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.
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In the paper
“Diploid controls were used to determine false positive rate of the centromeric probes.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
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In the paper
“Investigators were not blinded to group allocation.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Animal studies
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In the paper
“All cells tested negative for mycoplasma.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Cell culture
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“ongoing chromosome missegregation is required to replenish cytosolic DNA pools and to maintain cells in a pro-metastatic state.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > DISCUSSION
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In the paper
“For each probe, three normal peripheral blood samples (GM07535, GM06875 and GM00558), obtained from Coriell Institute (Camden, New Jersey) were also analyzed to derive cut-off values (false-positive).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Fluorescence in situ hybridization (FISH) analysis
Strength:plain· not yet calibratedn = 3Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CIN promotes formation and maintenance of metastasis”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
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In the paper
“For each sample a minimum of 20 inverted DAPI-stained metaphases were fully karyotyped and analyzed according to the International System of Human Cytogenetic Nomenclature (ISCN) 2013.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Single-cell karyotyping
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 701–800 of 1,551
Kim, J., Pena, J., McQueen, H. P., Kong, L., Michael, D., Lomashvili, E. M., & Cook, P. R. (2023) · Cancer Gene Therapy · doi:10.1038/s41417-023-00678-z · Cited by 17
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“By activating pro-tumour inflammatory signalling pathways, CIN promotes an inflammatory microenvironment that supports tumour growth and cancer cell survival [4,32].”
BackgroundInfluentialAneuploid embryonic stem cells drive teratoma metastasis
Xiao, R., Xu, D., Zhang, M., Chen, Z., Cheng, L., Du, S., Lu, M., Zhou, T., Li, R., Bai, F., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-45265-4 · Cited by 19
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Mechanical stress during confined migration causes aberrant mitoses and c-MYC amplification
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“This is evidenced by the enhanced CIN observed in circulating tumor cells and metastases compared to primary tumors (35–39).”
BackgroundCui, L., Xu, X. H., Fan, H., Wan, X., Chen, Q., Zhang, J., Tao, C., Du, Z., Wang, S., Zhang, J., et al. (2024) · Cancer Letters · doi:10.1016/j.canlet.2024.217183 · Cited by 17
Cancer knocks you out by fasting: Cachexia as a consequence of metabolic alterations in cancer
Cortellino, S., D’Angelo, M., Quintiliani, M., & Giordano, A. (2024) · Journal of Cellular Physiology · doi:10.1002/jcp.31417 · Cited by 18
“Tumor cells and anticancer therapies can trigger chronic inflammation through cGAS ‐ STING pathway activation, leading to TNF ‐ α and inflammatory cytokines secretion (Bakhoum et al., 2018; Mecca et al., 2024).”
ATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage
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Expanding the Role of STING in Cellular Homeostasis and Transformation
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“These results shed light on the apparently paradoxical roles of the cGAS–STING pathway in cancer [8,9,4,7,11-14].”
BackgroundInfluentialSelf-citationModelling chromosome structural and copy number changes to understand cancer genomes
Kneissig, M., Bernhard, S. V., & Štorchová, Z. (2019) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2019.02.005 · Cited by 15
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“Recent studies also point to a potential role of chronic activation of cytosolic DNA sensing pathways in promoting metastases (33) and suppressing HR-mediated DNA repair (34).”
BackgroundIncreased chromosomal instability characterizes metastatic renal cell carcinoma
Ma, Q., Wang, J., Qi, J., Ding, P., Guan, B., Zhang, J., Li, Z., Zhang, H., Li, T., Shi, Y. X., et al. (2020) · Translational Oncology · doi:10.1016/j.tranon.2020.100929 · Cited by 16
The Role of Non-Coding RNAs in Chromosomal Instability in Cancer
Mohapatra, S., Winkle, M., Ton, A. N., Nguyen, D., & Călin, G. A. (2022) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.122.001357 · Cited by 17
“In addition, it was shown that overexpression of AKT1 (AKT Serine/Threonine Kinase 1), a positive upstream regulator of miR-22, reduced homologous recombination via miR22 mediated suppression of MDC1 (Lee, Park et al. 2015).”
