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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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CIN generates micronuclei and cytosolic DNA”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
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In the paper
“There was no need to randomize animals.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Animal studies
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
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).”
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Items 601–700 of 1,551
Exploiting Radiation Therapy to Restore Immune Reactivity of Glioblastoma
Martino, M. D., Padilla, O. A., Daviaud, C., Wu, C., Gartrell, R. D., & Vanpouille‐Box, C. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.671044 · Cited by 26
Circulating Hybrid Cells: A Novel Liquid Biomarker of Treatment Response in Gastrointestinal Cancers
Walker, B. S., Sutton, T. L., Zarour, L. R., Hunter, J. G., Wood, S. G., Tsikitis, V. L., Herzig, D. O., Lopez, C. D., Chen, E. Y.-S., Mayo, S. C., et al. (2021) · Annals of Surgical Oncology · doi:10.1245/s10434-021-10379-2 · Cited by 23
Centrosome instability: when good centrosomes go bad
Ryniawec, J. M., & Rogers, G. C. (2021) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-021-03928-1 · Cited by 25
The Dynamic Instability of the Aneuploid Genome
Garribba, L., & Santaguida, S. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.838928 · Cited by 23
“It was already known that STING activation can lead to NF-kB pathway activation (Abe and Barber, 2014), but recently it has been observed that the activation of STING and non-canonical NF-kB pathway can mediate metastasis in a tumor cellautonomous fashion (Bakhoum et al., 2018).”
BackgroundIntegrated DNA and RNA sequencing reveals early drivers involved in metastasis of gastric cancer
Zhang, J., Liu, F., Yang, Y., Yu, N., Weng, X., Yang, Y., Gong, Z., Huang, S., Gan, L., Sun, S., et al. (2022) · Cell Death and Disease · doi:10.1038/s41419-022-04838-1 · Cited by 24
“could drive genomic instability and then generate more somatic mutations, including prometastatic drivers [30, 31].”
BackgroundSokač, M., Ahrenfeldt, J., Litchfield, K., Watkins, T. B. K., Knudsen, M., Dyrskjøt, L., Jakobsen, M. R., & Birkbak, N. J. (2022) · Cancer Research Communications · doi:10.1158/2767-9764.crc-22-0047 · Cited by 21
“Previous work has demonstrated how the cGAS-STING pathway is commonly activated by DNA from micronuclei bursting in the cytosol in tumors with high levels of CIN (43).”
BackgroundSelf-citationDhital, B., & Rodríguez-Bravo, V. (2023) · Chromosome Research · doi:10.1007/s10577-023-09724-w · Cited by 26
“In this regard, several seminal studies have unveiled that CIN-high tumors instigate chronic inflammatory responses via the cGAS-STING pathway and noncanonical NF-kB activation that mediate invasion and metastasis (Bakhoum and Cantley 2018; Bakhoum et al. 2018).”
BackgroundAneuploidy in human cancer: new tools and perspectives
Lakhani, A. A., Thompson, S. L., & Sheltzer, J. M. (2023) · Trends in Genetics · doi:10.1016/j.tig.2023.09.002 · Cited by 24
Yi, Q., Chen, Q., Yan, H., Zhang, M., Cai, L., Xiang, X., Pan, X., & Wang, F. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.005978 · Cited by 25
“Chromosomal instability resulting from chromosome missegregation during mitosis is a hallmark of cancer cells and contributes to tumorigenesis (1, 2).”
BackgroundCo-Operation between Aneuploidy and Metabolic Changes in Driving Tumorigenesis
Newman, D. L., & Gregory, S. L. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20184611 · Cited by 24
“There are several benefits of CIN for tumours: it varies them over time [54], contributing significantly to their chance of becoming metastatic [55] and resistant to chemotherapy [56,57].”
BackgroundTherapeutic Interventions Targeting Innate Immune Receptors: A Balancing Act
Cao, X., Cordova, A. F., & Li, L. (2021) · Chemical Reviews · doi:10.1021/acs.chemrev.1c00716 · Cited by 24
Lu, Y., Zhao, M., Chen, L., Wang, Y., Liu, T., & Liu, H. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1380517 · Cited by 25
“As the canonical PRR, cGAS is activated by endogenous and exogenous DNA, including invaded pathogens DNA, mitochondrial DNA, MNi DNA, genomic DNA, etc (7, 8).”
