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
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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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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
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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
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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
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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
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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
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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
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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
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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
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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 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 901–1,000 of 1,551
STINGing Viral Tumors: What We Know from Head and Neck Cancers
Saulters, E. L., Woolley, J. F., Varadarajan, S., Jones, T. M., & Dahal, L. N. (2021) · Cancer Research · doi:10.1158/0008-5472.can-21-0785 · Cited by 9
“Sustained release of cytosolic DNA, induced by tumor cell chromosomal instability, leads to chronic activation of STING and the downstream pathway that promotes tumor development (93).”
BackgroundHER2 Targeting in Esophagogastric Cancer: Redefining the Landscape and Breaking Barriers
Cytryn, S. L., & Janjigian, Y. Y. (2023) · Journal of the National Comprehensive Cancer Network · doi:10.6004/jnccn.2023.7010 · Cited by 10
Sakimura, S., Nagayama, S., Fukunaga, M., Hu, Q., Kitagawa, A., Kobayashi, Y., Hasegawa, T., Noda, M., Kouyama, Y., Shimizu, D., et al. (2021) · PLoS Genetics · doi:10.1371/journal.pgen.1009113 · Cited by 9
“compared CNA between primary and recurrence tumors and reported that primary breast tumor had near-diploid (2n) karyotypes, while metastases were enriched for cells with near-triploid (3n) karyotypes [11].”
ResultDuan, Q., Tang, C., Ma, Z., Chen, C., Shang, X., Yue, J., Jiang, H., Gao, Y., & Xu, B. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.672020 · Cited by 10
“In addition, tumor occurs by acquiring a series of mutations over time (18), and genomic instability and mutation are hallmarks of tumors (19, 20).”
BackgroundLahey, L. J., Wen, X., Mardjuki, R. E., Böhnert, V., Hess, G. T., Ritchie, C., Carozza, J. A., Maduke, M. C., Bassik, M. C., & Li, L. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.02.13.948273 · Cited by 9
“…(Gao et al., 2015), bacteria (Manzanillo et al., 2012; Nandakumar et al., 2019), damage (Harding et al., 2017; Hatch et al., 2013; McArthur et al., 2018), cancerous states (Bakhoum et al., 2018; Mackenzie et al., 2017), and senescence (Dou et al., 2017; Glück et al., 2017; Yang et al., 2017).”
BackgroundMardjuki, R. E., Wang, S., Carozza, J. A., Abhiraman, G. C., Lyu, X., & Li, L. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.01.12.575449 · Cited by 11
“Interestingly, while STING activation in cancer cells can promote metastasis 14,15 , STING activation in bystander cells of the tumor microenvironment delays primary tumor growth and metastasis and is responsible for the curative effect of radiation treatment 8,12,16–21 .”
BackgroundSTING in tumors: a focus on non-innate immune pathways
Yang, J., Yang, M., Wang, Y., Sun, J., Liu, Y., Zhang, L., & Guo, B. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1278461 · Cited by 11
“Approximately 55% of metastatic tumor-derived cells were reported to be cGAS positive (Bakhoum et al., 2018).”
BackgroundSmall spaces, big problems: The abnormal nucleoplasm of micronuclei and its consequences
Zych, M. G., & Hatch, E. M. (2024) · Current Opinion in Structural Biology · doi:10.1016/j.sbi.2024.102839 · Cited by 10
Rajabi, F., Smith, R., Liu-Bordes, W.-Y., Schertzer, M. J., Huet, S., & Londoño‐Vallejo, A. (2024) · Molecular Biology of the Cell · doi:10.1091/mbc.e24-08-0370 · Cited by 8
“…encompass both cell-autonomous mechanisms, such as the inflammatory response triggered by the detection of double-stranded DNA in the cytoplasm (Bakhoum et al. , 2018), as well as cell nonautonomous ones, such as a local senescent or proinflammatory microenvironment (Castro-Vega et al. , 2015;…”
InfluentialMarletta, S., Marcolini, L., Caliò, A., Pedron, S., Antonini, P., Martelli, F. M., Stefanizzi, L., & Martignoni, G. (2025) · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · doi:10.1007/s00428-025-04041-5 · Cited by 8
Zhang, H., Xu, X., Li, S., Huang, H., Zhang, K., Li, W., Wang, X., Yang, J., Yin, X., Qu, C., et al. (2025) · Colloids and Surfaces B Biointerfaces · doi:10.1016/j.colsurfb.2025.114573 · Cited by 9
Meléndez-Flórez, M. P., Ortega‐Recalde, O., Rangel, N., & Rondón‐Lagos, M. (2025) · Cancers · doi:10.3390/cancers17071222 · Cited by 12
“Paradoxically, cGAS/STING has also shown an oncogenic and metastatic potential, supporting the heterogenous role and complexity of this pathway and its modulation [135–137].”