BackgroundThe genetic script of metastasis
Jinesh, G. G., & Brohl, A. S. (2019) · Biological reviews/Biological reviews of the Cambridge Philosophical Society · doi:10.1111/brv.12562 · Cited by 16
“At the genetic level, metastasis is driven by cancer stem cells that display augmented genomic instability (Jinesh & Kamat, 2017b; Bakhoum et al., 2018; Seton-Rogers, 2018), at the metabolic level they display efficient glycolysis (Zhang et al., 2017a), at the immune level they evade phagocytosis…”
BackgroundZhao, X., Liu, B., William, W. N., Tsanov, K. M., Ho, Y.-J., Barriga, F. M., Lim, R. J., Trifas, M., Khandekar, A., Du, Y., et al. (2024) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2024.12.020 · Cited by 19
At the nucleus of cancer: how the nuclear envelope controls tumor progression
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Mechanisms of genome instability from cellular folate stress
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Organelle-specific signaling of cGAS–STING
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The fate of extra centrosomes in newly formed tetraploid cells: should I stay, or should I go?
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“There is evidence micronucleus instability can cause punctuated bursts of numerical and structural chromosomal alterations within a few cell divisions and promote inflammation, epithelial-tomesenchymal transition, and metastasis (Mackenzie et al., 2017; Bakhoum et al., 2018; Umbreit et al., 2020), but we are still lea…”
BackgroundRefphase: Multi-sample phasing reveals haplotype-specific copy number heterogeneity
Watkins, T. B. K., Colliver, E., Huska, M. R., Kaufmann, T. L., Lim, E. L., Duncan, C. B., Haase, K., Loo, P. V., Swanton, C., McGranahan, N., et al. (2023) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1011379 · Cited by 17
Self-citationMolecular Landscape and Clinical Implication of CCNE1- amplified Esophagogastric Cancer
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“35,60,61 No treatment information is available in MSK-MET.”
STING‐Activating Small Molecular Therapeutics for Cancer Immunotherapy
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Magkouta, S., Pappas, A., Vaitsi, P. C., Agioutantis, P. C., Pateras, I. S., Moschos, C., Iliopoulou, M. P., Kosti, C., Loutrari, H. V., Gorgoulis, V. G., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.134885 · Cited by 15
“This finding adds to emerging recent evidence on the role of secreted and cytosolic DNA in tumor progression and metastasis (27, 28).”
BackgroundYoshioka, K., & Matsuno, Y. (2020) · Cancer Science · doi:10.1111/cas.14746 · Cited by 15
KNTC1 knockdown suppresses cell proliferation of colon cancer
Zhengxiang, Z., Tao, Y., Zhiping, L., et al. (2021) · 3 Biotech · doi:10.1007/s13205-021-02800-0 · Cited by 15
Epigenetic Dysregulation Induces Translocation of Histone H3 into Cytoplasm
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STING Signaling and Skin Cancers
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“INTRODUCTION Chromosome instability (CIN), generated from increased chromosome missegregation in mitosis, is a driving force of human cancer and is, often correlated with poor prognosis, metastasis, and therapeutic resistance in various cancers [1, 2].”
Physical Forces and Transient Nuclear Envelope Rupture during Metastasis: The Key for Success?
Gauthier, B. R., Lorenzo, P. I., & Comaills, V. (2021) · Cancers · doi:10.3390/cancers14010083 · Cited by 15
“Using a mouse model, Bakhoum and coworkers showed that highly genetically unstable cancer cells with high chromosomal instability and an activated cGAS/STING pathway are more prone to form metastases than cancer cells with a more stable genome that do not activate the cGAS/STING pathway [65].”
BackgroundInfluentialZhang, N., Shang, M., Li, H., Wu, L., Dong, M., Huang, B., Lü, J., & Zhang, Y. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23073911 · Cited by 17
“Exogenous expression dnMCAK (a promoter of CCF) [38] in the breast cancer cells treated with H3K9me2 and H3K27me3”
BackgroundFOXM1 is critical for the fitness recovery of chromosomally unstable cells
Pan, F., Chocarro, S., Ramos, M. J., Chen, Y., de la Vega, A. A., Somogyi, K., & Sotillo, R. (2023) · Cell Death and Disease · doi:10.1038/s41419-023-05946-2 · Cited by 14
“The identification of specific targets against these bypass mechanisms could provide therapeutic strategies against CIN tumors [6, 7].”
