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.
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, 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.
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
“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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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
“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.
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
“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.
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
“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.
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
“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
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
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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 801–900 of 1,551
Twenty years of merotelic kinetochore attachments: a historical perspective
Cimini, D. (2023) · Chromosome Research · doi:10.1007/s10577-023-09727-7 · Cited by 13
Bhat‐Nakshatri, P., Khatpe, A. S., Chen, D., Batic, K., Mang, H. E., Herodotou, C., McGuire, P. C., Xuei, X., Erdoğan, C., Gao, H., et al. (2023) · Cancer Research Communications · doi:10.1158/2767-9764.crc-23-0330 · Cited by 13
Wang, L., Yu, Z., Zhang, J., & Guo, J. (2024) · Drug Discovery Today · doi:10.1016/j.drudis.2024.103892 · Cited by 12
D’Ambrosio, A., Bressan, D., Ferracci, E., Carbone, F. G., Mulé, P., Rossi, F., Barbieri, C., Sorrenti, E., Fiaccadori, G., Detone, T., et al. (2024) · Science Advances · doi:10.1126/sciadv.adh4435 · Cited by 13
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“However, chronic cGAS/STING activation was shown to promote breast cancer metastasis in mice implanted with the MDA-MB-231 and 4T1 breast cancer cell lines (Bakhoum et al., 2018).”
Human Papillomavirus-Induced Chromosomal Instability and Aneuploidy in Squamous Cell Cancers
Mallick, S., Choi, Y., Taylor, A. M., & Cosper, P. F. (2024) · Viruses · doi:10.3390/v16040501 · Cited by 17
“Furthermore, CIN has also been associated with immune suppression as well as increased metastasis via chronic activation of the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon gene) pathway [33,124].”
BackgroundTelomere dysfunction alters intestinal stem cell dynamics to promote cancer
LaBella, K. A., Hsu, W.-H., Li, J., Qi, Y., Liu, Y., Liu, J., Wu, C.-C., Liu, Y., Song, Z., Lin, Y., et al. (2024) · Developmental Cell · doi:10.1016/j.devcel.2024.03.020 · Cited by 13
Selection forces underlying aneuploidy patterns in cancer
Klockner, T. C., & Campbell, C. S. (2024) · Molecular & Cellular Oncology · doi:10.1080/23723556.2024.2369388 · Cited by 12
Role of the Innate Immune Response in Glomerular Disease Pathogenesis: Focus on Podocytes
Issa, W., Njeim, R., Carrazco, A., Burke, G. W., & Mitrofanova, A. V. (2024) · Cells · doi:10.3390/cells13131157 · Cited by 13
Innovating Cancer Treatment Through Cell Cycle, Telomerase, Angiogenesis, and Metastasis
Yousefi, T., Jobani, B. M., Taebi, R., & Qujeq, D. (2024) · DNA and Cell Biology · doi:10.1089/dna.2024.0109 · Cited by 12
“Metastasis involves a multitude of overlapping cellular pathways that regulate cancer cell behavior (Bakhoum et al., 2018; Das et al., 2020).”
Yang, H., Zhan, X., Jia, Z., Shi, W., Liu, T., Wei, Z., Li, H., Hou, X., Mu, W., Chen, Y., et al. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1369563 · Cited by 12
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The Role of Chronic Inflammation in Pediatric Cancer
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Deep visual proteomics reveals DNA replication stress as a hallmark of signet ring cell carcinoma
Kabatnik, S., Zheng, X., Pappas, G., Steigerwald, S., Padula, M. P., & Mann, M. (2025) · npj Precision Oncology · doi:10.1038/s41698-025-00819-7 · Cited by 12
TAX1BP1-dependent autophagic degradation of STING1 impairs anti-tumor immunity
Zhang, R., Yu, C., Zeh, H. J., Kroemer, G., Klionsky, D. J., Tang, D., & Kang, R. (2025) · Autophagy · doi:10.1080/15548627.2025.2471736 · Cited by 14
“Chronic activation of the STING1 pathway may drive tumorigenesis and metastasis through inflammation [15,16].”