Primary cilia prevent activation of the cGAS-STING pathway during mouse decidualization
Li, B., He, Y., Yao, W.-X., Jin, D.-D., Luo, H., Li, M., Wu, Y., & Yang, Z. (2025) · Communications Biology · doi:10.1038/s42003-025-08030-x · Cited by 8
Dai, W., Ko, J. M. Y., Yu, V. Z., Hou, Z., Chow, L. K.-Y., Chung, M. K. Y., Islam, K. A., Ng, B., Wong, C. W.-Y., Leung, K.-K., et al. (2025) · Cancer Letters · doi:10.1016/j.canlet.2025.217874 · Cited by 8
Chung, D. L., Hou, Z., Wang, Y., Islam, K. A., Liu, S., Liu, J., Chow, L. K.-Y., Wong, Y. Y.-W., Chak, C. P.-T., Zhang, Y., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-61597-1 · Cited by 8
“The genome instability index (GII) 60,61 is the percentage of single nucleotide polymorphisms (SNPs) across the genome present at an aberrant copy number relative to the baseline ploidy of the sample, considering chromosome size variations to ensure that large chromosomes do not have greater…”
Wang, S., Johnson, R. M., Carozza, J. A., Fernández, D., Scicinski, J. J., Verity, N. A., Mardjuki, R. E., Cao, X., Guo, Y., Papkoff, J. S., et al. (2025) · Cell Reports Medicine · doi:10.1016/j.xcrm.2025.102336 · Cited by 12
“21 Furthermore, cancer cells rapidly pump cGAMP out to the extracellular space for degradation by its extracellular hydrolase ENPP1 as another mechanism for immune evasion.”
InfluentialEmerging trends and converging evidence in tumor evolution: A comprehensive review
Jin, C., Li, W., Liu, B., Cao, L.-Q., Stefan, S. M., Yuan, L., Yu, X., Shi, L., & Yu, H. (2026) · Drug Resistance Updates · doi:10.1016/j.drup.2026.101380 · Cited by 12
Striking the right balance with type I interferon signalling in cancer
Chadwick, T. B., So, J., Hertzog, P. J., Haynes, N. M., & Parker, B. S. (2026) · Nature reviews. Cancer · doi:10.1038/s41568-026-00915-1 · Cited by 14
“This triggers continuous activation of IRF3 and NF-κB, promoting expression of pro-inflammatory cytokines and ISGs, and contributes to tumour progression in a context-dependent manner 8 .”
InfluentialSolomon, P. E., Kirkemo, L. L., Wilson, G. M., Leung, K., Almond, M. H., Sayles, L. C., Sweet-Cordero, A., Rosenberg, O. S., Coon, J. J., & Wells, J. A. (2022) · Molecular & Cellular Proteomics · doi:10.1016/j.mcpro.2022.100247 · Cited by 9
“Conversely, STING activation of noncanonical inflammatory pathways has been found to promote epithelial–mesenchymal transition and metastasis in cancers with high chromosomal instability that generate excessive dsDNA in the cytosol (74).”
Zhang, Y., Zhuang, T., Xin, Z., Sun, C., Li, D., Ma, N., Wang, X., & Wang, X. (2022) · Cells · doi:10.3390/cells12010066 · Cited by 8
“Chromosomal instability could cause the chronic leakage of DNA within tumor cells, then trigger a chronic inflammatory response that allows them to migrate to distant organs through a cytosolic DNA response [42].”
BackgroundEscape from Cellular Senescence Is Associated with Chromosomal Instability in Oral Pre-Malignancy
Prime, S. S., Cirillo, N., & Parkinson, E. K. (2023) · Biology · doi:10.3390/biology12010103 · Cited by 9
“Taken together, aneuploidy promotes the cancer phenotype [143–145] and leads to enhanced proliferation and spontaneous immortalization [146], altered metabolism [147], transcriptional reprogramming [148], immune evasion [149], migration [150] and invasion and metastases [151].”
