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.
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
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In the paper
“Our analysis was robust to imputation and we obtained similar results without imputed data (not shown).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Single-cell RNA sequencing
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“For the 4T1 experiments, Power analysis indicates that 10 mice per group will be sufficient to detect a difference at relative hazard ratios of <0.25 or >4.0 with 80% power and 95% confidence, given a median survival of 58 days in the control group and a total follow up period of 180 days.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Animal studies
Strength:hedged· not yet calibratedn = 10Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, to minimize the effects of experimental artifacts on the analysis, data was pre-processed to filter out cells with low total molecule counts (library size), low complexity and high mitochondrial content, identified by a bimodal fit.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Single-cell RNA sequencing
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The evolutionary benefits of the noncanonical pathway would justify the scarcity of inactivating mutations in cGAS and STING among breast and lung cancers (Extended Data Fig. 10e).”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > DISCUSSION
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“For disease-specific survival in MDA-MB-231 experiments, power analysis indicated that 10 mice per group will be sufficient to detect a difference at relative hazard ratios of <0.2 or >5 with 80% power and 95% confidence, given a median disease-specific survival of 3 months in the control group and a total follow up period of 250 days.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Animal studies
Strength:hedged· not yet calibratedn = 10Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Mitochondria were purified at 12,000xg to minimize their contamination in the cytosolic fraction.”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > METHODS > Quantification of cytosolic DNA
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“CIN promotes in vitro invasion and migration”
§ Chromosomal instability drives metastasis through a cytosolic DNA response > Extended Data
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
The role of CIN in metastasis has not been established.
“its role in metastasis has not been established.”
The paper relies on this without support.
The mouse xenograft and orthotopic models recapitulate human metastatic progression sufficiently to infer CIN's role in human metastasis.
“We injected MDA-MB-231 cells into the left cardiac ventricles of athymic mice to enable systemic dissemination while tracking metastatic colonization using a bioluminescence reporter.”
The paper relies on this without support.
The human tumor cohorts analyzed are representative of human metastatic disease generally.
“we applied the weighted-genomic integrity index (wGII) as a proxy for CIN8 on 79 primary tumor-brain metastases matched pairs from a recently published cohort9.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“While MN have been proposed to activate as tumor suppressor pathways, MN also play a critical pathogenic role in the evolution of cancer genomes and metastasis by driving genomic instability through chromothripsis (Bakhoum et al., 2018; Umbreit et al., 2020; Ye et al., 2019; Zhang et al., 2015).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Bakhoum et al., 2018
In the citing paper
“Moreover, STING-dependent activation of noncanonical NF-κB signaling, due to ruptured MN, promotes metastasis (Bakhoum et al., 2018).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Bakhoum et al., 2018
In the citing paper
“For example, in breast and lung cancers, suppression of chromosomal instability and associated cytoDNA decreases metastasis (Bakhoum et al., 2018).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Bakhoum et al., 2018
In the citing paper
“Researchers have observed differences in the expression of essential genes in the cGAS‐STING signaling mechanism between normal and malignant tissues, along with MB21D1‐encoding cGAS, transmembrane protein 173 (TMEM‐173)‐encoding STING, TANK‐binding kinase 1 (TBK‐1) and interferon regulatory factor 3 (IRF‐3).”
From Tumor microenvironment signaling and therapeutics in cancer progression (2023) · cites this paper as [253]
In the citing paper
“Comprehensive research and recent evidence proved that these four genes were significantly elevated in almost all cancer models, suggesting that cGAS‐STING signal transduction might be stimulated in all cancer types [252, 253].”
From Tumor microenvironment signaling and therapeutics in cancer progression (2023) · cites this paper as [253]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Noncanonical NF-κB protein ratios differ between the text and figure caption
MinorThe text describes ratios of p52 and phosphorylated p100 to total p100. The Extended Data Figure 8 caption instead names phosphorylated p52-to-p100 and p100-to-total p100 ratios.
“a trend toward higher ratios of p52 and phosphorylated p100 relative to total p100”
“Normalized ratio of phosphorylated p52-to-p100 (left) and p100-to-total p100 (right) protein levels.”
PCR indexing step is described as both 10 and 14 cycles
MinorThe methods give two different cycle counts for the same sample-index PCR amplification.
“A unique sample index for each library was introduced through 10 cycles of PCR amplification”
“(98°C for 45 s; 98°C for 20s, 60°C for 30s, and 72°C for 20 s x 14 cycles; 72°C for 1min; held at 4°C).”
