The DOI matches its Crossref record; 50 of the 51 references it cites were found in a registry or an index; none of the 39 sources its claims cite is checked for support yet.
A CXCL1 Paracrine Network Links Cancer Chemoresistance and Metastasis
Open accessAbstract
Metastasis and chemoresistance in cancer are linked phenomena but the molecular basis for this link is unknown. We uncovered a network of paracrine signals between carcinoma, myeloid and endothelial cells that drives both processes in breast cancer. Cancer cells that overexpress CXCL1 and 2 by transcriptional hyperactivation or 4q21 amplification are primed for survival in metastatic sites. CXCL1/2 attract CD11b+Gr1+ myeloid cells into the tumor, which produce chemokines including S100A8/9 that enhance cancer cell survival. While chemotherapeutic agents kill cancer cells, these treatments trigger a parallel stromal reaction leading to TNF-α production by endothelial and other stromal cells. TNF-α heightens the expression of CXCL1/2 in cancer cells, thus amplifying the CXCL1/2-S100A8/9 loop and causing chemoresistance. CXCR2 blockers break this cycle, augmenting the efficacy of chemotherapy against breast tumors and particularly against metastasis. This network of endothelial-carcinoma-myeloid signaling interactions provides a mechanism linking chemoresistance and metastasis, with opportunities for intervention.
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57 Own result · 35 Own interpretation · 24 Not checked yet · 3 Own method · 1 No basis given
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“Knockdown of CXCL1 and 2 using two independent shRNA hairpins (Figure S1C–D) significantly reduced mammary tumor growth in all three models (Figures 1C–D, 1G–H and S1E–F)”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
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“A significant reduction in CD11b+Gr1+ myeloid cells was observed in CXCL1/2 knockdown tumors in both models (Figure S2G–H).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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“This decrease was associated with reduced metastasis in the lungs (Figures 1E–F, 1I–J and S1G).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
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“Indeed, CXCL1 and CXCL2 showed a similar expression pattern in a combined cohort of 615 primary breast cancers (Figure 1A).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
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“Fluorescence in situ hybridization (FISH) of human tissue samples showed that CXCL1 and CXCL2 were amplified in 7.5% of primary breast tumors and in 19.9% of metastases (Figures 1B and S1A).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
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“LM2 cells showed upregulation of CXCL1/2 compared to the parental line (Figure S1B).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
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“Furthermore, lung colonization assays by tail vein injection of LM2 cells confirmed that the effect of CXCL1/2 depletion on metastasis is not solely a consequence of decreased tumor burden (Figure 1K–N).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
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“Compared to the high levels of CXCL1/2 expression in lung metastatic cell lines, the expression of CXCR1, CXCR2 and DARC was negligibly low both at the RNA and protein levels (Figure 2C and Figure S2F and (Muller et al., 2001)).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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- Not checked yetcites Muller et al., 2001 source
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“Detailed characterization of the myeloid cells showed a decrease in the CD11b+Ly6G+ granulocytic MDSC population in CXCL1/2 knockdown tumors compared to controls (Figure 2D and S2I).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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In the paper
“Reduction in CXCL1/2 levels in the LM2 xenograft and PyMT transplantation models was associated with a significant increase in apoptosis in the tumors (Figure 2A–B).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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“CXCR2 blockers break this cycle, augmenting the efficacy of chemotherapy against breast tumors and particularly against metastasis.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > Abstract
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In the paper
“Interestingly, among other CXCR2 ligands that we tested, CXCL3 knockdown in LM2 cells contributed to tumor growth but not metastasis (Figure S1K–M).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
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“No appreciable decrease was observed in the CD11b+Ly6C+, F4/80+ macrophages, SMA+ myofibroblast, Ter119+ erythroid cells or endothelial cells in the CXCL1/2 depleted tumors (Figure S2J–P, Table S1 and data not shown).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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In the paper
“PyMT-F and LM2 cells grew aggressively in the mammary fat pad and metastasized to the lungs.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
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In the paper
“However, CXCL1/2 knockdown was not accompanied by any visible changes in apoptosis in vitro or in angiogenesis and cell proliferation rates in tumors (Figure S2A–E).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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In the paper
“S100A8/9 addition only weakly activated NFκB in LM2 breast cancer cells and we detected no activation of the Akt or STAT3 pathways (Figure S4C and data not shown).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > S100A8/9 Promotes Breast Cancer Cell Survival Under Chemotherapy
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“Addition of an ERK1/2 inhibitor (FR180204) or a p70S6K inhibitor (PF4708671) abolished the chemo-protective effect of S100A8/9 whereas addition of a p38 inhibitor (SB203580) showed partial effect (Figure 4F), suggesting that the ERK1/2 and p70S6K signaling mediate the pro-survival effect of S100A8/9 in metastatic cells.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > S100A8/9 Promotes Breast Cancer Cell Survival Under Chemotherapy
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In the paper