BackgroundThe Search for Genomic Biomarkers of Response to Immunotherapy in Ovarian Cancer
Al-Rawi, D. H., Rusk, N., & Friedman, C. F. (2023) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-23-0048 · Cited by 8
Immune Regulation by Cytosolic DNA Sensors in the Tumor Microenvironment
Fukuda, K. (2023) · Cancers · doi:10.3390/cancers15072114 · Cited by 8
“Rather, noncanonical NF-κB (NF-κB2) signaling activation suppresses this signaling pathway [27].”
BackgroundInfluentialBakhoum, S. F. W. (2023) · Science · doi:10.1126/science.adg7671 · Cited by 8
Self-citationKimura, K., Chun, J. H., Lin, Y., Liang, Y., Jackson, T. L. B., & Huang, R. C. C. (2023) · PLoS ONE · doi:10.1371/journal.pone.0285536 · Cited by 8
“Inflammation aggravates the rampant chromosomal abnormalities often associated with metastatic cancer cells [65].”
BackgroundSTING promotes invasion and migration of uveal melanoma through p38‑MAPK signaling
Zhou, X., Meng, F., Xu, B., Ma, R., Cheng, Y., Wu, J., & Qian, J. (2023) · Oncology Reports · doi:10.3892/or.2023.8682 · Cited by 8
Demeule, M., Currie, J.-C., Charfi, C., Zgheib, A., Cousineau, I., Lullier, V., Béliveau, R., Marsolais, C., & Annabi, B. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1355945 · Cited by 8
STING is crucial for the survival of RUNX1::RUNX1T1 leukemia cells
Sun, Y., Wu, Y., Pang, G.-Z., Huang, J., Sheng, M., Xie, J., Chen, P., Wang, Y., Yin, D., Zhao, G., et al. (2024) · Leukemia · doi:10.1038/s41375-024-02383-8 · Cited by 8
Shao, C., Chen, J., Qiang, B., Ye, J., Yan, F., & Zhu, Y. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1451305 · Cited by 9
“Furthermore, studies have also found that inhibiting the cytoplasmic DNA sensing pathway or repairing chromosomal instability can effectively suppress the metastatic ability of cancer cells (59, 60).”
BackgroundChromosomal instability as an architect of the cancer stemness landscape
Baba, S. A., Zakeri, A., & Desgrosellier, J. S. (2024) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2024.1450614 · Cited by 9
Chaudhari, S., Pereira, S. D., Asare-Werehene, M., Naha, R., Kabekkodu, S. P., Tsang, B. K., & Satyamoorthy, K. (2021) · Journal of Ovarian Research · doi:10.1186/s13048-021-00787-z · Cited by 8
Tipping Cancer Cells Over the Edge: The Context-Dependent Cost of High Ploidy
Andor, N., Altrock, P. M., Jain, N., & Gomes, A. P. (2021) · Cancer Research · doi:10.1158/0008-5472.can-21-2794 · Cited by 7
“were found to be enriched for cells with near-triploid karyotypes (78).”
BackgroundJiang, G., Hong, J., Shao, F., Wen, Q., Cheng, F., Yu, T., & Zhu, J. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.795129 · Cited by 9
“Besides their role in synthetic lethality, PARP inhibitors can lead to the production of neoantigens and DNA accumulation in the cytosol, which can trigger interferon pathways that enhance the immune response (59, 60).”
Backgroundp52 signaling promotes cellular senescence
Bernal, G. M., Wu, L., Voce, D. J., Weichselbaum, R. R., & Yamini, B. (2022) · Cell & Bioscience · doi:10.1186/s13578-022-00779-6 · Cited by 8
“A variety of stimuli, including signals emanating from surface receptor/ligand binding [11] or pathways induced by the innate immune response [12, 13], converge on NIK or its upstream regulators to induce p52 nuclear translocation [14, 15].”
BackgroundZhang, W., Chen, S., Guan, H., & Zhou, P. (2022) · Radiation Medicine and Protection · doi:10.1016/j.radmp.2022.05.002 · Cited by 10
Bakhoum, S. F. (2022) · Trends in cancer · doi:10.1016/j.trecan.2022.07.006 · Cited by 9
Self-citationJiang, X., Zhang, B., Du, F., Guo, J., Wang, D., Li, Y.-E., Deng, S.-H., Cui, B., & Liu, Y. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1013828 · Cited by 8
“For example, chromosome segregation errors can directly lead to the activation of immune signaling pathways (55).”