Citations
Cites
Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2
Love, M. I., Huber, W., & Anders, S. (2014) · Genome Biology · doi:10.1186/s13059-014-0550-8 · Cited by 95,106
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
STAR: ultrafast universal RNA-seq aligner
Dobin, A., Davis, C. A., Schlesinger, F., Drenkow, J., Zaleski, C., Jha, S., Batut, P., Chaisson, M., & Gingeras, T. R. (2013) · Bioinformatics · doi:10.1093/bioinformatics/bts635 · Cited by 51,709
HTSeq—a Python framework to work with high-throughput sequencing data
Anders, S., Pyl, P. T., & Huber, W. (2015) · Bioinformatics · doi:10.1093/bioinformatics/btu638 · Cited by 21,464
Trapnell, C., Williams, B. A., Pertea, G., Mortazavi, A., Kwan, G., van Baren, M. J., Salzberg, S. L., Wold, B. J., & Pachter, L. (2010) · Nature Biotechnology · doi:10.1038/nbt.1621 · Cited by 15,556
Massively parallel digital transcriptional profiling of single cells
Zheng, G. X. Y., Terry, J. M., Belgrader, P., Ryvkin, P., Bent, Z. W., Wilson, R., Ziraldo, S. B., Wheeler, T. D., McDermott, G. P., Zhu, J., et al. (2017) · Nature Communications · doi:10.1038/ncomms14049 · Cited by 7,353
Cyclic GMP-AMP Synthase Is a Cytosolic DNA Sensor That Activates the Type I Interferon Pathway
Sun, L., Wu, J., Du, F., Chen, X., & Chen, Z. J. (2013) · Science · doi:10.1126/science.1232458 · Cited by 4,996
circlize implements and enhances circular visualization in R
Gu, Z., Gu, L., Eils, R., Schlesner, M., & Brors, B. (2014) · Bioinformatics · doi:10.1093/bioinformatics/btu393 · Cited by 4,290
Györffy, B., Lanczky, A., Eklund, A. C., Denkert, C., Budczies, J., Li, Q., & Szallasi, Z. (2010) · Breast Cancer Research and Treatment · doi:10.1007/s10549-009-0674-9 · Cited by 4,169
Nextflow enables reproducible computational workflows
Di Tommaso, P., Chatzou, M., Floden, E. W., Barja, P. P., Palumbo, E., & Notredame, C. (2017) · Nature Biotechnology · doi:10.1038/nbt.3820 · Cited by 4,001
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Items 1,201–1,300 of 1,551
Tambekar, A., Guhe, V., & Singh, S. (2024) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2024.110201 · Cited by 2
Yang, J., Feng, J., Duan, Z., Liu, X., Zhang, H., Zhang, M., Ma, Z., Hu, Z., Xiang, L., & Qi, X. (2025) · Clinical & Experimental Metastasis · doi:10.1007/s10585-025-10337-2 · Cited by 2
“…BM group, suggesting that this group had stronger genomic instability, which was in accordance with the hypothesis that large-scale genomic alterations, such as copy number changes, is often evident at metastatic sites and genomic instability drives tumor progression and metastasis [48 ].”
CIN s of the cytoplasm: dissecting ds RNA signaling in chromosomal instability
Skolariki, A., Jady‐Clark, R. L., & Parkes, E. E. (2025) · Molecular Oncology · doi:10.1002/1878-0261.70047 · Cited by 2
“Chromosomal instability (CIN) is a fundamental driver of tumorigenesis and metastasis, fueling genetic diversity and adaptation under selective pressure [1].”
边, 孜. (2025) · Advances in Clinical Medicine · doi:10.12677/acm.2025.1551504 · Cited by 2
Xiao, J., Kim, J. P., Park, B. K., Baylink, D. J., Kwon, C., Tran, V., Lee, S., Codorniz, K., Tan, L. D., Moreno, P. L., et al. (2025) · Experimental Hematology and Oncology · doi:10.1186/s40164-025-00669-w · Cited by 2
“2D), a finding which addresses concerns raised in prior studies that identified elevated NFκB2-mediated DDR pathways in blood and solid cancers [10, 11].”