Context-dependent effects of whole-genome duplication during mammary tumor recurrence
Newcomb, R., Dean, E., McKinney, B. J., & Alvarez, J. V. (2021) · Scientific Reports · doi:10.1038/s41598-021-94332-z · Cited by 14
“WGD is also prevalent in metastatic disease [7] and in breast cancer has been observed in a greater proportion of metastases than primary tumors [5].”
BackgroundAneuploidy, inflammation and diseases
Kirsch‐Volders, M., & Fenech, M. F. (2022) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2022.111777 · Cited by 12
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STING Agonists in Head and Neck Squamous Cell Carcinoma
Wallington, D. G., Contessa, J. N., & Hayman, T. J. (2022) · The Cancer Journal · doi:10.1097/ppo.0000000000000620 · Cited by 12
The progress in our understanding of CIN in breast cancer research
Liao, Y.-Y., & Cao, W. (2023) · Frontiers in Oncology · doi:10.3389/fonc.2023.1067735 · Cited by 12
“CIN involves the activation of the CGAS–STING pathway, which promotes metastasis (3).”
BackgroundHaj, M., Levon, A., Frey, Y., Hourvitz, N., Campisi, J., Tzfati, Y., Elkon, R., Ziv, Y., & Shiloh, Y. (2023) · Aging Cell · doi:10.1111/acel.13869 · Cited by 12
“MN eventually rupture spilling their DNA content into the cytosol thereby activating the cGAS- STING cytosolic DNA- sensing pathway (Bakhoum et al., 2018; Dou et al., 2017; Harding et al., 2017; MacDonald et al., 2023).”
BackgroundPolyglutamine binding protein 1 (PQBP1) inhibits innate immune responses to cytosolic DNA
Shannon, J. L., Murphy, M. S., Kantheti, U., Burnett, J. M., Hahn, M., Dorrity, T. J., Bacas, C. J., Mattice, E. B., Corpuz, K. D., & Barker, B. R. (2018) · Molecular Immunology · doi:10.1016/j.molimm.2018.05.014 · Cited by 12
Cytosolic Genomic DNA functions as a Natural Antisense
Asada, K., Ito, K., Yui, D., Tagaya, H., & Yokota, T. (2018) · Scientific Reports · doi:10.1038/s41598-018-26487-1 · Cited by 13
Song, J., Zhang, L., Li, C., Maimaiti, M., Sun, J. P., Hu, J., Li, L., Zhang, X., Wang, C., & Hu, H. (2022) · Computational and Structural Biotechnology Journal · doi:10.1016/j.csbj.2022.04.002 · Cited by 12
“For instance, the dysregulation of the cGAS-STING signaling has been linked to cancer and metastasis [8–10], Huntington disease [11], age-dependent macular degeneration (AMD) [12], amyotrophic lateral sclerosis (ALS) [13–14], Parkinson’s disease [15], nonalcoholic steatohepatitis (NASH) [16] and…”
BackgroundBalaji, A., Saha, S., Deshpande, S., Poola, D., & Sengupta, K. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.1068347 · Cited by 12
“CIN leads to transcriptional imbalances in a cell- and tissue-specific manner (Bakhoum et al., 2018; Benhra et al., 2018).”
BackgroundThe evolution of spindles and their mechanical implications for cancer metastasis
Chen, Y., Nam, S., Chaudhuri, O., & Huang, H. (2019) · Cell Cycle · doi:10.1080/15384101.2019.1632137 · Cited by 12
“[18] Bakhoum SF, Ngo B, Laughney AM, et al.”
BackgroundOvercoming Immune Therapy Resistance in Cancer Through Innate Immune Reprogramming
Mandracci, G., Soliman, N., & Khawanky, N. E. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26199554 · Cited by 15
“Meanwhile, mitochondria under metabolic stress or defective mitophagy release mitochondrial DNA [91,92].”