BackgroundInfluentialRole of PRMT1 and PRMT5 in Breast Cancer
Martinez, S., Sentis, S., Poulard, C., Trédan, O., & Romancer, M. L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25168854 · Cited by 25
“Therapies that disrupt DNA damage repair to elevate cytosolic DNA levels synergize with anti-tumor immunotherapy by activating the cGAS pathway [107]. cGAS is a cytosolic DNA sensor that activates the type I interferon pathway and promotes tumor metastasis in breast cancer [108,109].”
BackgroundThe cGAS‒STING pathway in colorectal cancer: bridging innate immunity and therapeutic strategies
Li, W., Dong, G.-H., Bi, Y., Han, Y.-Y., Sun, L., Wang, T., Lin, Z., & Ren, X.-S. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-025-03544-y · Cited by 27
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“Discussion DNA damage–induced genome instability is a hallmark of malignantdiseases (30), andmaypromote tumormetastasis (31).”
BackgroundNuclear AIM2‐Like Receptors Drive Genotoxic Tissue Injury by Inhibiting DNA Repair
Jiang, H., Swacha, P., & Gekara, N. O. (2021) · Advanced Science · doi:10.1002/advs.202102534 · Cited by 22
cGAS-STING signalings potentiate tumor progression via sustaining cancer stemness
Liu, F.-R., Jiang, M., Mei, Z., Lin, C.-J., & Tian, L. (2022) · Translational Oncology · doi:10.1016/j.tranon.2022.101404 · Cited by 24
Kuang, X., & Li, J. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.895961 · Cited by 23
“Beyond inhibition of the type I interferon response, activation of the cGAS-STING pathway alternatively induces other inflammatory pathways, including noncanonical NF-kB (25).”
BackgroundInfluentialKim, J. C., Liu, X., Fitzgerald, K., Eng, J. S., Orf, J., O’Brien, S. A., Belmontes, B., Casbon, A.-J., Novitskiy, S. V., Tarbell, K. V., et al. (2023) · Cancer Immunology, Immunotherapy · doi:10.1007/s00262-022-03327-w · Cited by 22
“While the upstream signals responsible for constitutive STING activation in MC38 cells are unclear, pathways such as genomic instability [17], activation of endogenous viral elements [18], defects in endogenous nucleic acid degradation [19], or deregulation of STING itself [20] have been implicated in STING activation.”
BackgroundMoutafi, M. K., Koliou, G.-A., Papaxoinis, G., Economopoulou, P., Kotsantis, I., Gkotzamanidou, M. A., Anastasiou, Μ., Pectasides, D. G., Kyrodimos, E., Delides, A., et al. (2023) · Cancer Research Communications · doi:10.1158/2767-9764.crc-23-0051 · Cited by 27
The Killer’s Web: Interconnection between Inflammation, Epigenetics and Nutrition in Cancer
Mecca, M., Picerno, S., & Cortellino, S. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25052750 · Cited by 24
“Recently, it has been discovered that the genetic instability of tumor cells induces an inflammatory response due to the release of nuclear DNA into the cytoplasm, caused by DNA repair defects [2,3].”
BackgroundTargeting STING signaling for the optimal cancer immunotherapy
Xu, Y., & Xiong, Y. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1482738 · Cited by 24
Motile ciliogenesis and the mitotic prism
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“collect the STING-cGAMP complexes (3).”
Context-dependent impact of type I interferon signaling in cancer
Ruiz-Iglesias, A., Guilbaud, E., Galluzzi, L., & Mañes, S. (2025) · Molecular Cancer · doi:10.1186/s12943-025-02495-4 · Cited by 25
“One major driver of type I IFN responses in malignant cells is chromosomal instability (CIN), a metastable genomic state associated with the accumulation of inter-ferogenic micronuclei and cytosolic DNA fragments activating CGAS [105].”
Li, Z. Y., Zheng, W., Liu, Y., Cao, R., Wei, J., & Jia, H. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-025-03555-9 · Cited by 22
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Liquid–Liquid Phase Separation in Cancer Signaling, Metabolism and Anticancer Therapy
Igelmann, S., Lessard, F., & Ferbeyre, G. (2022) · Cancers · doi:10.3390/cancers14071830 · Cited by 22
“However, many tumors express high levels of genes in the cGAS/STING pathway [44,45].”