Hitchhiking albumin to STING tumours
Ye, S., & Gao, J. (2025) · Nature Biomedical Engineering · doi:10.1038/s41551-025-01401-z · Cited by 2
The Presence of Genomic Instability in Cerebrospinal Fluid in Patients with Meningeal Metastasis
Wang, P., Zhang, H., Chen, P., Sun, Z., Zhang, Z., Yin, Q., Sun, H., & Yu, J. (2021) · Cancer Management and Research · doi:10.2147/cmar.s295368 · Cited by 2
“A number of researches have shown that cells with high genetic instability facilitates migration and invasion, and the upregulated mRNA expression of NF-κB and hPTTG1 in tumors with high genetic instability genes is closely connected with shorter disease-free survival in lung and breast cancers.(23,24) MM is usually a…”
BackgroundLohard, S., Juin, P. P., & Barillé‐Nion, S. (2020) · Molecular & Cellular Oncology · doi:10.1080/23723556.2020.1735912 · Cited by 2
“Even though IFN-I signatures were correlated to apoptosis/antiproliferative responses in tumors and to favorable clinical outcome in the context of anthracycline-based chemotherapy,(9,10) chronic IFN-I signalingmay have also pro-tumor effects including immune suppression and metastasis promotion.(11) Finally, how anti…”
BackgroundSun, R., & Νικολακόπουλος, Α. Ν. (2021) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1008838 · Cited by 2
Metastasis and organotropism: A look through the lens of large-scale clinical sequencing data
Coulton, A., & Turajlic, S. (2022) · Cancer Cell · doi:10.1016/j.ccell.2022.01.011 · Cited by 2
Wang, J., Ding, Z., Shu, W., & Zhuge, Y. (2023) · Cellular Signalling · doi:10.1016/j.cellsig.2023.110728 · Cited by 2
Li, D., Qian, X., Wang, Y., et al. (2024) · Clinica Chimica Acta · doi:10.1016/j.cca.2024.117822 · Cited by 2
Robust Somatic Copy Number Estimation using Coarse-to-fine Segmentation
Culibrk, L., Grewal, J., Pleasance, E., Williamson, L., Mungall, K., Laskin, J. J., Marra, M. A., & Jones, S. J. M. (2024) · Current Bioinformatics · doi:10.2174/0115748936312589240910071837 · Cited by 4
Harnessing Tumor Immune Ecosystem Dynamics to Personalize Radiation TherapyPreprint
Grass, G. D., Alfonso, J. C. L., Welsh, E. A., Ahmed, K. A., Teer, J. K., Harrison, L. B., Cleveland, J. L., Mulé, J. J., Eschrich, S. A., Enderling, H., et al. (2020) · SSRN Electronic Journal · doi:10.2139/ssrn.3581358 · Cited by 2
Probing pathophysiology of extracellular cGAMP with substrate-selective ENPP1Preprint
Carozza, J. A., Cordova, A. F., AlSaif, Y., Böhnert, V., Skariah, G. M., & Li, L. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.05.04.442665 · Cited by 2
“Now, cGAMP signaling seems to have an impact in every disease the field has investigated: cGAMP signaling occurs in cancer cells (Bakhoum et al., 2018; Deng et al., 2014; Harding, 2017; Mackenzie et al., 2017; Woo et al., 2014), in neurodegenerative diseases (Sliter et al., 2018), during myocardial…”
BackgroundMartinez, C. A., Spurr, L. F., Iyer, S., Pugh, S. A., Bridgewater, J. A., Primrose, J. N., Domingo, E., Maughan, T., D'Angelica, M. I., Talamonti, M. S., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.09.22.459429 · Cited by 2
cGAS recruitment to micronuclei is dictated by pre-existing nuclear chromatin statusPreprint
MacDonald, K. M., Nicholson-Puthenveedu, S., Tageldein, M. M., Arrowsmith, C. H., & Harding, S. M. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.01.13.476191 · Cited by 2
Radiation-induced persistent DNA damage response and late toxicity in cardiac tissuePreprint
Shigemori, K., Jiang, Y., Martin, J., Hawkins, M., Ryan, A. J., & Parkes, E. E. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.02.27.530210 · Cited by 2
Multi-scale characterisation of homologous recombination deficiency in breast cancerPreprint
Jacobson, D. H., Shi, P., Fisher, J., & Secrier, M. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.08.23.554414 · Cited by 2
WRAD core perturbation impairs DNA replication fidelity promoting immunoediting in pancreatic cancerPreprint
Citron, F., Ho, I.-L., Balestrieri, C., Liu, Z., Yen, E.-Y., Cecchetto, L., Perelli, L., Zhang, L., Castillo, L. A., Blazanin, N., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.10.21.619543 · Cited by 2
Self-citationSharma, A., Steger, R. F., Li, J. M., Baude, J. A., Heom, K. A., Dey, S. S., & Stowers, R. S. (2025) · bioRxiv · doi:10.1101/2025.03.18.643983 · Cited by 3
“The greater effect on gene expression in the presence of multiple cues in metastatic MDA-MB-231 cells might be due to their higher genomic instability 48,49 , signaling pathway crosstalk 50 , as well as a greater genetic and phenotypic heterogeneity 51,52 .”
Aberrant inheritance of extrachromosomal DNA amplifications promotes cancer evolutionPreprint
Marom, S., DAYAN, I., Kadali, V. N., Giurgiu, M., Koifman, G., Hakeny, K., Chaurasia, M., Benamozig, O., Nevo, R., Azuri, I., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.19.677276 · Cited by 2
“Their fragility and frequent rupture trigger innate immune signaling through the cGAS–STING pathway, suggesting a mechanism by which ecDNA may impact metastatic potential 7,51 .”