BackgroundBaldi, G. G., Orbach, D. H., Bertulli, R., Magni, C., Sironi, G., Casanova, M., & Ferrari, A. (2019) · Expert Opinion on Emerging Drugs · doi:10.1080/14728214.2019.1591367 · Cited by 14
“Metastasis and outcome in synovial sarcoma are strongly associated with chromosome complexity and genome instability, which is more common in synovial sarcoma of adults than children [23,25].”
BackgroundVoutsadakis, I. A. (2019) · Molecular Diagnosis & Therapy · doi:10.1007/s40291-019-00420-2 · Cited by 15
“Spillage of DNA in the cytosol leads to immune signaling activation through the cGAS/STING/ non-canonical NF-κB pathway [4, 131].”
BackgroundPan-cancer whole genome comparison of primary and metastatic solid tumorsPreprint
Martínez-Jiménez, F., Movasati, A., Brunner, S. R., Nguyen, L., Priestley, P., Cuppen, E. P. J. G., & van Hoeck, A. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.06.17.496528 · Cited by 15
Micronuclei: origins, assays, mechanisms, diseases and treatments
Duan, H., Peng, X., Qin, S., Zhou, Y., Xiao, D., Tao, Y., & Liu, S. (2026) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02538-8 · Cited by 17
FoxM1 insufficiency hyperactivates Ect2–RhoA–mDia1 signaling to drive cancer
Limzerwala, J. F., Jeganathan, K. B., Kloeber, J. A., Davies, B. A., Zhang, C., Sturmlechner, I., Zhong, J., Velasco, R. O. F., Fields, A. P., Yuan, Y., et al. (2020) · Nature Cancer · doi:10.1038/s43018-020-00116-1 · Cited by 15
Liu, M., Chen, M., Huang, J.-M., Liu, Q., Wang, L., Liu, R., Yang, N., Huang, W., & Zhang, W. (2022) · BMC Medical Genomics · doi:10.1186/s12920-022-01410-w · Cited by 14
Cytosolic DNA sensors and glial responses to endogenous DNA
Suptela, A. J., & Marriott, I. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1130172 · Cited by 15
DNA damage repair and cancer immunotherapy
Xiang, Z., Liu, H., & Hu, Y. (2023) · Genome Instability & Disease · doi:10.1007/s42764-023-00098-1 · Cited by 13
Alshebremi, M., Tomchuck, S. L., Myers, J. T., Kingsley, D. T., Eid, S., Abiff, M., Bonner, M., Saab, S. T., Choi, S. H., & Huang, A. Y.-C. (2023) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2022-006608 · Cited by 14
“Detection of cytosolic dsDNA in the context of viral and bacterial infections, 26–29 aging and damaged cells, 30 or cancer, 31–33 is performed by the cytoplasmic DNA sensor, cGAS. cGAS catalyzes the formation of the second messenger cyclic dinucleotide (CDN), 2 ′ 3 ′ -cyclic- GMP-AMP (cGAMP).”
Chromosomal instability and inflammation: a catch-22 for cancer cells
van den Brink, A., Rodríguez, M. F. S. P., & Foijer, F. (2023) · Chromosome Research · doi:10.1007/s10577-023-09730-y · Cited by 17
Lewicky, J. D., Martel, A. L., Gupta, M. R., Roy, R., Rodriguez, G. M., Vanderhyden, B. C., & Le, H. (2023) · Cancers · doi:10.3390/cancers15164127 · Cited by 16
Modeling specific aneuploidies: from karyotype manipulations to biological insights
Truong, M. A., Cané‐Gasull, P., & Lens, S. M. A. (2023) · Chromosome Research · doi:10.1007/s10577-023-09735-7 · Cited by 16
Chen, F., Zhao, D., Huang, Y., Wen, X., & Feng, S. (2023) · Life Sciences · doi:10.1016/j.lfs.2023.122239 · Cited by 15
Pontius, W., Hong, E. S., Faber, Z. J., Gray, J., Peacock, C. D., Bayles, I., Lovrenert, K., Chin, D. H., Gryder, B. E., Bartels, C. F., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-42656-x · Cited by 14
“Excitingly, two of these genes, NFKB2 and RELB , converge at the pathway level, as both are components of non-canonical NFkB signaling - a known driver of metastasis in other chromosomally unstable cancers 24 .”