BackgroundSpecies-specific self-DNA detection mechanisms by mammalian cyclic GMP-AMP synthases
Mosallanejad, K., Kennedy, S. N., Bahleda, K. M., Slavik, K. M., Zhou, W., Govande, A. A., Hancks, D. C., Kranzusch, P. J., & Kagan, J. C. (2023) · Science Immunology · doi:10.1126/sciimmunol.abp9765 · Cited by 21
Jiang, H., Kong, N., Liu, Z., West, S. C., & Chan, Y. W. (2023) · Advanced Science · doi:10.1002/advs.202204388 · Cited by 22
Biomaterial-enabled therapeutic modulation of cGAS-STING signaling for enhancing antitumor immunity
Liu, Y., Yang, F., Wang, X., Yang, B., Li, M., & Luo, Z. Y. (2023) · Molecular Therapy · doi:10.1016/j.ymthe.2023.03.026 · Cited by 24
Super-enhancer-associated gene CAPG promotes AML progression
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“[30] from epithelial– esenchymal transition (EMT)/ igration/metastasis genes that were upregulated in the metastatic subpopulation of chro oso ally unstable cancer cells.”
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RetractedChronic chromosome instability induced by Plk1 results in immune suppression in breast cancer
Kandala, S., Ramos, M., von Voithenberg, L. V., Diaz-Jimenez, A., Chocarro, S., Keding, J., Brors, B., Imbusch, C. D., & Sotillo, R. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.113266 · Cited by 25
Liver Metastasis in Cancer: Molecular Mechanisms and Management
Xu, W., Xu, J., Liu, J., Wang, N., Zhou, L., & Guo, J. (2025) · MedComm · doi:10.1002/mco2.70119 · Cited by 26
Karyotype Aberrations in Action: The Evolution of Cancer Genomes and the Tumor Microenvironment
Baudoin, N. C., & Bloomfield, M. (2021) · Genes · doi:10.3390/genes12040558 · Cited by 20
An immune-related signature that to improve prognosis prediction of breast cancer.
Zhang, Y., Di, X., Chen, G., Liu, J., Zhang, B., Feng, L., Cheng, S., & Wang, Y. (2021) · PubMed Central · Cited by 20
Pathophysiological Roles of the cGAS-STING Inflammatory Pathway
Maekawa, H., Fain, M. E., & Wasano, K. (2023) · Physiology · doi:10.1152/physiol.00031.2022 · Cited by 21
Molecular subtyping in colorectal cancer: A bridge to personalized therapy (Review)
Wang, C., Zhang, H., Liu, Y., Wang, Y., Hu, H., & Wang, G. (2023) · Oncology Letters · doi:10.3892/ol.2023.13816 · Cited by 22
Recent trends in STING modulators: Structures, mechanisms, and therapeutic potential
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“The cGAS – STING pathway would be the fi rst candidate to explain the functional interactions of TAK-931-induced RS and/or CIN with in fl ammatory signaling, since the cGAS-STING pathway plays an important role in the cytosolic DNA-sensing machinery to activate the innate immune pathway 54 – 56 .”
BackgroundPlavc, G., & Strojan, P. (2020) · Radiology and Oncology · doi:10.2478/raon-2020-0060 · Cited by 20
Wang, W., Fu, R., Gao, R., Luo, L., Wang, Z., Xue, Y., Sun, J., Pan, M., Hong, M., Qiao, L., et al. (2024) · ACS Biomaterials Science & Engineering · doi:10.1021/acsbiomaterials.3c01665 · Cited by 20
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“Recently, it was discovered that chromosome segregation errors as well as replication stress activate the anti-viral immune cGAS-STING pathway, which responds to genomic double-stranded DNA in the cytosol [2,23].”