STING activation reshapes the tumor microenvironment leading to tumor regression in osteosarcomaPreprint
Young, E. P., Johnson, C. A., Lee, A. G., Morris, D., Tsui, J. L., Breese, M. R., Cámara, J. A., Schott, C. R., Abram, C. L., Leung, S. G., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.10.24.684275 · Cited by 2
Integrative spatial multi-omics reveals prognostic tumor niches in female genital tumorsPreprint
Tian, X., Lin, S., Wu, Y., He, Y., Zhang, Z., Zhao, Y., Zhang, P., Zhao, L., Yang, W., Ye, M., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.24.690313 · Cited by 2
Park, W., Umeda, S., Hilmi, M., O'Connor, C. A., Sharma, R., Tezcan, N., Zhang, H., Zhu, Y., Schwartz, C., Yaqubie, A., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.03.15.711961 · Cited by 2
Self-citationrDNA breaks activate dsRNA pattern recognition through sense-antisense transcriptionPreprint
Chen, J., Kim, S., Chen, S., Mo, Z., Jiang, Y., Liu, K. F., Li, Q., & Greenberg, R. A. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.26.728043 · Cited by 2
Mimoune, N., Bahouh, M. W., Boukhechem, S., Marouf, N., Khelef, D., & Kaidi, R. (2021) · JOURNAL of SIBERIAN MEDICAL SCIENCES · doi:10.31549/2542-1174-2021-2-77-103 · Cited by 1
Multimodal immunostimulation to control BRCA1-defective ovarian carcinoma
Klapp, V., & Galluzzi, L. (2021) · Trends in cancer · doi:10.1016/j.trecan.2021.11.006 · Cited by 1
Kim, S., Choe, M. H., Oh, J. S., & Kim, J. (2022) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2022.10.092 · Cited by 1
Gjerstorff, M. F. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1219870 · Cited by 1
Interferon signaling restrains renal cell carcinoma heterogeneity
Holíček, P., Fucikova, J. P., & Galluzzi, L. (2023) · Trends in cancer · doi:10.1016/j.trecan.2023.08.008 · Cited by 1
Advancements in tyrosine kinase-mediated regulation of innate nucleic acid sensing
Liu, S., & Xu, P. (2024) · Journal of Zhejiang University (Medical Sciences) · doi:10.3724/zdxbyxb-2023-0480 · Cited by 1
Post-traumatic Bullous Pilomatrixoma Exploring the Pathogenesis
Martínez-Ortega, J. I., Ortega-Valerio, G., & Cibrian, A. G. R. (2024) · American Journal of Dermatopathology · doi:10.1097/dad.0000000000002681 · Cited by 1
Sampaio, L. R., Dias, R. D. B., Goes, J. V. C., de Melo, R. P. M., Borges, D. D. P., Melo, M. M. D. L., de Oliveira, R. T. G., Ribeiro, H. L., Magalhães, S. M. M., & Pinheiro, R. F. (2024) · Medical Oncology · doi:10.1007/s12032-024-02376-8 · Cited by 1
“Of utmost importance, the increased expression of IRF3 , IRF7, and NFκB has been constantly reported in myeloid bone marrow tumors [17–19].”
Functional correlation between WRN and SAMHD1 in DNA end-resection
Perdichizzi, B., & Pichierri, P. (2024) · PubMed · doi:10.17912/micropub.biology.001157 · Cited by 1
“Fork stalling occurs when cells are exposed to genotoxic agents such as HU and camptothecin (CPT) or when they encounter sequences that are intrinsically difficult to replicate (Bakhoum et al., 2018).”
BackgroundLi, G., Zhao, R., Xie, Z., Qu, X., Duan, Y., Zhu, Y., Liang, H., Tang, D., Li, Z., & He, W. (2024) · Frontiers in Medicine · doi:10.3389/fmed.2024.1372495 · Cited by 1
“Studies have shown an essential link between chromosomal instability and tumor metastasis and that cell membrane dsDNA produced by persistent chromosome segregation errors is sensed by the STING pathway (28, 29).”
BackgroundProfiling Numerical and Structural Chromosomal Instability in Different Cancer Types
Zhang, X., & Kschischo, M. (2024) · Methods in molecular biology · doi:10.1007/978-1-0716-3946-7_20 · Cited by 1
Exploring chromosomal instability and clonal heterogeneity in breast cancer
Castellanos, G., Camargo-Herrera, L. V., Rangel, N., Jiménez, G., Martínez‐Agüero, M., & Rondón‐Lagos, M. (2024) · Endocrine Related Cancer · doi:10.1530/erc-24-0096 · Cited by 2
Zhou, X., Ba, Y., Xu, N., Xu, H., Zhang, Y., Liu, L., Weng, S., Liu, S., Xing, Z., Chen, S., et al. (2025) · Molecular Medicine · doi:10.1186/s10020-024-01049-6 · Cited by 1
“Coincidentally, Subtype 1 held the worst outcome and enriched in drug resistant pathways showing consistency with previous research which revealed that tumors of CIN associated with malignance, metastasis, therapy resistance(He et al. 2018; Sansregret et al. 2018; Bakhoum et al. 2018).”