Mărcuț, L. F., Brata, R. D., Barb, A. C., Manole, A., Stef, D. G., Dumitru, C. Ș., Zara, F., & Pătrașcu, R. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262311271 · Cited by 11
“In contrast, chronic or dysregulated pathway activation shifts signaling toward NF-κ B-driven inflammation, PD-L1 upregulation, and accumulation of myeloid-derived suppressor cells, ultimately fostering an immunosuppressive microenvironment [74].”
The cGAS-STING pathway in cancer: friend or foe
Li, Q., Song, Q., Ma, L., Kang, K., Zhu, X., Li, Y., Lin, X., Lu, X., Zeng, Z., Li, G., et al. (2026) · Cell Death and Disease · doi:10.1038/s41419-026-08607-2 · Cited by 15
“Investigations into the underlying mechanisms revealed that in metastatic tumors, activation of the cGAS ‒ STING pathway results in the upregulation of the non-canonical NF-κ B pathway, thereby promoting metastasis [100].”
Intermetallic nanoassemblies potentiate systemic STING activation
Zhou, X., Ling, X., Sun, X., Wan, Z., Dwyer, T., Moore, T. C., Li, Q., Dobson, H. E., Wu, Q., Kong, X., et al. (2026) · Science · doi:10.1126/science.adx1893 · Cited by 16
Peng, Y., Meng, G., Sheng, X., & Gao, H. (2021) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.16615 · Cited by 11
Harnessing cGAS‐STING Pathway for Cancer Immunotherapy: From Bench to Clinic
Lee, D., Huntoon, K. M., Kang, M., Lü, Y., Gallup, T. D., Jiang, W., & Kim, B. Y. S. (2022) · Advanced Therapeutics · doi:10.1002/adtp.202200040 · Cited by 10
Nakajima, S., Kaneta, A., Okayama, H., Saito, K., Kikuchi, T., Endo, E., Matsumoto, T., Fukai, S., Sakuma, M., Sato, T., et al. (2023) · Cancers · doi:10.3390/cancers15102826 · Cited by 12
“Substantial amounts of cytoplasmic dsDNA are found under pathological conditions, including cancer [20], and it has been reported that cytoplasmic dsDNA in cancer cells may contribute to type I IFN-dependent priming of tumor cellspecific T cell immunity [21].”
BackgroundLymph node metastasis: An immunological burden
Lund, A. W. (2023) · The Journal of Experimental Medicine · doi:10.1084/jem.20230904 · Cited by 12
Mechanisms controlling the mechanical properties of the nuclei
Bastianello, G., & Foiani, M. (2023) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2023.102222 · Cited by 12
Jin, T., Ding, L., Chen, J., et al. (2024) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.18182 · Cited by 11
A survey of chromosomal instability measures across mechanistic models
Lynch, A. R., Bradford, S., Zhou, A. S., Oxendine, K., Henderson, L., Horner, V. L., Weaver, B. A. A., & Burkard, M. E. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2309621121 · Cited by 13
“Indeed, CIN accelerates tumor evolution, and portend increased metastasis (3, 4), therapeutic resistance (5–7), and worse prognosis (8–10).”
Advances in the prerequisite and consequence of STING downstream signalosomes
Lu, X., Li, X., Li, L., Han, C., & Li, S. (2024) · Medical Review · doi:10.1515/mr-2024-0016 · Cited by 11
“Contrary to its established tumor-suppressive function [101, 102, 104], additional research has revealed that the STING system may also be involved in increasing tumor burden and worsening illnessoutcomesinmousetumormodels[65, 105](Figure2).”
BackgroundTBK1-Zyxin signaling controls tumor-associated macrophage recruitment to mitigate antitumor immunity
Zhou, R., Wang, M., Li, X., Liu, Y., Yao, Y., Wang, A., Chen, C., Zhang, Q. Y., Wu, Q., Zhang, Q., et al. (2024) · The EMBO Journal · doi:10.1038/s44318-024-00244-9 · Cited by 10
“…activation of cGAS-STING signaling could robustly inhibit tumor growth; however, tumor-derived cGAMP and chronic in fl ammation caused by DNA-damage response (DDR), chromosomal instability (CIN), mtDNA release, and dying cells may promote tumor progression (Bakhoum et al, 2018; Hou et al, 2018).”