The yin and yang of chromosomal instability in prostate cancer
Carceles‐Cordon, M., Orme, J. J., Domenech, J. M. D., & Rodríguez-Bravo, V. (2024) · Nature Reviews Urology · doi:10.1038/s41585-023-00845-9 · Cited by 13
“This compendium of genomic alterations consistently detected in patient prostate tumour samples is highly reminiscent of chromosomal instability (CIN — a previously defined but not fully understood pan-cancer driver of tumour aggressiveness, heterogeneity, evolution and metastasis 18–21 ).”
InfluentialBudrewicz, J., & Chavez, S. L. (2024) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2024.1344092 · Cited by 14
Jacobo, M. J., Donnella, H. J., Sobti, S., Kaushik, S., Goga, A., & Bandyopadhyay, S. (2024) · Scientific Reports · doi:10.1038/s41598-024-53999-w · Cited by 13
Wang, S., Zheng, Q.-Y., Hong, W.-F., Tang, B., Hsu, S.-J., Zhang, Y., Zheng, X., Zeng, Z.-C., Gao, C., Ke, A., et al. (2024) · Radiotherapy and Oncology · doi:10.1016/j.radonc.2024.110424 · Cited by 17
O’Donoghue, J. C., & Freeman, F. E. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1403538 · Cited by 15
“Furthermore, this type of cGAS/STING activation is linked to chronic NF-k B activation, driven by chromosomal instability-induced tumour cell-intrinsic micronuclei containing dsDNA (46).”
BackgroundIntegrating model systems and genomic insights to decipher mechanisms of cancer metastasis
Leung, M. M., Swanton, C., & McGranahan, N. (2025) · Nature Reviews Genetics · doi:10.1038/s41576-025-00825-2 · Cited by 15
“It is proposed that chromosomal mis-segregation may lead to the release of DNA into the cytosol of tumour cells, triggering activation of the cGAS–STING innate immune signalling pathway, which leads to an inflammatory response and the promotion of EMT 40 .”
Self-citationHayman, T. J., Bhatia, A. K., Jethwa, K. R., Young, M. R., & Park, H. S.-M. (2021) · Translational Cancer Research · doi:10.21037/tcr-20-2096 · Cited by 13
“It has been shown that chronic STING pathway activation leads to protumorigenic effects by establishing an immunosuppressive microenvironment, thereby promoting therapy resistance and metastasis (71-73).”
BackgroundConnolly, N. P., Galisteo, R., Xu, S., Bar, E. E., Peng, S., Tran, N. L., Ames, H. M., Kim, A. J., Woodworth, G. F., & Winkles, J. A. (2021) · Glia · doi:10.1002/glia.24018 · Cited by 15
“Given the finding that high Fn14 expression in the tumor cells more than TAMs appears to drive the aggressive GBM phenotype observed here, it is possible that Fn14 signaling coordinates some form of myeloid mimicry to enable tumor growth, brain invasion, and immune evasion (Bakhoum et al., 2018).”
BackgroundRecombination-dependent replication: new perspectives from site-specific fork barriers
Carr, A. M., & Lambert, S. (2021) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2021.07.008 · Cited by 14
Yano, S., Akiyama, K., Tsuchiya, R., Kubotani, H., Chiba, T., Nagata, T., & Tsuruta, F. (2021) · Scientific Reports · doi:10.1038/s41598-021-97640-6 · Cited by 12
Zhu, Z., Wang, W., Feng, L., Jordan, T., Li, G., Silverman, S., Qiu, S., Joy, A. A., Chen, C., Hockley, D. L., et al. (2021) · Cell Reports Medicine · doi:10.1016/j.xcrm.2021.100404 · Cited by 15
Role of Base Excision Repair in Innate Immune Cells and Its Relevance for Cancer Therapy
Zhao, S., Habib, S. L., Senejani, A. G., Sebastian, M. M., & Kidane, D. (2022) · Biomedicines · doi:10.3390/biomedicines10030557 · Cited by 14
“Recent work has implicated chromosol instability contribute to inducing innate immune inflammatory pathways [97].”