Energetics of whole genome doubling and genomic instability
Beck, R. J., Tagal, V., Amin, S. B., Bakhoum, S. F., Maley, C. C., Verhaak, R. G. W., Gomes, A. P., & Andor, N. (2025) · Cancer Letters · doi:10.1016/j.canlet.2025.217878 · Cited by 3
Self-citationLei, Y. Y., Hu, Y. S., Cao, Y. Y., et al. (2025) · Food and Chemical Toxicology · doi:10.1016/j.fct.2025.115648 · Cited by 2
View Micronuclei in the Extent of Evolution: New Insight Into an Old Issue
Yang, S., Yao, H., Zhang, Y., Zhang, W., Jin, S., Huang, K., Song, J., Feng, Y., Li, X., & Wang, X. (2025) · Journal of Cellular Physiology · doi:10.1002/jcp.70079 · Cited by 1
“Their ability to activate cGAS ‐ STING can also promote tumor evolution and progression (Bakhoum et al. 2018; Furman et al. 2019; Harding et al. 2017; Mackenzie et al. 2017; Morehouse et al. 2020; H. Zhao et al. 2021).”
Khan, F., Liu, Y., Whitfield, D., Pang, L., Ali, H. A., Huang, Y., Zhou, F., Hagan, R. S., Frenis, K., Rowe, R. G., et al. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2420793122 · Cited by 1
“These findings align with a recent report showing that the STING - TBK1 signaling driven by cytosolic DNA can promote BCBM development ( 51 ).”
RetractedChromosomal Instability and Chromoanagenesis as Forces for Genomic Evolution
Castellano‐Pozo, M., & Comaills, V. (2025) · Methods in molecular biology · doi:10.1007/978-1-0716-4750-9_36 · Cited by 4
Epigenetics of mitochondrial and inflammation in cardiac fibrosis
He, H., Lin, L.-C., Liu, Z., Liu, P., Mao, S., Cao, W., Zhao, J., & Tao, H. (2025) · Cellular Signalling · doi:10.1016/j.cellsig.2025.112133 · Cited by 1
Impact of Chromosomal Instability and Aneuploidy in Cancer Development
Mennie, A. K., Dhital, B., & Ly, P. (2025) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-071124-101613 · Cited by 3
“Elevated CIN is implicated in progression to metastatic disease (Bakhoum et al. 2018, Li et al. 2023) and generally associated with poor prognosis (Carter et al. 2006, Kronenwett et al. 2004, Nakamura et al. 2003).”
Self-citationThe Link Between Chromosomal Instability and Immunity in Cancer
Kumari, L., Kumar, Y., & Bhatia, A. (2025) · Springer eBooks · doi:10.1007/978-3-032-00749-0_51 · Cited by 1
Lei, Y., He, D., Si, J., et al. (2025) · Annals of Medicine · doi:10.1080/07853890.2025.2581815 · Cited by 1
“(3) Modulation of the immune microenvironment, whereby in responsive patients, the immune system may selectively clear ‘immunogenic’ tumour cells with CIS-H, further reducing the survival of genomically unstable subclones and suppressing CIS progression [63,64].”
Dhakal, S., Siraji, M. I., Grøndal, S. M., Skarsten, G. N., Moutoussamy, E. E., Gausdal, G., Lorens, J. B., & Bougnaud, S. (2025) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-24-0440 · Cited by 1
ALFA-K: Local adaptive mapping of karyotype fitness landscapes
Beck, R. J., Li, T., & Andor, N. (2025) · Nature Communications · doi:10.1038/s41467-025-67750-0 · Cited by 3
“…as interferon gamma as a measure of missegregation rate 25 , as chromosome missegregations can trigger micronuclei formation, whose rupture activates the cyclic GMP-AMP synthase – stimulator of interferon genes (cGAS – STING) pathway and induces interferon-stimulated gene expression 30 .”
Heng, H. H. (2025) · Environmental Disease · doi:10.4103/ed.ed_26_25 · Cited by 1
Zhu, T., He, L., Li, S., et al. (2026) · Frontiers in Genetics · doi:10.3389/fgene.2025.1749780 · Cited by 1
“Research suggests that this instability can activate the cGAS–STING pathway, leading to type I interferon production and subsequent recruitment of CD8 + T cells (Bakhoum et al., 2018).”
Mitochondrial Adaptations Underlying Tetraploidization in Human Cancer, Fungal, and Yeast Models
Jèmaà, M., Bedoui, A., Ammous-Boukhris, N., et al. (2026) · Biology · doi:10.3390/biology15020181 · Cited by 1
“…cancer cells are specifically dependent on mitochondrial metabolism and should be hyper-sensitive to inhibitors and inducers of oxidative stress [38] and dysregulated mitophagy leading to accumulation of dysfunctional mitochondria [39]. https://doi.org/10.3390/biology15020181 The canonical…”
InfluentialPotential of Micronuclear Epigenetic Signatures in Analyses of Toxicity and Genomic Instability
Paul, S., Das, A., Bandyopadhyay, A. K., & Giri, A. K. (2026) · Cell Biology International · doi:10.1002/cbin.70142 · Cited by 1
“Agustinus et al. (2023) highlight the potential for epigenetic remodeling following the reintegration of extranuclear MN‐DNA into the nuclear genome.”