Decoding chromosomal instability insights in CRC by integrating omics and patient-derived organoids
Papaccio, F., Cabeza-Segura, M., García-Micó, B., Gimeno-Valiente, F., Zúñiga, S., Gambardella, V., Gutiérrez-Bravo, M. F., Martínez‐Ciarpaglini, C., Rentero-Garrido, P., Fleitas, T., et al. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-025-03308-8 · Cited by 12
“4), as previously reported with CIN cancer cell lines [71].”
Chen, W., Jiang, Y., Zeng, J., Liu, D., Feng, X., Cheng, Y., Lu, D., Sun, Y., Zhu, Q., Zhang, X., et al. (2025) · Oncogene · doi:10.1038/s41388-025-03366-4 · Cited by 11
Cytosolic dsDNA is a novel senescence marker associated with pyroptosis activation
Zhou, R., Xie, X., Qin, Z., Li, X., Liu, J., Li, H., Zheng, Q., & Luo, Y. (2021) · Tissue and Cell · doi:10.1016/j.tice.2021.101554 · Cited by 11
Tu, S., Mao, D., Shi, M., Zhang, H., Liu, C., Li, X., Zhao, Y., Chen, Y., & Liu, Y. (2022) · Phytotherapy Research · doi:10.1002/ptr.7433 · Cited by 12
Budke, B., Zhong, A., Sullivan, K. D., Park, C., Gittin, D. I., Kountz, T. S., & Connell, P. P. (2022) · Nucleic Acids Research · doi:10.1093/nar/gkac491 · Cited by 11
“For example, both radiation-induced DSBs and genomic instability can promote the liberation of nucleic acids into the cytoplasm after mitosis, which ultimately leads to the activation of non-canonical NF- B (22,39).”
BackgroundGrowth-promoting function of the cGAS-STING pathway in triple-negative breast cancer cells
Liu, L., Shen, Y.-C., Wang, Y., Wu, W., Chang, L., Chen, Y.-H., Lee, C.-C., & Wang, S. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.851795 · Cited by 12
Apoptosis as a Barrier against CIN and Aneuploidy
Weiss, J. G., Villunger, A., Gallob, F., & Rieder, P. (2022) · Cancers · doi:10.3390/cancers15010030 · Cited by 11
Lin, P., Chen, Y., Xu, J., et al. (2023) · Journal of Thoracic Disease · doi:10.21037/jtd-22-1732 · Cited by 11
Reece, A. S., & Hulse, G. K. (2023) · Pediatric Reports · doi:10.3390/pediatric15010009 · Cited by 11
MCAK Inhibitors Induce Aneuploidy in Triple-Negative Breast Cancer Models
Smith, J. C., Husted, S., Pilrose, J. M., Ems-McClung, S. C., Stout, J. R., Carpenter, R. L., & Walczak, C. (2023) · Cancers · doi:10.3390/cancers15133309 · Cited by 11
“Expression of a dominant-negative MCAK led to increased CIN, which correlated with an increase in metastasis in xenograft models [31].”