BackgroundRole of Senescence in Tumorigenesis and Anticancer Therapy
Stoczyńska-Fidelus, E., Węgierska, M., Kierasińska, A., Ciunowicz, D., & Rieske, P. (2022) · Journal of Oncology · doi:10.1155/2022/5969536 · Cited by 15
“As a result of centrosome aberrations, the accumulation of double-stranded DNA (dsDNA) is observed, which induces the cGAS-STING pathway; thus, continuous chromosome segregation errors promote cellular invasion and metastasis in a STING-dependent manner [38, 39].”
BackgroundBochtler, T., Wohlfromm, T., Hielscher, T., et al. (2022) · Genes Chromosomes and Cancer · doi:10.1002/gcc.23047 · Cited by 14
“Accordingly, chromosomal instability has been associated with metastasis, treatment resistance, and poor prognosis in many cancer types.(20,31) On the other hand, an exceedingly”
BackgroundThe multifaceted role of micronuclei in tumour progression: A whole organism perspective.
Guscott, M. A., Saha, A., Maharaj, J., & McClelland, S. E. (2022) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2022.106300 · Cited by 16
Liu, C., Rong, X., Li, X., Gao, N., Qu, L., Peng, Y., Shi, J., Yu, M., Sheng, W., & Zhu, B. (2023) · Sensors and Actuators B Chemical · doi:10.1016/j.snb.2023.133841 · Cited by 14
Decoding Cancer Evolution: Integrating Genetic and Non-Genetic Insights
Ashouri, A., Zhang, C., & Gaiti, F. (2023) · Genes · doi:10.3390/genes14101856 · Cited by 17
Yoshioka, K., Matsuno, Y., Hyodo, M., & Fujimori, H. (2019) · Cancers · doi:10.3390/cancers11111643 · Cited by 14
Yao, M., Wu, Y., Cao, Y., Liu, H., Ma, N., Chai, Y., Zhang, S., Zhang, H., Nong, L., Li, L., et al. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.667920 · Cited by 14
“Detection of the Autophagy Activity in Breast Cancer Cells Recently, it has been revealed that MN formed in MDA-231 cells could trigger SASP activity to promote metastasis and progression (15).”
BackgroundDIAPH1 regulates chromosomal instability of cancer cells by controlling microtubule dynamics
Miao, S., Schäfer, P., Nojszewski, J., et al. (2021) · European Journal of Cell Biology · doi:10.1016/j.ejcb.2021.151156 · Cited by 14
The STING Signaling: A Novel Target for Central Nervous System Diseases
Song, M. S., Ren, J., Zhu, Z., Yi, Z., Wang, C., Liang, L., Tian, J., Mao, G., Mao, G., & Chen, M. (2025) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-025-01550-4 · Cited by 13
“Tumor cells displaying chromosomal instability may chronically activate innate immune pathways to boost invasion and metastasis of cancer cells via disruption of the disruption of epithelial responses to cytosolic DNA (Bakhoum et al. 2018).”
The cGAS-STING axis in kidney disease: mechanisms and therapeutic potential
Li, J., Liu, X., & Feng, H. (2025) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2025.178155 · Cited by 15
Elmetwalli, A. (2025) · Drug Resistance Updates · doi:10.1016/j.drup.2025.101326 · Cited by 16
Wang, L., Zhu, S., Ding, Z., Hong, J., Zheng, L., Sun, J., Tang, Y., Chen, X., Yong, X., Hu, M., et al. (2026) · Journal of Translational Medicine · doi:10.1186/s12967-025-07645-2 · Cited by 16
“At its core, cGAS, a cytosolic DNA sensor, detects double-stranded DNA (dsDNA) originating from diverse sources, including invading pathogens, mitochondrial stress, micronuclei rupture, retroelements, and the chromosomal instability characteristic of malignant cells [1, 7, 21].”
InfluentialAND logic nanoparticle for precision immunotherapy of metastatic cancers
Ye, S., Chen, S., Basava, V. S., Torres, K., Zhao, Y., Huang, G., Chen, M., & Gao, J. (2026) · Nature Nanotechnology · doi:10.1038/s41565-026-02130-3 · Cited by 18
“On the other hand, chronic STING activation was shown to promote tumour progression through inflammation 36,37 .”
