nanjangud, G., Pe’er, D., Cleveland, D. W., Powell, S. N., Lammerding, J., Swanton, C., & Cantley, L. C.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Weill Cornell Medicine (US)
- University of California San Diego (US)
- Cornell University (US)
- The Francis Crick Institute (GB)
- University Hospital Zurich (CH)
- Broad Institute (US)
- University College London (GB)
- Moffitt Cancer Center (US)
- Corresponding author
- Cantley, Lewis C.
- ORCID
- Bakhoum, Samuel F.
- Ngo, Bryan
- Laughney, Ashley M.
- Murphy, Charles J.
- Ly, Peter
- Shah, Pragya
- Watkins, Thomas B. K.
- Taunk, Neil K.
- Pauli, Chantal
- Chadalavada, Kalyani
- Rajasekhar, Vinagolu K.
- Genovese, Giulio
- Venkatesan, Subramanian
- Birkbak, Nicolai J.
- McGranahan, Nicholas
- Lundquist, Mark
- LaPlant, Quincey
- Healey, John H.
- Elemento, Olivier
- Chung, Christine H.
- Lee, Nancy Y.
- Nanjangud, Gouri
- Pe’er, Dana
- Cleveland, Don W.
- Powell, Simon N.
- Lammerding, Jan
- Swanton, Charles
- Cantley, Lewis C.
- Venue
- Nature
- Published
- 2018-01-17
- Volume
- 553
- Issue
- 7689
- Pages
- 467-472
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC5785464
- OpenAlex
- W2783667606
- Cited by
- 1,593
- References
- 59
- Citations by year
- 2026: 215 · 2025: 213 · 2024: 223 · 2023: 216 · 2022: 190 · 2021: 203 · 2020: 149 · 2019: 105 · 2018: 76
- FWCI
- 55.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- National Science Foundation (1254846, CA008748, 1257284)
- Breast Cancer Research Foundation (CA008748)
- Elsa U. Pardee Foundation
- Memorial Sloan-Kettering Cancer Center (CA008748, P30 CA008748)
- Johns Hopkins University
- Francis Crick Institute (10169)
- Gray Foundation
- Cancer Research UK (20466, 19310, 17786)
- Rosetrees Trust (M231-CD1)
- National Institutes of Health (NIH-R01, W81XWH)
- Medical Research Council (MR/P014712/1)
- National Heart, Lung, and Blood Institute (R01HL082792)
- National Cancer Institute (R01CA169306, U54CA210184, R01CA187069, K99CA218871, P30CA008748, R35CA197588)
- National Institute of General Medical Sciences (R35GM122476)
- Division of Chemical, Bioengineering, Environmental, and Transport Systems (CBET-1254846)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- chromosomal instability, metastasis, cytosolic DNA sensing, cGAS-STING pathway, micronuclei, chromosome segregation errors, NF-κB signaling, innate immunity, tumor inflammation, aneuploidy, tumor invasion
- MeSH terms
- STING Protein, Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase, Animals, Brain Neoplasms, Breast Neoplasms, Carcinoma, Squamous Cell, Cell Line, Cytosol, DNA, Neoplasm, Female, Head and Neck Neoplasms, Humans, Inflammation, Membrane Proteins, Mesoderm, Neoplasm Metastasis, Nucleotidyltransferases, NF-kappa B, Chromosome Segregation, Xenograft Model Antitumor Assays, Chromosomal Instability, Micronuclei, Chromosome-Defective, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-19, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-19 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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