InfluentialUnraveling syndrome-driven osteosarcoma: genetic insights and therapeutic frontiers
Zhou, Y., Wang, W., Qiu, J., Huang, J., Fu, L., & Songfeng, X. (2026) · Orphanet Journal of Rare Diseases · doi:10.1186/s13023-026-04243-3 · Cited by 1
“Critically, seminal studies have established that loss of TP53 function is a fundamental prerequisite for cells to undergo and survive chromothripsis [57, 58].”
Conversation with Future Clinical Cytogeneticists: The New Frontiers
Ye, J. C., Chowdhury, R., & Heng, H. H. (2026) · Genes · doi:10.3390/genes17020232 · Cited by 3
Saskova, K., Landfors, M., Hlaváč, V., Šeborová, K., Brůha, J., Honkova, K., Tomášová, K., Selvi, S., Drábová, J., Hackenhaar, F. S., et al. (2026) · Mutagenesis · doi:10.1093/mutage/geag010 · Cited by 1
Targeting the cGAS-STING-TBK1 pathway in cancer therapy
Jiang, L., Zhong, Y., Zhang, Z., Yang, Q., Sun, S., Sun, H., & Liu, Z. (2026) · Future Medicinal Chemistry · doi:10.1080/17568919.2026.2628553 · Cited by 2
Veith, T. A., Beck, R. J., Brown, J. S., & Andor, N. (2026) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1013897 · Cited by 1
“Chromosomal instability, a hallmark of cancer associated with advanced disease and poor outcomes [3], is a powerful evolutionary process that rapidly generates genetic diversity.”
Zeste White 10 May Serve as a Prognostic Biomarker and Therapeutic Target for Human Breast Cancer
Bellah, S. F., Hossen, M. A., Billah, S., et al. (2026) · Breast Cancer Basic and Clinical Research · doi:10.1177/11782234261428784 · Cited by 1
A Decade of cGAS Discovery: Point of Convergence in Oral Diseases
Sun, L., Gao, P., Xiao, P., Li, S., & Liu, D. (2026) · International Dental Journal · doi:10.1016/j.identj.2025.109382 · Cited by 1
“14 Therefore, the cGAS-STING pathway exhibits dual functionality in the TME: either facilitate tumour progression or provoke anti-tumour immunity.”
Νikolouzakis, Τ. Κ., Souglakos, J., Kantidakis, E. E., Achilleos, K., van Staden, T., & Chrysos, E. (2026) · Cancers · doi:10.3390/cancers18071062 · Cited by 1
Nuclear envelope proteins in cancer: revisiting the significance of LEM-domain proteins
Jobe, A., Mirza, S., & Vijayan, R. (2026) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2026.1789623 · Cited by 1
“Additionally, chromosomal instability arising from nuclear defects has been shown to promote metastatic progression through cytosolic DNA sensing pathways (Bakhoum et al., 2018).”
Investigating the Consequences of Aneuploidy in Cancer and Normal Tissue
Modi, J. N., & Taylor, A. M. (2026) · Advances in experimental medicine and biology · doi:10.1007/978-3-032-22637-2_15 · Cited by 1
Mitochondrial Stress Orchestrates Tumor Immune Evasion and Immunotherapy Resistance
Bılır, A., Yıldırım, B., & Karalök, M. H. (2026) · Cells · doi:10.3390/cells15100890 · Cited by 1
“Early experimental studies have shown that mitochondrial DNA stress, such as that induced by TFAM deficiency, is sufficient to activate innate immune signaling in the absence of infection, establishing a direct link between mitochondrial dysfunction and immune activation [30].”
Pérot, G., Guerriau, C., Roussel, N., Sarot, É., Valle, C., Pomiès, P., Tirode, F., Poncet, D., & Chibon, F. (2026) · BMC Cancer · doi:10.1186/s12885-026-16151-7 · Cited by 1
PKCα-mediated nuclear translocation of cGAS stabilizes β-catenin and drives metastasis
Zhang, Q., Tong, C., Zhao, M., Ma, M., Huang, S., He, Y., Song, Y., Liu, M., Yi, L., Yao, F., et al. (2026) · Molecular Cell · doi:10.1016/j.molcel.2026.05.023 · Cited by 1
GPAT4 regulates antitumor immune response through activating the mtDNA-cGAS axis in cancer cells
Ruan, Z., Liang, W., Gong, Y.-T., Guan, W., Zhou, X.-A., Jiang, K., Yang, Q., & Hu, M.-M. (2026) · Cell Insight · doi:10.1016/j.cellin.2026.100343 · Cited by 1
“…pathway (Hu & Shu, 2018, 2020, 2023; Ishikawa & Barber, 2008; Zhong et al., 2008), play central roles in recognizing cellular stress, inducing type I interferon responses, and remodeling the immune microenvironment (Bakhoum et al., 2018; Hopfner & Hornung, 2020; Zhang & Zhong, 2022).”