BackgroundMapping chromosomal instability induced by small-molecular therapeutics in a yeast model
Sheng, H., Qi, L., Sui, Y., et al. (2019) · Applied Microbiology and Biotechnology · doi:10.1007/s00253-019-09845-5 · Cited by 8
Wang, Z., Zhang, L., He, L., Cui, D., Liu, C., Yin, L., Zhang, M., Jiang, L., Gong, Y., Wang, W., et al. (2020) · Chinese Journal of Cancer Research · doi:10.21147/j.issn.1000-9604.2020.03.05 · Cited by 8
Parallels Between the Antiviral State and the Irradiated State
McGee, H. M., Marciscano, A. E. E., Campbell, A. M., Monjazeb, A. M., Kaech, S. M., & Teijaro, J. R. (2020) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/djaa190 · Cited by 8
“(29) demonstrated that cancer cells with chromosomal instability co-opt cGAS-STING signaling to promote metastatic dissemination.”
BackgroundFrigola, J., Carbonell, C., Iranzo, P., Pardo, N., Callejo, A., Cedrés, S., Martínez‐Martí, A., Navarro, A., Soleda, M., Jimenez, J., et al. (2022) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2021-004197 · Cited by 8
“We also identified differences regarding the SCNAs burden and immune infiltration levels between primary and metastatic lesions, although distinct metastatic sites may behave differently.”
Fanconi Anemia Pathway Deficiency Drives Copy Number Variation in Squamous Cell CarcinomasPreprint
Webster, A., Sanders, M. A., Patel, K., Dietrich, R., Noonan, R. J., Lach, F. P., White, R. R., Goldfarb, A. M., Hadi, K., Edwards, M. M., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.08.14.456365 · Cited by 8
Xie, T., Liu, Z., Li, Y., Wang, S., Zhai, Y., Teng, F., Hao, X., Wang, Y., Wang, H., Zhang, X., et al. (2022) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-22-0474 · Cited by 9
“Chromosomal instability (CIN) is associated with tumor evolution and metastases (25).”
BackgroundCharacterizing chromosomal instability-driven cancer evolution and cell fitness at a glance
Tijhuis, A. E., & Foijer, F. (2024) · Journal of Cell Science · doi:10.1242/jcs.260199 · Cited by 8
Cancer cells’ chamber of secrets: the link between micronuclei, chromothripsis and malignancy
Mcneil, T. R., Sikder, S., & Dalal, Y. (2025) · Open Biology · doi:10.1098/rsob.240388 · Cited by 7
“Studies investigating the link between MN, cancer risk, metastasis and prognosis highlight MN’s role in contributing to cancer progression [6–8].”
Chromosomal instability in development and disease: Beyond cancer evolution
Milán, M. (2025) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2025.102537 · Cited by 8
Egan, D., Glennon, K., Treacy, A. D., et al. (2025) · npj Precision Oncology · doi:10.1038/s41698-025-00973-y · Cited by 7
“Genomic instability promotes metastasis by inducing the release of DNA into the cytoplasm, thus activating the STING pathway and down-stream noncanonical NF-κ B signaling 20 .”
The Interplay of Aging and Cancer: Mechanisms, Implications, and Therapeutic Strategies
Wang, L., Luo, Y., Chen, X., Wang, Y., & Zhang, Y. (2025) · MedComm – Oncology · doi:10.1002/mog2.70041 · Cited by 8
Chemotherapy-induced CA-repeat DNA fragments in breast cancer trigger antitumor immune responses
Zhang, X., Huang, P., Chen, H., Yang, C., Yang, X., Liu, Y., Wu, B., Zeng, W., Saw, P. E., Ye, S., et al. (2025) · Nature Immunology · doi:10.1038/s41590-025-02289-2 · Cited by 7
“…study and others have shown that ligation of absent in melanoma 2 (AIM2) by cytosolic DNA might induce a tolerogenic phenotype in DCs or macrophages by upregulating various immune checkpoint molecules, including PD-L1 and IDO 14–16 , facilitating cancer cell dissemination and metastasis 17 .”
Alam, A., Siddiqui, M. F., Hamoudi, R., Kishore, U., Fernández-Cabezudo, M. J., & al-Ramadi, B. K. (2025) · Computational and Structural Biotechnology Journal · doi:10.1016/j.csbj.2025.11.061 · Cited by 9
“At the same time, HJURP amplifies chromosomal instability (CIN), leading to DNA missegregation that paradoxically activates pro-metastatic NF-κ B signaling and an EMT phenotype [100].”