BackgroundCancer stem-like cells in uveal melanoma: novel insights and therapeutic implications
Loda, A., Semeraro, F., Parolini, S., Ronca, R., & Rezzola, S. (2024) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2024.189104 · Cited by 11
Cancer as a form of life: Musings of the cancer and evolution symposium
Paul, D. (2021) · Progress in Biophysics and Molecular Biology · doi:10.1016/j.pbiomolbio.2021.05.003 · Cited by 11
Type I Interferon Induction in Cutaneous DNA Damage Syndromes
Klein, B., & Günther, C. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.715723 · Cited by 16
Targeting cytokinesis bridge proteins to kill high-CIN type tumors
Xie, B., Liang, X., Yue, W., Ma, J., Li, X., Zhang, N., Wang, P., Liu, C., Shi, X., Qiao, J., et al. (2021) · Fundamental Research · doi:10.1016/j.fmre.2021.08.015 · Cited by 10
Potential role of cGAS/STING pathway in regulating cancer progression
Dhanisha, S. S., & Guruvayoorappan, C. (2022) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2022.103780 · Cited by 11
Tumor Cells Transmit Drug Resistance via Cisplatin-Induced Extracellular Vesicles
Wang, J., Liu, Q., Zhao, Y., Fu, J., & Su, J. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241512347 · Cited by 11
Chan, F.-F., Yuen, V. W., Shen, J., Chin, D. W., Law, C., Wong, B. P., Chan, C. Y., Cheu, J. W., Ng, I. O., Wong, C. C., et al. (2023) · Hepatology · doi:10.1097/hep.0000000000000709 · Cited by 11
“[25,26] Consistent with the extensive DNA damage in CAF-1 KO cells, it exhibited increased micronuclei formation and dsDNA on IF visualization (Figure 7A).”
Role of micronucleus-activated cGAS-STING signaling in antitumor immunity
Qin, S. H. E. N., Xu, P., & Chen, M. (2024) · Journal of Zhejiang University (Medical Sciences) · doi:10.3724/zdxbyxb-2023-0485 · Cited by 11
D’Antoni, S., Spatuzza, M., Bonaccorso, C. M., & Catania, M. V. (2024) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2024.105731 · Cited by 11
“Chromosomal instability is a hallmark of malignancies (Negrini et al., 2010) and a driver of tumorigenesis, malignancy progression and a promoter of metastasis formation (Bakhoum et al., 2018).”
Mutations in the non-catalytic polyproline motif destabilize TREX1 and amplify cGAS-STING signaling
Shim, A., Luan, X., Zhou, W., Crow, Y. J., & Maciejowski, J. (2024) · Human Molecular Genetics · doi:10.1093/hmg/ddae089 · Cited by 10
VHL loss enhances antitumor immunity by activating the anti-viral DNA-sensing pathway
Jiao, M., Hu, M., Pan, D., Liu, X., Bao, X., Kim, J., Li, F., & Li, C. (2024) · iScience · doi:10.1016/j.isci.2024.110285 · Cited by 10
“64 In fact, the paradoxical roles of VHL mutations in promoting tumor development while making them susceptible to ICB therapy are not unique.”
Paizal, J. P., Au, S. H., & Bakal, C. (2024) · Scientific Reports · doi:10.1038/s41598-024-64733-x · Cited by 10
“5) 17 .”
BackgroundWang, Y., Ma, Y., He, L., Du, J., Li, X., Jiao, P., Wu, X., Xu, X., Zhou, W., Yang, L., et al. (2024) · Chinese Journal of Cancer Research · doi:10.21147/j.issn.1000-9604.2024.03.05 · Cited by 10
Wu, Z., Zhang, W., Wang, L., Leng, J., Li, Y., Fan, Z., Zhan, M., Cao, L., Jiang, Y., Jiang, Y., et al. (2024) · Clinical and Translational Medicine · doi:10.1002/ctm2.1815 · Cited by 10
“19 Meanwhile, Hu et al. 20 found that intrinsic STING activation in cancer cells helps to inhibit lung adenocarcinoma metastasis.”
Propagation of neuronal micronuclei regulates microglial characteristics
Yano, S., Asami, N., Kishi, Y., Takeda, I., Kubotani, H., Hattori, Y., Kitazawa, A., Hayashi, K., Kubo, K., Saeki, M., et al. (2025) · Nature Neuroscience · doi:10.1038/s41593-024-01863-5 · Cited by 15
“Because cGAS contributes to the increased metastasis of cancer cells 87 , it is plausible that this migration may be dependent on cGAS.”