Suaste, V., Presterud, R., Wennerström, A. B., Wang, H., Zhang, J., Lund, S. O., Holmen, H. G., Lüders, T., Rowe, A., Berge, R. K., et al. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27135652 · Cited by 1
“It is possible that interferon stimulation is a direct cause of the DNA repair defect as A-T cells have increased levels of DNA damage and genome instability, giving rise to cytosolic damaged self-DNA, which is sensed and acted upon by the cGAS-STING pathway [40–42].”
Oncogenic EGFR rewires STING-TBK1 signalosomes to license DNA damage tolerance in NSCLC
Shen, Q., Chen, M., Chen, Y., Zhang, Q., Wu, Q., Yu, X., Zhang, F., Liu, S., Chen, C., Ye, C., et al. (2026) · The EMBO Journal · doi:10.1038/s44318-026-00856-3 · Cited by 1
“Chromosomal instability has been shown to drive metastasis in a STING-dependent manner, highlighting a context-dependent role of STING signaling in cancer progression (Bakhoum et al, 2018).”
Xu, Z., Guo, J., Liu, Z., Yu, J., Yuan, R., Min, Y., Wei, Z., & Peng, X. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103270 · Cited by 1
Cai, Y., Chen, Z., Xiong, J., Zhao, Y., & Zhou, J. (2026) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2026.189666 · Cited by 1
Replication stress in cancer: origins, consequences and therapeutic opportunities
Chen, J., & Zou, L. (2026) · Nature reviews. Cancer · doi:10.1038/s41568-026-00979-z · Cited by 2
Crossley, M. P., & Cimprich, K. A. (2018) · Nature · doi:10.1038/d41586-018-02804-6 · Cited by 1
Making Mistakes Empowers Cancer Cells
Balanis, N. G., & Graeber, T. G. (2018) · Trends in cancer · doi:10.1016/j.trecan.2018.05.001 · Cited by 1
“[7] provides a striking example of how non-CNA based aspects of chromosomal instability enable the cancer phenotype of metastasis.”
BackgroundVedoya, G. M., Galarza, T. E., Mohamad, N. A., et al. (2022) · Life Sciences · doi:10.1016/j.lfs.2022.120853 · Cited by 1
The Metabolism of Cancer Cells During Metastasis
Farshbafnadi, M., & Rezaei, N. (2023) · Springer eBooks · doi:10.1007/978-3-030-80962-1_60-1 · Cited by 1
Zhuang, G., Zhang, X., Du, W., Xu, L., Ma, J., Luo, H., Tang, H., Wang, W., Wang, P., Li, M., et al. (2024) · Journal of Translational Medicine · doi:10.1186/s12967-024-04865-w · Cited by 1
“Previous studies have shown that SVs play critical roles in tumor development, progression, and resistance to treatment by changing gene copy numbers, activating oncogenes, disrupting suppressor genes, or creating novel gene fusions [1–3].”
BackgroundZhou, P., Wang, P., & Li, B. (2024) · Discover Oncology · doi:10.1007/s12672-024-01482-3 · Cited by 1
Unveiling the Tumor Suppressors: Insights from Drosophila
Kuang, X., & Ma, X. (2025) · Advances in experimental medicine and biology · doi:10.1007/978-3-031-97035-1_1 · Cited by 1
Chromosome instability: From molecular mechanisms to disease
de Cárcer, G., Huertas, P., & Lopez-Contreras, A. J. (2018) · DNA repair · doi:10.1016/j.dnarep.2018.04.006 · Cited by 1
Colorectal Cancer Genetics: An Overview of the Actionable Building Blocks
Bairi, K. E., Lengyel, C. G., Marra, A., & Afqir, S. (2020) · Springer eBooks · doi:10.1007/978-3-030-53821-7_2 · Cited by 1
MYC Dysregulates Mitotic Spindle Function Creating a Dependency on TPX2Preprint
Rohrberg, J., Corella, A. N., Taileb, M., et al. (2018) · SSRN Electronic Journal · doi:10.2139/ssrn.3189389 · Cited by 1
How the Genome Folds, Divides, Lives, and DiesPreprint
Johnson, W. L., Xie, K. T., Kwon, M., Liu, S., & Pellman, D. S. (2017) · Cold Spring Harbor Symposia on Quantitative Biology · doi:10.1101/sqb.2017.82.035527 · Cited by 1
“…will hopefully lead to new ideas about therapy; for example, recent work has revealed unexpected links between nuclear envelope integrity and innate immune signaling that may, in some contexts, serve as a unique cancer vulnerability (Harding et al. 2017; Mackenzie et al. 2017; Bakhoum et al. 2018).”