Endo, Y., Suzuki, K., Kimura, Y., Tamaki, S., Aizawa, H., Abe, I., Watanabe, F., Kato, T., Saito, M., Futsuhara, K., et al. (2022) · International Journal of Oncology · doi:10.3892/ijo.2022.5351 · Cited by 13
“Bakhoum et al (51) showed that CIN promotes metastasis by sustaining a tumor‑cell autono‑ mous response to cytosolic DNA in breast cancer.”
BackgroundMitotic SENP3 activation couples with cGAS signaling in tumor cells to stimulate anti-tumor immunity
Hu, G., Chen, Y., Yang, X., Wang, Y., He, J., Wang, T., Fan, Q., Deng, L., Tu, J., Tan, H., et al. (2022) · Cell Death and Disease · doi:10.1038/s41419-022-05063-6 · Cited by 14
“Moreover, MN derived from chromosomal instability is also reported to promote inflammation-driven metastasis [21, 22].”
BackgroundWu, Z., Lin, Y., Liu, L.-M., Hou, Y., Qin, W., Zhang, L., Jiang, S., Yang, Q., & Bai, Y. (2022) · Journal of Immunology Research · doi:10.1155/2022/7978042 · Cited by 13
“Moreover, cGAS-STING-dependent DNA-sensing of micro-nuclei in tumor cells can couple chromosome instability to tumor metastasis [32], suggesting a contradictory role for the pathway in cancer biology.”
He, X., Sun, Y., Lu, J., Naz, F., Ma, S., & Liu, J. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1117760 · Cited by 14
Prognostic significance of STING expression in solid tumor: a systematic review and meta-analysis
Kim, Y.-H., Cho, N.-Y., Jin, L., Jin, H. Y., & Kang, G. H. (2023) · Frontiers in Oncology · doi:10.3389/fonc.2023.1244962 · Cited by 13
Tetraploidization Increases the Motility and Invasiveness of Cancer Cells
Jèmaà, M., Daams, R., Charfi, S., Mertens, F., Huber, S. M., & Massoumi, R. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241813926 · Cited by 13
“In addition to the internal biological properties of polyploid cells, intriguing studies have shown that polyploidy is required to maintain cells in a pro-metastatic state by activating the internal immune system and mimicking chronic inflammation, which helps cells spread [8,41] The major impact of this study opens n…”
BackgroundTrafficking and effect of released DNA on cGAS-STING signaling pathway and cardiovascular disease
Zhou, Z., Ouyang, C., Chen, Q., Ren, Z., Guo, X., Lei, M., Liu, C., & Yang, X. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1287130 · Cited by 15
Kirby, T. J., Zahr, H. C., Fong, E. H. H., & Lammerding, J. (2024) · Cell Death Discovery · doi:10.1038/s41420-024-01998-1 · Cited by 14
Self-citationPD-L1 promotes oncolytic virus infection via a metabolic shift that inhibits the type I IFN pathway
Hodgins, J. J., Abou‐Hamad, J., O’Dwyer, C., Hagerman, A., Yakubovich, E., de Souza, C. T., Marotel, M., Buchler, A., Fadel, S., Park, M. M., et al. (2024) · The Journal of Experimental Medicine · doi:10.1084/jem.20221721 · Cited by 19
Menz, A., Zerneke, J., Viehweger, F., Büyücek, Ş., Dum, D., Schlichter, R., Hinsch, A., Bawahab, A. A., Fraune, C., Bernreuther, C., et al. (2024) · Cancers · doi:10.3390/cancers16132425 · Cited by 14
“For example, Bakhoum et al. [42] reported that genetically instable tumors can activate STING-dependent noncanonical NF-κ B signaling that facilitates metastasis.”
BackgroundZannini, L., Cardano, M., Liberi, G., & Buscemi, G. (2024) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-024-05380-3 · Cited by 16
“Furthermore, in line with the strong association between inflammation and cancer, cGAS activation by MN has been linked to cancer progression, promoting cellular invasion and metastasis [19].”
BackgroundLv, X., Jia, M., Feng, X., Jian, J., Yang, J., Ma, D., Ji, M., Diao, Y., & Shen, J.-C. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.70166 · Cited by 15
Pagotto, S., Veronese, A., Soranno, A., et al. (2019) · Cancers · doi:10.3390/cancers11040575 · Cited by 13
“CIN is positively correlated with tumor stage, relapse, metastasis, treatment and resistance [25,26], and is predominately caused by defects in the mitotic chromosome segregation [27].”