BackgroundEWSR1 maintains centromere identity
Kitagawa, R., Niikura, Y., Becker, A., Houghton, P. J., & Kitagawa, K. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112568 · Cited by 24
Chromosomal instability-induced cell invasion through caspase-driven DNA damage
Barrio, L., Gaspar, A.-E., Muzzopappa, M., Ghosh, K., Romão, D., Clemente‐Ruiz, M., & Milán, M. (2023) · Current Biology · doi:10.1016/j.cub.2023.09.004 · Cited by 21
GAS-STING: a classical DNA recognition pathways to tumor therapy
Wang, X., Lin, M., Zhu, L., & Ye, Z. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1200245 · Cited by 22
“However, persistent activation of cGAS-STING led to a reduction in type I IFNs production and an increase in atypical NF-k B signaling in tumor cells with chromosomal instability (147).”
BackgroundMulti-scale characterisation of homologous recombination deficiency in breast cancer
Jacobson, D. H., Shi, P., Fisher, J., & Secrier, M. (2023) · Genome Medicine · doi:10.1186/s13073-023-01239-7 · Cited by 18
“LGALS9 has previously been associated with antimetastatic potential in breast cancer [107], potentially indicating a compensation for increased chromosomal instabilility which may drive metastasis [108].”
BackgroundKushwah, A. S., Masood, S., Mishra, R., & Banerjee, M. (2023) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2023.104240 · Cited by 22
Mistriotis, P., Wisniewski, E. O., Bishwa, R., Kaláb, P., & Κωνσταντόπουλος, Κ. (2024) · Trends in Cell Biology · doi:10.1016/j.tcb.2024.01.001 · Cited by 18
Therapeutic landscape in systemic lupus erythematosus: mtDNA activation of the cGAS-STING pathway
Gu, X., Chen, Y., Cao, K., Tu, M., Liu, W., & Ju, J. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.112114 · Cited by 24
Untangling the evolutionary roots of lung cancer
Devarakonda, S. H. K., & Govindan, R. (2019) · Nature Communications · doi:10.1038/s41467-019-10879-6 · Cited by 18
How Cells Handle DNA Breaks during Mitosis: Detection, Signaling, Repair, and Fate Choice
Thompson, R. H., Gatenby, R., & Sidi, S. (2019) · Cells · doi:10.3390/cells8091049 · Cited by 19
“Interestingly, overexpression of Mad2 was found to partially rescue this phenotype [69].”
BackgroundAlam, M., Ansari, M. M., Noor, S., Mohammad, T., Hasan, G. M., Kazim, S. N., & Hassan, M. I. (2022) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2022.03.157 · Cited by 21
Yang, H., Xia, Y., Ma, Y., Gao, M., Hou, S., Xu, S., & Wang, Y. (2024) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-24-00015 · Cited by 24
“Furthermore, non-canonical NF-κB responses may be induced by stimulating the cGAS-STING pathway, which in turn promotes the nuclear translocation of p52-RELB (p52-REL proto-oncogene, NF-κB subunit) (Bakhoum et al., 2018; Hou et al., 2018).”
Zheng, C., Chen, Y., He, T., Ye, X., Xu, D., Wang, X., Wen, X., Li, C., Yao, Q., Chen, S., et al. (2024) · Molecular Medicine · doi:10.1186/s10020-024-00924-6 · Cited by 21
“In addition, STING activates the NF-κB pathway and induces the expression of genes such as TNF-α and IL-6 (Bakhoum et al. 2018).”
BackgroundNuclear PD-L1 triggers tumour-associated inflammation upon DNA damage
Nihira, N. T., Wu, W., Hosoi, M., Togashi, Y., Sunada, S., Miyoshi, Y., Miki, Y., & Ohta, T. (2025) · EMBO Reports · doi:10.1038/s44319-024-00354-9 · Cited by 20
Li, X., Xu, S., Su, Z., Shao, Z., & Huang, X. (2025) · ACS Omega · doi:10.1021/acsomega.4c10865 · Cited by 23
Genomics and precision surgery for head and neck squamous cell carcinoma
Galmiche, A., Saidak, Z., Bouaoud, J., Mirghani, H., Page, C., Dakpé, S., & Clatot, F. (2020) · Cancer Letters · doi:10.1016/j.canlet.2020.04.004 · Cited by 18
SWAN pathway-network identification of common aneuploidy-based oncogenic drivers
Bowers, R. R., Jones, C. M., Paz, E. A., Barrows, J. K., Armeson, K. E., Long, D. T., & Delaney, J. R. (2022) · Nucleic Acids Research · doi:10.1093/nar/gkac200 · Cited by 18
“However, in some cancer cells this pathway was found to be attenuated by an unknown mechanism (76), allowing for cell survival and increased metastasis.”