BackgroundLimited Environmental Serine Confers Sensitivity to PHGDH Inhibition in Brain MetastasisPreprint
Ngo, B., Kim, E., Osorio-Vasquez, V., Doll, S., Bustraan, S., Luengo, A., Davidson, S. M., Ali, A., Ferraro, G. D., Kang, D. S., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.03.03.974980 · Cited by 1
“Metastasis is an evolutionary process whereby the adaptive potential of tumor cells enables their ability to colonize specific tissues.(1) Despite efforts to identify novel oncogenic mutations that drive metastasis, whole-genome sequencing studies have revealed striking similarities in the array of driver gene mutatio…”
BackgroundMethodSelf-citationYao, M., Wu, Y., Cao, Y., Liu, H., Ma, N., Chai, Y., Zhang, S., Zhang, H., Nong, L., Li, L., et al. (2021) · Research Square · doi:10.21203/rs.3.rs-201782/v1 · Cited by 1
Kumar, S., Zhao, J., Talluri, S., Buon, L., Mu, S., Potluri, B., Liao, C., Shi, J., Chakraborty, C., Gonzalez, G. B., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.04.20.488830 · Cited by 1
Local Adaptive Mapping of Karyotype Fitness LandscapesPreprint
Beck, R. J., & Andor, N. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.07.14.549079 · Cited by 1
“Finally the R 2 value between ⃗f a and ⃗f b is calculated and used as the metric to evaluate the inference pipeline performance.”
Bhat-Nakshatri, P., Khatpe, A., Chen, D., Batic, K., Mang, H. E., Herodotou, C., McGuire, P. C., Xuei, X., Gao, H.-Y., Liu, Y.-L., et al. (2023) · bioRxiv · doi:10.1101/2023.07.26.550741 · Cited by 1
Baba, S. A., Labhsetwar, S., Klemke, R. L., et al. (2023) · Data in Brief · doi:10.1016/j.dib.2023.109647 · Cited by 1
“Recent high-profile work has further characterized CIN as a driver of antiviral innate immune signaling in breast cancer cells [9] , resulting in tumor progression and metastasis [1] .”
BackgroundMethodInfluentialDumont, A., Gautier, F., Batard, Q., Guette, C., Guillonneau, F., Campone, M., Juin, P. P., & Barillé‐Nion, S. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.10.06.561231 · Cited by 1
Ke, A., Gao, C., Wang, S., et al. (2023) · Research Square · doi:10.21203/rs.3.rs-3499737/v1 · Cited by 1
VHL loss enables immune checkpoint blockade therapy by boosting type I interferon responsePreprint
Jiao, M., Bao, X., Hu, M., Pan, D., Liu, X., Kim, J., Li, F., & Li, C. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.11.28.569047 · Cited by 1
NF1 modulates microtubule repair and sensitivity to antibody-drug conjugatesPreprint
Duso, B. A., Messuti, E., Tini, G., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.12.06.569572 · Cited by 1
Schlafen-11 and -9 are innate immune sensors for intracellular single-stranded DNAPreprint
Zhang, P., Hu, X., Li, Z., Liu, Q., Liu, L., Jin, Y., Liu, S., Zhao, X. H., Wang, J., Hao, D., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.02.24.581893 · Cited by 1
Chocteau, F., Gautier, F., Josso, V., Douillard, E., Juin, P. P., & Barillé‐Nion, S. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.12.21.629876 · Cited by 1
Constitutive cGAS-STING activation in ALT+ cellsPreprint
Geelen, D., Beacom, A., Vaurs, M., Mahieu, M., Boutoual, R., Derumier, A., Hoerr, R. E., Loriot, A. E., Nassour, J., & Decottignies, A. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.18.649516 · Cited by 2
“In addition, in cancer cells with elevated chromosomal instability, cGAS-STING activation fosters pro-tumoral activity that depends on NF-κB and IL-6 (Bakhoum et al., 2018; Hong et al., 2022; Lanng et al., 2024).”
Johnson, R. M., Wang, S., Carozza, J. A., Fernández, D., Scicinski, J. J., Verity, N. A., Mardjuki, R. E., Cao, X., Papkoff, J. S., Ray, N., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.05.18.654655 · Cited by 1
“To avoid self-STING activation-mediated cell death, cancer cells often suppress STING pathway through epigenetic silencing ( 33 ) or rewiring its downstream to noncanonical, pro-metastatic nuclear factor-kappa-B (NF-κ B) pathway ( 21 ).”
InfluentialDabke, K., Gull, N., Kreimer, S. D., Peng, P.-C., Diaz, M., Cheikh, B. B., Dhawan, A., Evans, K., Ng, N. D., Yuan, X., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.06.01.655822 · Cited by 1
Renaud-Pageot, C., Capocefalo, D., Lemaire, S., Forest, A., Cantini, L., & Almouzni, G. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.09.672651 · Cited by 1
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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