Duan, W., Hosea, R., Wang, L., Ruan, C., Zhao, F., Liu, J., Zhao, H., Miyagishi, M., Wu, S., & Kasim, V. (2025) · Advanced Science · doi:10.1002/advs.202409769 · Cited by 10
Tumor Metastasis: Mechanistic Insights and Therapeutic Intervention
Tang, L., Peng, S., Zhuang, X., He, Y., Song, Y., Nie, H., Zheng, C., Pan, Z., Lam, A. K.-Y., He, M., et al. (2025) · MedComm – Oncology · doi:10.1002/mog2.70012 · Cited by 11
Targeting vulnerabilities of aneuploid cells for cancer therapy
Zerbib, J., Bloomberg, A., & Ben‐David, U. (2025) · Trends in cancer · doi:10.1016/j.trecan.2025.04.005 · Cited by 12
Sun, R., Peng, J. C., Wang, Z., Yan, B., Zhu, S., Huang, Z., Zhang, J., Ding, D., Li, X., Wang, L., et al. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2413732122 · Cited by 11
Beernaert, B., Jady‐Clark, R. L., Shah, P., Ramon‐Gil, E., Lawson, N. M., Brodtman, Z. D., Tagore, S., Stihler, F., Carter, A., Clarke, S., et al. (2026) · Science Advances · doi:10.1126/sciadv.aeb1611 · Cited by 13
“In CIN settings, we and others have reported the chronic stimulation of the innate immune cyclic GMP (guanosine 5 ′ -monophosphate)- AMP (adenosine 5 ′ - monophosphate) synthase (cGAS)- stimulator of interferon (IFN) genes (STING) pathway ( 15 – 18 ).”
Self-citationNakamura, K. D., Ishii, Y., Takasu, S., Nohmi, T., Shibutani, M., & Ogawa, K. (2021) · Archives of Toxicology · doi:10.1007/s00204-021-03099-9 · Cited by 11
Nájera, G. S., Narganes-Carlón, D., & Crowther, D. J. (2021) · Scientific Reports · doi:10.1038/s41598-021-94897-9 · Cited by 9
“…and chronic inflammatory diseases like non-alcoholic fatty liver disease 109 , systemic lupus erythematosus 110 , vascular and pulmonary syndrome 111 , macular degeneration 112 , Bloom syndrome 113 , Aicardi-Goutières syndrome 114 , cancer 115 , DNA damage 116 , neurodegeneration 117 and beyond.”
BackgroundSilva, A. N. S., Saito, Y., Yoshikawa, T., et al. (2021) · British journal of surgery · doi:10.1093/bjs/znab460 · Cited by 10
Gudiño, R. C., McManus, K. J., & Hombach‐Klonisch, S. (2023) · Cancers · doi:10.3390/cancers15061735 · Cited by 10
Zheng, W., Pu, M., Li, X., Du, Z., Jin, S., Li, X., Zhou, J., & Zhang, Y. (2023) · Scientific Reports · doi:10.1038/s41598-023-35842-w · Cited by 11
“The CIN has also been linked to metastasis through the cGAS-STING cytosolic DNA-sensing pathway 43 .”
BackgroundHow Does cGAS Avoid Sensing Self-DNA under Normal Physiological Conditions?
Zheng, W., Chen, N., Meurens, F., Zheng, W., & Zhu, J. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241914738 · Cited by 10
“…with high chromosomal instability promotes invasion and metastasis, attributed to a switch from IFN-I and canonical NF-κ B signaling to non-canonical NF-κ B cascades [74]. cGAS is a major factor in promoting hepatocellular carcinoma cell (HCC) tumor growth by suppressing ferroptosis in vivo [75].”