Genome instability triggers intercellular DNA transfer between human cells
Maurais, E. G., Mazzagatti, A., Lin, Y.-F., Narożna, M., Hu, Q., Dahiya, R., Santiago-Ferrer, D., Herlihy, C. P., Krebs, M., Pateraki, N., et al. (2026) · Cell · doi:10.1016/j.cell.2026.04.041 · Cited by 12
“45,47 Beyond activation of cell-autonomous signaling programs—such as the cytosolic DNA sensing cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway 48–50 —it is poorly understood whether cytoplasm-exposed micronuclei and/or cytoplasmic DNA fragments can impact neighboring…”
Self-citationAn MRI Radiomics Approach to Predict the Hypercoagulable Status of Gliomas
Saidak, Z., Laville, A., Soudet, S., Sevestre, M., Constans, J., & Galmiche, A. (2024) · Cancers · doi:10.3390/cancers16071289 · Cited by 7
“…found in gliomas (IDH1 mutational status, genomic EGFR amplification, presence of tumor aneuploidy and chromosomal instability) in accordance with the important role played by TF in gliomagenesis, and the regulatory role played by some of these alterations in F3 expression [12–14 , 17 ].”
BackgroundMethodInfluentialZeng, X., Zhao, F., Tu, X., Zhang, Y., Yang, W., Hou, J., Jiang, Q., Zhu, S., Wu, Z., Hao, Y., et al. (2025) · Journal of Clinical Investigation · doi:10.1172/jci188120 · Cited by 10
“Intracardiac injection to induce brain metastases was performed as described previously (49, 64).”
Xu, L., He, J. G., Cai, Q., Li, M., Pu, X., & Guo, Y. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.117289 · Cited by 7
Targeting Genome Stability in Melanoma—A New Approach to an Old Field
Osrodek, M., & Woźniak, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22073485 · Cited by 11
“When looking at a general landscape of cancer development and progression, genomic instability can be viewed as a metastatic fuel [18,19].”
BackgroundMiyahira, A. K., Zarif, J. C., Coombs, C. C., Flavell, R. R., Russo, J. W., Zaidi, S., Zhao, D., Zhao, S. G., Pienta, K. J., & Soule, H. R. (2021) · The Prostate · doi:10.1002/pros.24262 · Cited by 8
“However, how chromosomally unstable tumor cells cooperate with chronic activation of innate immune pathways to evade immune surveillance remains unknown.(97) A recent study showed that the ectonucleotidase ENPP1 plays a pro‐metastatic role by degrading extracellular cGAMP and producing immune suppressive adenosine.”
BackgroundLuthra, A., Mastrogiacomo, B., Smith, S. A., Chakravarty, D., Schultz, N. D., & Sánchez-Vega, F. (2022) · Genes Chromosomes and Cancer · doi:10.1002/gcc.23023 · Cited by 7
“52,53 Chromosomal instability can be quantified using a variety of metrics.”
BackgroundTamaki, S., Suzuki, K., Abe, I., Endo, Y., Kakizawa, N., Watanabe, F., Saito, M., Tsujinaka, S., Miyakura, Y., Ohta, S., et al. (2022) · Scientific Reports · doi:10.1038/s41598-022-15071-3 · Cited by 9
Zhang, M., Wang, X., Liu, C., Zheng, Z., Wan, J., Yang, Y., Chen, S., & Liu, H. (2022) · Molecular Carcinogenesis · doi:10.1002/mc.23470 · Cited by 7
“In addition, H2AX phosphorylation and γH2AX foci formation are now generally accepted as consistent and quantitative markers of cellular DNA double‐strand breaks, which are often seen in CIN.29 The results supported that GTSE1 contributed to the formation of γH2AX foci.”
BackgroundLakbir, S., Lahoz, S., Cuatrecasas, M., Camps, J., Glas, R. A., Heringa, J., Meijer, G. A., Abeln, S., & Fijneman, R. J. A. (2022) · European Journal of Cancer · doi:10.1016/j.ejca.2022.09.034 · Cited by 11
Kimmel, G. J., Beck, R. J., Yu, X., Veith, T. A., Bakhoum, S. F. W., Altrock, P. M., & Andor, N. (2023) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1010815 · Cited by 7
“These transcriptomes originated from three cell lines, where members of the kinesin superfamily of proteins were knocked down to increase or decrease mis-segregation rate in a controlled fashion [59].”