BackgroundDu, Y., Luo, Y., Hu, Z., Lu, J., Liu, X., Xing, C., Wu, J., Duan, T., Chu, J., Wang, H. Y., et al. (2022) · Advanced Science · doi:10.1002/advs.202103701 · Cited by 18
Emerging Perspectives of Bone Metastasis in Hepatocellular Carcinoma
Yuan, X., Zhuang, M., Zhu, X., Cheng, D., Liu, J., Sun, D., Qiu, X., Lu, Y., & Sartorius, K. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.943866 · Cited by 18
Patil, S., Deshpande, S., & Sengupta, K. (2022) · Human Molecular Genetics · doi:10.1093/hmg/ddac235 · Cited by 18
The second half of mitosis and its implications in cancer biology
Moreno-Andrés, D., Holl, K., & Antonin, W. (2022) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2022.11.013 · Cited by 22
Kumar, S., Zhao, J., Talluri, S., Buon, L., Mu, S., Potluri, L. B., Liao, C., Shi, J., Chakraborty, C., Gonzalez, G. B., et al. (2023) · Gastroenterology · doi:10.1053/j.gastro.2023.04.035 · Cited by 18
Classen, S., Petersen, C., & Borgmann, K. (2023) · Strahlentherapie und Onkologie · doi:10.1007/s00066-023-02103-8 · Cited by 19
“However, also immunosuppressive and tumorigenesis-favoring effects, including promotion of metastasis formation, have been observed [16, 17] and discussed detailed in Sect.”
BackgroundWang, D., Yan, K. H., Yu, H., Li, H., Zhou, W., Hong, Y., Guo, S., Wang, Y., Xu, C., Pan, C., et al. (2023) · Cancer Research · doi:10.1158/0008-5472.can-23-0394 · Cited by 18
Stimulating STING for cancer therapy: Taking the extracellular route
Li, L. (2024) · Cell chemical biology · doi:10.1016/j.chembiol.2024.04.004 · Cited by 20
Genomic loss of heterozygosity and survival in the REAL3 trial
Smyth, E. C., Cafferkey, C., Loehr, A., Waddell, T. K., Begum, R., Peckitt, C., Harding, T. C., Nguyen, M., Okines, A. F. C., Raponi, M., et al. (2018) · Oncotarget · doi:10.18632/oncotarget.26336 · Cited by 18
“Recent seminal work has demonstrated that chromosomal instability drives metastasis independently of aneuploidy and has described increased levels chromosomal instability in a cohort of matched primary tumour and brain metastases, in addition to a series of matched breast cancer primaries and metastases [32].”
BackgroundEssers, P., van der Heijden, M., Verhagen, C. V. M., Ploeg, E. M., de Roest, R. H., Leemans, C. R., Brakenhoff, R. H., van den Brekel, M. W. M., Bartelink, H. G. M. M., Verheij, M., et al. (2019) · Cancer Research · doi:10.1158/0008-5472.can-18-3388 · Cited by 17
“In line with such 131 an influence, a recent study highlights the association between chromosomal instability and 132 lymph node status in HNSCC (25).”
BackgroundResultInfluentialSPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
Lazar, I., Fabre, B., Feng, Y., Khateb, A., Turko, P., Gómez, J. M. M., Frederick, D. T., Levesque, M. P., Feld, L., Zhang, G., et al. (2020) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-20-0291 · Cited by 17
“However, activation of these pathways is also linked with the propensity to metastasize (16).”
BackgroundTian, J., Lu, Z., Niu, S., Zhang, S., Ying, P., Wang, L., Zhang, M., Cai, Y., Dong, T., Zhu, Y., et al. (2021) · Clinical and Translational Medicine · doi:10.1002/ctm2.485 · Cited by 18
Advances in Vaccine-Based Therapies for Pancreatic Cancer
McMillan, M. T., & Soares, K. C. (2025) · Journal of Gastrointestinal Cancer · doi:10.1007/s12029-025-01165-4 · Cited by 19
“This likely explains the increased rates of metastasis and poor overall survival observed with CIN-high tumors [60–62], including PDAC [63–65].”