BackgroundMancarella, D., Ellinghaus, H., Sigismondo, G., Veselinov, O., Kühn, A., Goyal, A., Hartmann, M., Fellenberg, J., Krijgsveld, J., Plass, C., et al. (2024) · International Journal of Cancer · doi:10.1002/ijc.34883 · Cited by 12
Signal‐transducing innate receptors in tumor immunity
Hangai, S., Kimura, Y., Taniguchi, T., & Yanai, H. (2021) · Cancer Science · doi:10.1111/cas.14848 · Cited by 12
Establishment and characterization of a new human colon cancer cell line, PUMC-CRC1
Bian, X., Cao, F., Wang, X., Hou, Y., Zhao, H., & Liu, Y. (2021) · Scientific Reports · doi:10.1038/s41598-021-92491-7 · Cited by 10
Nondiploid cancer cells: Stress, tolerance and therapeutic inspirations
Du, M., Zhang, S., Liu, X., Xu, C., & Zhang, X. (2022) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2022.188794 · Cited by 10
Seton-Rogers, S. E. (2018) · Nature reviews. Cancer · doi:10.1038/nrc.2018.16 · Cited by 10
ENPP1 is an innate immune checkpoint of the anticancer cGAMP-STING pathwayPreprint
Wang, S., Böhnert, V., Joseph, A. J., Sudaryo, V., Swinderman, J. T., Yu, F. B., Lyu, X., Skariah, G. M., Subramanyam, V., Gilbert, L. A., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.06.01.543353 · Cited by 10
Ongoing genome doubling promotes evolvability and immune dysregulation in ovarian cancerPreprint
McPherson, A., Vázquez-Garćıa, I., Myers, M. A., Zatzman, M., Al-Rawi, D. H., Weiner, A. C., Freeman, S. S., Mohibullah, N., Satas, G., Williams, M. J., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.07.11.602772 · Cited by 10
Self-citationcGAS regulates the DNA damage response to maintain proliferative signaling in gastric cancer cells
Liu, B., LIU, H., Ren, F., LIU, H., Bukhari, I., FU, Y., WU, W., ZHAO, M., ZHU, S., MO, H., et al. (2021) · Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics · doi:10.32604/or.2022.03529 · Cited by 10
“In the last decades, genome instability has been recognized as a crucial mechanism of gastric carcinogenesis [19,20].”
BackgroundMultilevel Heterogeneity of Colorectal Cancer Liver Metastasis
Chen, H., Zhai, C., Xu, X., Wang, H., Han, W., & Shen, J. (2023) · Cancers · doi:10.3390/cancers16010059 · Cited by 10
“Previous studies found that chromosome instability is significantly higher in metastatic breast cancer cells than in primary cells, and it is also a driver of metastasis [33].”
BackgroundResearch progress on mitochondria regulating tumor immunity
Li, J., Xu, P., & Chen, S. (2024) · Journal of Zhejiang University (Medical Sciences) · doi:10.3724/zdxbyxb-2023-0484 · Cited by 11
Wang, H., Zhang, Y., Tian, Y., Yang, W., Wang, Y., Hou, H., Pan, H., Pei, S., Zhu, H., Gu, Z., et al. (2024) · Cancer Research · doi:10.1158/0008-5472.can-23-0744 · Cited by 9
Elucidation of how the Mir-23-27-24 cluster regulates development and aging
Yap, X.-L., & Chen, J. (2024) · Experimental & Molecular Medicine · doi:10.1038/s12276-024-01266-3 · Cited by 9
“Although such instability can be a natural element of cellular processes, uncontrolled genomic instability results in diseases such as cancer and aging 42,43 .”
BackgroundChk2 sustains PLK1 activity in mitosis to ensure proper chromosome segregation
Black, E. M., Parrado, C. A. R., Trier, I., Li, W., Joo, Y. K., Pichurin, J., Liu, Y., & Kabeche, L. (2024) · Nature Communications · doi:10.1038/s41467-024-54922-7 · Cited by 10
“Increased numbers of micronuclei are a hallmark and driver of cancer, as they can deleteriously affect gene expression, DNA damage repair, and in fl ammation 2,85 – 89 .”
Ibarra-Arellano, M. A., Caprio, L., Hada, A., Stotzem, N., Cai, L. L., Shah, S. B., Walsh, Z. H., Melms, J. C., Wünnemann, F., Bestak, K., et al. (2025) · Communications Biology · doi:10.1038/s42003-025-07796-4 · Cited by 15
“FluorescentimageswereobtainedontheZeissCelldiscoverer 7usingthePlanApochromat20×/0.7objective,0.5×magni fi cation changer, and Axiocam 506.”