BackgroundRe-awakening Innate Immune Signaling in Cancer: The Development of Highly Potent ENPP1 Inhibitors
Cogan, D. A., & Bakhoum, S. F. W. (2020) · Cell chemical biology · doi:10.1016/j.chembiol.2020.11.001 · Cited by 15
“Yet, evidence suggests that tumors employ negative feedback mechanisms to suppress cGAS-STING signaling and instead co-opt its chronic activation to spread to distant organs (Bakhoum et al., 2018).”
BackgroundSelf-citationSTimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors
Perera, S. A., Kopinja, J. E., Ma, Y., Muise, E. S., Laskey, J., Chakravarthy, K., Chen, Y., Cui, L., Presland, J. P., Sathe, M., et al. (2021) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-21-0136 · Cited by 14
“Not only has it been shown that strong acute activation can negate the adaptive immune response (32), but chronic activation promotes noncanonical NF-kB signaling–driven metastasis (42).”
BackgroundThe STING pathway: An uncharacterized angle beneath the gut–retina axis
Qin, X., Zou, H., & Niu, C. (2022) · Experimental Eye Research · doi:10.1016/j.exer.2022.108970 · Cited by 13
Marletta, S., Caliò, A., Bogina, G. S., Rizzo, M., Brunelli, M., Pedron, S., Marcolini, L., Stefanizzi, L., Gobbo, S., Princiotta, A., et al. (2023) · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · doi:10.1007/s00428-023-03549-y · Cited by 13
“Blockage of the STING pathway in morphologically aggressive renal cell carcinomas prevents local progression and metastasis development, eliciting a stronger antitumoral response [38].”
BackgroundSensing Self and Non-Self DNA by Innate Immune Receptors and Their Signaling Pathways
Sok, S. P. M., Ori, D., Nagoor, N. H., & Kawai, T. (2018) · Critical Reviews in Immunology · doi:10.1615/critrevimmunol.2018026540 · Cited by 13
Cytoplasmic DNA can be detected by RNA fluorescence in situ hybridization
Greenberg, E., Hochberg-Laufer, H., Blanga, S., Kinor, N., & Shav‐Tal, Y. (2019) · Nucleic Acids Research · doi:10.1093/nar/gkz645 · Cited by 11
“Finally, these findings can be of use for the future study of DNA translocation into the nucleus and its packaging after transfection, and possibly for the detection of traces of DNA in the cytoplasm of cells, as has recently been reported for some diseased states (21,22).”
BackgroundPrecision targeting of STING: Challenges, innovations, and clinical outlook for cancer therapy
Shi, J., Zhang, Y., Zhao, N., Seki, E., Ma, L., Kocic, G. M., Li, X., Terzić, J., & Zheng, T. (2025) · The Innovation · doi:10.1016/j.xinn.2025.101074 · Cited by 16
Genome instability and crosstalk with the immune response
Chabanon, R. M., Danlos, F. X., Ouali, K., & Postel-Vinay, S. C. (2025) · Genome Medicine · doi:10.1186/s13073-025-01509-6 · Cited by 16
“Indeed, cells with pre-existing CIN were shown to exhibit elevated levels of micronuclei, which activate cGAS when dsDNA becomes accessible upon micronuclei envelope disruption [17].”
InfluentialZhao, K., Cui, S., Wang, N., Wei, Q., Wang, X., Hou, K., Zhu, J., & Kong, F. (2026) · Journal of Translational Medicine · doi:10.1186/s12967-026-07748-4 · Cited by 14
The cGAS-STING pathway: Mechanism and medical implications
Hooftman, A., Keller, A., & Ablasser, A. (2026) · Cell · doi:10.1016/j.cell.2026.06.001 · Cited by 24
The cGAS/STING signaling pathway: a cross-talk of infection, senescence and tumors
Zeng, P.-H., & Yin, W.-J. (2022) · Cell Cycle · doi:10.1080/15384101.2022.2109899 · Cited by 12
“Interestingly, when the STING in the cells decreased, the malignant phenotype of the cells was inhibited [125].”
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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