Regulation of the Cell-Intrinsic DNA Damage Response by the Innate Immune Machinery
Hayman, T. J., & Glazer, P. M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222312761 · Cited by 19
“However, it is worth noting that there have been several lines of evidence that suggest that chronic activation of SASP or cGAS–STING signaling leads to a phenotype of immunosuppression, increased tumor progression, and metastasis [55,63,93,97].”
BackgroundA small-molecule inhibitor and degrader of the RNF5 ubiquitin ligase
Ruan, J., Liang, D., Yan, W., Zhong, Y., Talley, D. C., Rai, G., Tao, D., LeClair, C. A., Simeonov, A. M., Zhang, Y., et al. (2022) · Molecular Biology of the Cell · doi:10.1091/mbc.e22-06-0233 · Cited by 19
“However, some studies have reported that activation of the cGAS-cGAMPSTING pathway by chromosomal instability can conversely drive metastasis (Bakhoum and Cantley, 2018; Bakhoum et al., 2018).”
BackgroundLv, J., Xing, C., Chen, Y., Bian, H., Lv, N., Wang, Z., Liu, M., & Su, L. (2022) · Pharmaceuticals · doi:10.3390/ph15101241 · Cited by 17
Chromosomal Instability as Enabling Feature and Central Hallmark of Breast Cancer
Castellanos, G., Valbuena, D. S., Pérez, E., Villegas, V. E., & Rondón‐Lagos, M. (2023) · Breast Cancer Targets and Therapy · doi:10.2147/bctt.s383759 · Cited by 22
“In fact, in vivo studies in cancer showed that CIN promoted chronic inflammatory signaling through cGAS/STING and caused aggressive metastatic tumor growth.(121) Additionally, in cancer-related inflammation, the induction of CIN by inflammatory mediators, has been suggested as an additional mechanism involved in this…”
BackgroundLi, J., Yang, F., Wang, Z., Zheng, S., Zhang, S., Wang, C., He, B., Wang, J., & Wang, H. (2023) · Cell Proliferation · doi:10.1111/cpr.13590 · Cited by 17
The Role of the Toll-like Receptor 2 and the cGAS-STING Pathways in Breast Cancer: Friends or Foes?
Cossu, C., Lorenzo, A. D., Fiorilla, I., Todesco, A. M., Audrito, V., & Conti, L. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms25010456 · Cited by 19
“Persistent activation of cGAS-STING signaling has been observed in different tumor types with high levels of CIN, including breast cancer, resulting in tumor progression, invasion, and metastasis formation [75,77] through both cell-intrinsic and cell extrinsic mechanisms.”
BackgroundMa, X., Chen, M.-M., & Meng, L. (2024) · Acta Pharmacologica Sinica · doi:10.1038/s41401-023-01210-7 · Cited by 21
“…could trigger non-canonical NF-κ B signaling instead of canonical NF-κ B or type I IFN signaling, as evidenced by up-regulation of p52 and phosphorylated p100, along with decreased expression of NF receptor-associated factor 2 (TRAF2), an inhibitor of non-canonical NF-κ B pathway [8, 50].”
Ecto-nucleotide pyrophosphatase/phosphodiesterase 1 inhibitors: Research progress and prospects
Guan, D., Fang, L., Feng, M., Guo, S., Xie, L., Chen, C., Sun, X., Wu, Q., Yuan, X., Xie, Z., et al. (2024) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2024.116211 · Cited by 24
Chen, S., Zhang, D., Du, Y., Shi, J., Gu, S., Zhou, X., Yu, H., Wang, F., Chen, J., & Cui, H. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-07290-5 · Cited by 17
“There are potential interactions between IRF3 and components of the NF-κ B signaling pathway [18, 19], which provide an in fl ammatory tumor micro-environment promoting tumor survival and metastasis [20].”
Xu, L., Qu, J., Song, N., Zhang, L., Zeng, X. Q., Che, X., Hou, K., Shi, S., Feng, Z., Qu, X., et al. (2020) · Oncology Reports · doi:10.3892/or.2020.7812 · Cited by 19
“Therefore, metastasis is the key challenge to overcome in patients with TNBC. Recent findings demonstrated that genomic instability is a driver of metastasis, particularly in TNBC (4,5).”