InfluentialYonesaka, K., Kurosaki, T., Tanizaki, J., Kawakami, H., Tanaka, K., Maenishi, O., Takamura, S., Sakai, K., Chiba, Y., Teramura, T., et al. (2025) · Cells · doi:10.3390/cells14060447 · Cited by 9
“Conversely, persistent activation of STING pathway by CIN can cause chronic inflammation, which in turn promotes cancer metastasis [21,28].”
InfluentialShen, Y., Fang, H., Xie, H., Zhu, S., Wang, X., Liu, S., Sui, J., Xu, Y. J., Bo, Y., Zhao, J., et al. (2025) · Cell Communication and Signaling · doi:10.1186/s12964-025-02458-8 · Cited by 11
“Additionally, mitochondrial ROS can also promote tumor cell survival via NF-κB signaling [62].”
Darwinian Selection Transforms Organisms to Bio-Robots
Skopec, R. (2018) · Current Trends in Biomedical Engineering & Biosciences · doi:10.19080/ctbeb.2018.14.555881 · Cited by 9
“There’s reason to think that our fluid force field is also extendable [1].”
BackgroundHao, F. (2022) · Clinical & Translational Oncology · doi:10.1007/s12094-022-02826-7 · Cited by 10
“However, chronic and persistent overreaction of STING signaling may play a key role in promoting the progression of certain inflammation-aggravated cancers, suggesting a complex interplay between host and tumoral cGAS-STING signaling in mediating downstream anti-tumor immune response [74, 75].”
BackgroundNovel GIRlncRNA Signature for Predicting the Clinical Outcome and Therapeutic Response in NSCLC
Zhang, Q., Liu, X., Chen, Z., & Zhang, S. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.937531 · Cited by 9
“These results accord with the fact that genome instability contributes to neoplasia and metastasis (Bakhoum et al., 2018; Nguyen et al., 2022).”
ResultSpoor, J. K. H., den Braber, M., Dirven, C. M. F., Pennycuick, A., Bártková, J., Bartek, J. J., van Dis, V., van den Bosch, T. P. P., Leenstra, S., & Venkatesan, S. (2024) · Frontiers in Oncology · doi:10.3389/fonc.2023.1218297 · Cited by 9
“Interestingly, all gliomas in our cohort had a missegregation frequency of at least 50%, making the overall chromosome missegregation frequency generally higher compared to that of recent studies in other cancer types (15, 16, 21, 30).”
MethodResultSelf-citationArginine methylation-dependent cGAS stability promotes non-small cell lung cancer cell proliferation
Liu, X., Zheng, W., Zhang, L., Cao, Z., Cong, X., Hu, Q., Hou, J., Jin, X., Yuan, Q., Lin, L., et al. (2024) · Cancer Letters · doi:10.1016/j.canlet.2024.216707 · Cited by 10
Tumor Organoids: The Era of Personalized Medicine
Rassomakhina, N. V., Ryazanova, A. Y., Likhov, A. R., Bruskin, S. A., Maloshenok, L. G., & Zherdeva, V. V. (2024) · Biochemistry (Moscow) · doi:10.1134/s0006297924140086 · Cited by 9
Novel insights into immune cells modulation of tumor resistance
Zhou, Y., Na, C., & Li, Z. (2024) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2024.104457 · Cited by 9
Tayoun, T., Oulhen, M., Aberlenc, A., Farace, F., & Pawlikowska, P. (2021) · Cells · doi:10.3390/cells10020337 · Cited by 10
“GI has also been associated with epithelial-mesenchymal transition (EMT) through the activation of the cytosolic DNA response pathway [26].”
BackgroundConsequences of mitotic failure – The penalties and the rewards
Štorchová, Z. (2021) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2021.03.007 · Cited by 9
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
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