InfluentialSelf-citationGriseofulvin Radiosensitizes Non–Small Cell Lung Cancer Cells and Activates cGAS
Wang, X., Raman, N., Lemtiri-Chlieh, G., Chang, J., Jagtap, S., Chowdhury, D. D., Ballew, M., Carrieri, F. A., Nguyen, T., Nugent, K. M., et al. (2023) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-22-0191 · Cited by 7
“MN formation has been previously shown to activate the cytoplasmic double-stranded DNA sensor pathway cGAS, which in turn activates an innate immune response (18).”
BackgroundRacine, F., Soudet, S., Sevestre, M., Galmiche, A., & Saidak, Z. (2022) · Current Opinion in Otolaryngology & Head & Neck Surgery · doi:10.1097/moo.0000000000000870 · Cited by 7
“Chromosomal instability, a common characteristic of malignant cells, may also activate the expression of TF, as suggested by in vitro studies examining the consequences of the cell response to cytosolic DNA [14].”
BackgroundInfluentialZhu, X., Zhao, W., Zhou, Z. M., & Gu, X. (2023) · Journal of Molecular Evolution · doi:10.1007/s00239-023-10117-0 · Cited by 7
“Among them, one subclone acquires sufficient driver mutations in a short period of time and thus equips tumors with malignant phenotypes, such as invasion, angiogenesis, and immune escape (Sotillo et al. 2010; Gao et al. 2016; San-sregret et al. 2017; Mackenzie et al. 2017; Bakhoum et al. 2018).”
BackgroundProtopapa, M., Kouloulias, V., Kougioumtzopoulou, A., Liakouli, Z., Papadimitriou, C., & Zygogianni, A. G. (2019) · Clinical & Translational Oncology · doi:10.1007/s12094-019-02165-0 · Cited by 7
Dysregulation in nucleic acid‐sensing pathway genes is associated with cancer patients’ prognosis
Yan‐Fei, H., Yang, H. K., Zhou, Y., Yang, H., Yu‐Qing, Y., Ipsita, P., Hui-ying, H., Weigang, F., & Tian, X. (2020) · Cancer Science · doi:10.1111/cas.14450 · Cited by 6
Arias-García, M., Yin, Z., Roumeliotis, T. I., Butera, F., Wang, L., Rickman, R. H., Choudhary, J. S., Wong, S. T. C., Yuan, Y., & Bakal, C. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/689737 · Cited by 7
“Science 316, 17531756. 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., et al. (2018). Chromosomal instability drives metastasis through a cytosolic DNA response. Nature 553, 467-472. Bartolini, F., and Gundersen, G.G. (2006). Generation…”
BackgroundInfluentialCancer tolerance to chromosomal instability is driven by Stat1 inactivation in vivoPreprint
Schubert, M., Hong, C., Jilderda, L. J., Requesens, M., Tijhuis, A. E., Simon, J. E., Bakker, P. L., Cooper, J. L., Damaskou, A., Wardenaar, R., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.12.03.471107 · Cited by 9
“To detect transposon integration sites, we used QISeq (2).”
MethodIntegrating SNVs and CNAs on a phylogenetic tree from single-cell DNA sequencing dataPreprint
Zhang, L., Bass, H. W., Irianto, J., & Mallory, X. (2023) · Genome Research · doi:10.1101/gr.277249.122 · Cited by 8
“Further, such genomic instability is especially common in metastasis (Bakhoum et al. 2018).”
Inhibition of anti-tumor immunity by melanoma cell-derived Activin-A depends on STING
Pinjušić, K., Ambrosini, G., Lourenço, J., Fournier, N., Iseli, C., Guex, N., Egorova, O., Nassiri, S., & Constam, D. B. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1335207 · Cited by 6
“…associated with an in fl amed cell state has been shown to facilitate metastatic growth in preclinical models of breast cancer by activating NF k B (77), and it also mediates tumor immune evasion and immunotherapy resistance in genetically unstable BRCA1 mutant ovarian cancer by driving…”
BackgroundEpigenomics‐guided precision oncology: Chromatin variants in prostate tumor evolution
Furlano, K., Keshavarzian, T., Biernath, N., Fendler, A., Santis, M. D., Weischenfeldt, J., & Lupien, M. (2025) · International Journal of Cancer · doi:10.1002/ijc.35327 · Cited by 6
“104 Overall, chromatin-based epigenetic modifications are key drivers of metastatic prostate cancer, contributing to aggressive phenotypes by promoting JAK – STAT signaling and EMT, as well as enabling cancer cells to adopt immune-like characteristics.”