The head and neck cancer genome in the era of immunotherapy
Wijetunga, N. A., Yu, Y., Morris, L. G. T., Lee, N. Y., & Riaz, N. (2020) · Oral Oncology · doi:10.1016/j.oraloncology.2020.105040 · Cited by 17
Self-citationMechanisms of Immune Modulation by Radiation
Spina, C. S., & Drake, C. G. (2021) · Seminars in Radiation Oncology · doi:10.1016/j.semradonc.2021.02.001 · Cited by 17
DNA Damage Response Evaluation Provides Novel Insights for Personalized Immunotherapy in Glioma
Chen, M., Huang, B., Zhu, L., Wang, Q., Pang, Y. K., Cheng, M., Lian, H., Liu, M., Zhao, K., Xu, S., et al. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.875648 · Cited by 17
“Additionally, chronic activation of the cGAS-STING pathway has been found to drive tumor metastasis and cancer progression (44), which may partly elucidate the high malignancy and poor survival of patients with increased DDR scores.”
BackgroundThe cGAS-STING signaling pathway is modulated by urolithin A
Madsen, H. B., Park, J. H., Chu, X., Hou, Y., Li, Z., Rasmussen, L. J., Croteau, D. L., Bohr, V. A., & Akbari, M. (2023) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2023.111897 · Cited by 16
“…pathway in different stages of cancer progression (Bakhoum et al., 2018; Hong et al., 2022), it is necessary to further investigate the effects of UA treatment on cancer progression in appropriate mouse models of human cancer with chromosomal instability (Bakhoum et al., 2018; Li et al., 2021a).”
InfluentialTowards understanding cancer dormancy over strategic hitching up mechanisms to technologies
Yang, S., Seo, J., Choi, J., Kim, S.-H., Kuk, Y., Park, K. C., Kang, M., Byun, S., & Joo, J. (2025) · Molecular Cancer · doi:10.1186/s12943-025-02250-9 · Cited by 20
Zhao, K., Vos, J. L., Lam, S. Z., Boe, L. A., Muldoon, D. M., Han, C. Y., Valero, C., Lee, M., Fitzgerald, C. W. R., Lee, A. S., et al. (2025) · Nature Genetics · doi:10.1038/s41588-025-02204-3 · Cited by 17
“These immunological consequences, together with the increase in intratumoral heterogeneity 19–21 and metastatic potential 22–24 , may in part explain why CNA is more selected for than mutagenesis during the metastatic process.”
Cao, L., Li, W., Li, Z., Wei, X., Ding, J., Zhou, C., Chen, X., Huang, Z., Shao, Z., Shen, J., et al. (2025) · Science Immunology · doi:10.1126/sciimmunol.adn1630 · Cited by 20
DNA Damage Response Inhibitors in Cholangiocarcinoma: Current Progress and Perspectives
Geyik, Ö. G., Anichini, G., Ulukaya, E., Marra, F., & Raggi, C. (2022) · Cells · doi:10.3390/cells11091463 · Cited by 18
The senescence-associated secretory phenotype in ovarian cancer dissemination
Veenstra, J. P., Bittencourt, L. F. F., & Aird, K. M. (2022) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00049.2022 · Cited by 20
Targeting protein kinases benefits cancer immunotherapy
Zhang, Z., Bu, L., Luo, J., & Guo, J. (2022) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2022.188738 · Cited by 18
Li, L., Yuan, Q., Chu, Y.-M., Jiang, H., Zhao, J., Su, Q., Huo, D., & Zhang, X. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1106638 · Cited by 16
“Numerous studies have shown that abnormal centromere function can lead to abnormal chromosome segregation, thereby promoting tumor development (Daniela et al., 2001; Goncalves Dos Santos Silva et al., 2008; Thompson and Compton, 2008; Turajlic and Swanton, 2016; Jamal-Hanjani et al., 2017; Bakhoum et al., 2018).”
BackgroundWithers, S. S., Moeller, C. E., Quick, C. N., Liu, C., Baham, S. M., Looper, J., Subramanian, R., & Kousoulas, K. G. (2023) · PLoS ONE · doi:10.1371/journal.pone.0284645 · Cited by 22
“The mechanism of STING downregulation in OSA cells was not evaluated in this study; however, prior reports describe epigenetic silencing, increased STING degradation, cGAMP hydrolysis, altered post-translational modifications, and inhibition of STING signalosome assembly [29, 36, 37].”