Peng, L., Zhao, A., Li, R., Liu, Y., Tang, D., Deng, D., Zhuang, Q., Liang, R., Zhang, S., & Song, W. C. (2025) · Advanced Science · doi:10.1002/advs.202502750 · Cited by 8
Decoding STING’s roles in cancer: immunity, pain, dormancy, and autophagy
Lin, H., Tang, Y., & Liang, X. (2025) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-025-05281-4 · Cited by 6
“However, oxidative stress, metabolic alterations, and CIN can damage DNA within the nucleus and mitochondrial DNA of tumor cells, releasing endogenous DNA into the cytoplasm [26–28].”
Alnwisser, B., Alshehri, S., Qattan, A. T., Zou, M., Aboussekhra, A., Alzahrani, A. S., & Shi, Y. (2025) · Frontiers in Oncology · doi:10.3389/fonc.2025.1536270 · Cited by 7
“Chromosomal instability is known to drive metastasis through the activation of a cytosolic DNA response (40).”
Luo, R., Li, X., Zhang, M., Huang, D., Le, H., He, T., Wang, X., Kou, X., Wu, X., Wu, Q., et al. (2025) · ACS Nano · doi:10.1021/acsnano.5c09178 · Cited by 6
Liu, X., Xiao, X., Feng, Y., Li, Y., Yao, S., Han, Y., & Xia, S. (2025) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2025.167965 · Cited by 6
Wu, J., Li, B., Chen, Y., et al. (2025) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo-2025-592 · Cited by 6
“Our research also showed that andrographolide-treatment could promote DC maturation, mechanistically link to ox-mtDNA’s cGAS-STING-MHCI antigen presentation axis (17).”
cGAS Inhibits ALDH2 to Suppress Lipid Droplet Function and Regulate MASLD Progression
Wang, Y., Deng, Y., Chen, J., Hahn, Q., Umbaugh, D. S., Zhang, Z., Zhang, Y., Rowe, S. E., Li, L., Herring, L. E., et al. (2025) · Advanced Science · doi:10.1002/advs.202508576 · Cited by 6
Bai, G., Liu, H., Li, W., Chen, S., Wang, L., Wang, Z., Zhou, Y., Pan, Y., Liu, Y., Chen, Q., et al. (2025) · Journal of Nanobiotechnology · doi:10.1186/s12951-025-03689-0 · Cited by 8
“After tumor-derived double-stranded DNA (dsDNA) leaks into the cytoplasm, its accumulation hijacks the cytosolic DNA sensor cGAS to catalyze the synthesis of cyclic GMP-AMP (cGAMP) and thus activates the adaptor protein STING [7].”
Research advances in stimulator of interferon genes (STING) agonists for cancer immunotherapy
Shen, W.-R., Shi, X.-R., He, Y., Zhang, Z.-Z., & Chen, S. (2025) · Surgery · doi:10.1016/j.surg.2025.109847 · Cited by 8
Transactions on micronuclear DNA and implications for immune signaling
Maciejowski, J., & Greenberg, R. A. (2025) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2025.10.007 · Cited by 6
Pavani, G., Matada, G. S. P., Ghara, A., Paik, A., David, A. R., & Kavyasree, C. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.116052 · Cited by 6
A prognostic signature based on adenosine metabolism related genes for ovarian cancer
Liang, W., Chao Hui, Z. H. O. U., Wang, J., et al. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.1003512 · Cited by 6
“Moreover, genomic errors contributed by HRD could lead to the formation of micronuclear envelopes which are highly rupture-prone and further produce cytosolic double-stranded DNA (dsDNA) (43).”
BackgroundBaba, S. A., Sun, Q., Mugisha, S., Labhsetwar, S., Klemke, R. L., & Desgrosellier, J. S. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e20182 · Cited by 5
“However, only AXL was enriched in aCSCs [7], upregulated by CIN [8], and a member of the “Response to Stress” gene set, unique to aCSCs [7] (Fig.”
BackgroundMethodInfluentialChromosomal instability drives immunosuppression and metastatic dissemination
Vitale, I., Galassi, C., & Galluzzi, L. (2023) · Cell Research · doi:10.1038/s41422-023-00876-2 · Cited by 6
Niu, Y., Liu, Y., Ma, X., Liu, L., Li, S., Li, R. Q., Wang, T., Song, H., & Niu, D. (2023) · Mucosal Immunology · doi:10.1016/j.mucimm.2023.10.004 · Cited by 6
cGAS Mediates the Inflammatory Responses of Human Microglial Cells to Genotoxic DNA Damage
Suptela, A. J., Radwan, Y., Richardson, C. A., Yan, S., Afonin, K. A., & Marriott, I. (2023) · Inflammation · doi:10.1007/s10753-023-01946-8 · Cited by 6
Marugán, C., Sanz‐Gómez, N., Ortigosa, B., Monfort‐Vengut, A., Bertinetti, C., Teijo, A., González, M., de la Vega, A. A., Lallena, M. J., Moreno‐Bueno, G., et al. (2024) · Molecular Oncology · doi:10.1002/1878-0261.13602 · Cited by 6
“In addition, other studies identified similar CIN signatures for a variety of cancers, correlating with increased tumoral aggressiveness [11 – 15] and metastasis capacity [16].”
BackgroundInfluentialNaso, F. D., Polverino, F., Cilluffo, D., Latini, L., Stagni, V., Asteriti, I. A., Rosa, A., Soddu, S., & Guarguaglini, G. (2024) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2024.167116 · Cited by 7
“Chromosomal instability (CIN) is a cancer-driver condition strictly linked with tumour aggressiveness, metastatisation, relapses and chemo-resistance [1,2].”
Yu, M., Chen, Q., & Lu, Y. (2024) · World Journal of Gastrointestinal Oncology · doi:10.4251/wjgo.v16.i7.3230 · Cited by 6
Fang, X., Yu, W.-Y., Zhu, C.-M., Zhao, N., Zhao, W., Xie, T., Wei, L., Sun, X.-R., Xie, J., & Zhao, Y. (2024) · Acta Pharmacologica Sinica · doi:10.1038/s41401-024-01372-y · Cited by 6
“Further, a driving role of CIN in metastasis by inducing responses to cytosolic DNA in an aneuploidy-independent manner is reported in both lung and breast tumors [5].”
Fu, Q., Lu, Z., Chang, Y., Jin, T., & Zhang, M. (2024) · Industrial Crops and Products · doi:10.1016/j.indcrop.2024.119589 · Cited by 6
Morel, K. L., German, B., Hamid, A., Nanda, J. S., Linder, S., Bergman, A. M., van der Poel, H. G., Hofland, I., Bekers, E. M., Trostel, S. Y., et al. (2024) · Journal of Clinical Investigation · doi:10.1172/jci175680 · Cited by 6
“In both breast and PCa, low ZFP36 expression is a negative prognostic indicator, and it is associated with rapid tumor progression and poor clinical outcome (16, 54). substituted a lethal epithelial response to inflammation with that of myeloid-derived cells, resulting in increased metastasis (62).”
D’Souza, D. P., Bik, L., Giwa, O. D., Cohen, S., Barazany, H. L., Siegal, T., & Frenkel‐Morgenstern, M. (2024) · Nucleic Acids Research · doi:10.1093/nar/gkae1126 · Cited by 6
Science in Focus: Biological Optimisation of Radiotherapy Fraction Size in an Era of Immune Oncology
Wilkins, A. C., Melcher, A. A., & Somaiah, N. (2018) · Clinical Oncology · doi:10.1016/j.clon.2018.07.001 · Cited by 6
Vedoya, G. M., Nigro, M. M. L., & Martín, G. (2020) · Toxicology in Vitro · doi:10.1016/j.tiv.2020.105018 · Cited by 6
Harnessing Genomic Stress for Antitumor Immunity
Pu, C., Tao, S., Xu, J., & Huang, M. (2020) · Antioxidants and Redox Signaling · doi:10.1089/ars.2020.8221 · Cited by 6
“As aforementioned, abnormality of chromosome segregation during mitosis leads to formation of micronuclei (10, 11, 75, 124).”
Cancer as a System Dysfunction
Saeed, K., Ryder, E. F., & Manning, A. L. (2021) · Systems · doi:10.3390/systems9010014 · Cited by 6
Processes shaping cancer genomes – From mitotic defects to chromosomal rearrangements
Keuper, K., Wieland, A., Räschle, M., & Štorchová, Z. (2021) · DNA repair · doi:10.1016/j.dnarep.2021.103207 · Cited by 6
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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