Background
Metadata
- Authors
- Bakhoum, S. F., Ngo, B., Laughney, A. M., Cavallo, J.-A., Murphy, C. J., Ly, P., Shah, P., Sriram, R. K., Watkins, T. B. K., Taunk, N. K., Duran, M., Pauli, C., Shaw, C., Chadalavada, K., Rajasekhar, V. K., Genovese, G., Venkatesan, S., Birkbak, N. J., McGranahan, N., Lundquist, M., LaPlant, Q., Healey, J. H., Elemento, O., Chung, C. H., Lee, N. Y., Imielenski, M., Nanjangud, G., Pe’er, D., Cleveland, D. W., Powell, S. N., Lammerding, J., Swanton, C., & Cantley, L. C.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Weill Cornell Medicine (US)
- University of California San Diego (US)
- Cornell University (US)
- The Francis Crick Institute (GB)
- University Hospital Zurich (CH)
- Broad Institute (US)
- University College London (GB)
- Moffitt Cancer Center (US)
- Corresponding author
- Cantley, Lewis C.
- ORCID
- Bakhoum, Samuel F.
- Ngo, Bryan
- Laughney, Ashley M.
- Murphy, Charles J.
- Ly, Peter
- Shah, Pragya
- Watkins, Thomas B. K.
- Taunk, Neil K.
- Pauli, Chantal
- Chadalavada, Kalyani
- Rajasekhar, Vinagolu K.
- Genovese, Giulio
- Venkatesan, Subramanian
- Birkbak, Nicolai J.
- McGranahan, Nicholas
- Lundquist, Mark
- LaPlant, Quincey
- Healey, John H.
- Elemento, Olivier
- Chung, Christine H.
- Lee, Nancy Y.
- Nanjangud, Gouri
- Pe’er, Dana
- Cleveland, Don W.
- Powell, Simon N.
- Lammerding, Jan
- Swanton, Charles
- Cantley, Lewis C.
- Venue
- Nature
- Published
- 2018-01-17
- Volume
- 553
- Issue
- 7689
- Pages
- 467-472
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC5785464
- OpenAlex
- W2783667606
- Cited by
- 1,593
- References
- 59
- Citations by year
- 2026: 215 · 2025: 213 · 2024: 223 · 2023: 216 · 2022: 190 · 2021: 203 · 2020: 149 · 2019: 105 · 2018: 76
- FWCI
- 55.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- National Science Foundation (1254846, CA008748, 1257284)
- Breast Cancer Research Foundation (CA008748)
- Elsa U. Pardee Foundation
- Memorial Sloan-Kettering Cancer Center (CA008748, P30 CA008748)
- Johns Hopkins University
- Francis Crick Institute (10169)
- Gray Foundation
- Cancer Research UK (20466, 19310, 17786)
- Rosetrees Trust (M231-CD1)
- National Institutes of Health (NIH-R01, W81XWH)
- Medical Research Council (MR/P014712/1)
- National Heart, Lung, and Blood Institute (R01HL082792)
- National Cancer Institute (R01CA169306, U54CA210184, R01CA187069, K99CA218871, P30CA008748, R35CA197588)
- National Institute of General Medical Sciences (R35GM122476)
- Division of Chemical, Bioengineering, Environmental, and Transport Systems (CBET-1254846)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- chromosomal instability, metastasis, cytosolic DNA sensing, cGAS-STING pathway, micronuclei, chromosome segregation errors, NF-κB signaling, innate immunity, tumor inflammation, aneuploidy, tumor invasion
- MeSH terms
- STING Protein, Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase, Animals, Brain Neoplasms, Breast Neoplasms, Carcinoma, Squamous Cell, Cell Line, Cytosol, DNA, Neoplasm, Female, Head and Neck Neoplasms, Humans, Inflammation, Membrane Proteins, Mesoderm, Neoplasm Metastasis, Nucleotidyltransferases, NF-kappa B, Chromosome Segregation, Xenograft Model Antitumor Assays, Chromosomal Instability, Micronuclei, Chromosome-Defective, Mice
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