“AC treated tumors significantly upregulated CXCL1/2 expression (Figure 5C–D) and this effect was associated with increased recruitment of S100A9-expressing cells (Figure 5E) and CD11b+Ly6G+ granulocytic cells (Figure 5F).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > The CXCL1/2–S100A8/9 Survival Axis Is Hyperactivated by Chemotherapy
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In the paper
“Within the recruited CD11b+Ly6G+ population in the PyMT immunocompetent transplant tumors, 6, 12 and 25% of the cells expressed CD80, F4/80 and Sca1, respectively, and a minority expressed CD86, CD117, IL4Rα, VEGFR1 and CD34 (Table S2).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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In the paper
“Chemotherapy treatment of mice bearing LM2 tumors initially resulted in significant apoptosis and a concomitant delay in tumor growth (Figure 5A–B).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > The CXCL1/2–S100A8/9 Survival Axis Is Hyperactivated by Chemotherapy
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In the paper
“CXCL1/2 depleted tumors showed a decrease in CD4+ and CD8+ lymphocytes, no major change in γδ-TCR+ and CD25+ T-regulatory cells, and moderate increases in B220+ lymphocyte and CD49b+ NK cell numbers (Table S1).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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In the paper
“Coinjection of wild-type MPRO cells with LM2 cancer cells enhanced mammary tumor growth and lung metastasis, an effect that was significantly blunted by S100a8/9 knockdown in the MPRO cells (Figure S3E–F).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Promote Metastasis Through Myeloid Cell-derived S100A8/9
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In the paper
“Interestingly, a reduction both in monocytic CD11b+Ly6C+ and granulocytic CD11b+Ly6G+ cells occurred in the lungs of mice bearing CXCL1/2 depleted tumors with minimal changes in the number of F4/80+ macrophages (Figure S2R–T).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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In the paper
“However, this protection was more limited in co-culture with CD11b+Gr1+ cells derived from S100A9−/− marrow (Figure 4D), confirming that the pro-survival properties of myeloid factors under stress chemotherapy conditions are partly due to S100A8/9.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > S100A8/9 Promotes Breast Cancer Cell Survival Under Chemotherapy
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In the paper
“In contrast, Fascin that is part of a lung metastasis gene signature (Minn et al., 2005) did not show the same trend upon chemotherapy treatment as S100A8/9 (Figure S5E), further confirming the specificity of the association of S100A8/9 with chemotherapy resistance.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > S100A8/9 association with resistance to perioperative chemotherapy
What the sources say
- Not checked yetcites Minn et al., 2005 source
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In the paper
“To identify cancer cell survival factors derived from the recruited myeloid cells, we identified candidates that are abundantly expressed in tumor-derived CD11b+Gr1+ cells and are not of epithelial origin (Figure 3C,D and Figure S3A). S100A8 and A9 fulfilled these criteria.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Promote Metastasis Through Myeloid Cell-derived S100A8/9
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In the paper
“In line with our hypothesis, CD11b+Gr1+ cells and specifically the CD11b+Ly6G+ subpopulation expressed CXCR2 (Figure 2E, S2Q).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
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In the paper
“However, when AC was combined with the CXCR2 inhibitor, lung metastatic burden was markedly reduced and the interaction between the drugs exhibited synergism (Figure 7C,D).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > Blocking CXCL1 Signaling Increases the Effectiveness of Chemotherapy
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In the paper
“However metastatic cells were not completely eliminated and micrometastases were detected throughout the lungs (Figure 7C,D).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > Blocking CXCL1 Signaling Increases the Effectiveness of Chemotherapy
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In the paper
“Biologically, less than 0.1% of the circulating cancer cells are estimated to withstand the harsh stresses of infiltrating and colonizing distant metastatic sites (Weiss, 2000).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > INTRODUCTION
What the sources say
- Not checked yetcites Weiss, 2000
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In the paper
“Drug resistance in cancer can be cell-intrinsic (Poulikakos and Rosen, 2011) or a combination of host and tumor mediated pathways (Bergers and Hanahan, 2008; Ebos et al., 2009).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > INTRODUCTION
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In the paper
“CXCL1 emerged among a set of genes whose expression is associated with lung relapse in breast tumors, including tumors that had not been exposed to prior chemotherapy (Minn et al., 2007; Minn et al., 2005), and as a gene that increases the aggressiveness of circulating breast tumor cells (Kim et al., 2009).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Additionally, high expression of CXCL1 in breast tumors without gene amplification is also possible (Bieche et al., 2007).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
What the sources say
- Not checked yetcites Bieche et al., 2007 source
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“While chemotherapeutic agents kill cancer cells, these treatments trigger a parallel stromal reaction leading to TNF-α production by endothelial and other stromal cells.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > Abstract
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In the paper
“Based on these results, we postulated that CXCL1/2 mediates tumor cell survival via paracrine mechanisms.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
hedgeddirect- Asserted: fails — The authors may not put it forward as true.
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In the paper
“CXCL1/2 attract CD11b+Gr1+ myeloid cells into the tumor, which produce chemokines including S100A8/9 that enhance cancer cell survival.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“CXCL1 and 2 are 90% identical by amino-acid sequence and signal through the same receptor CXCR2 (Balkwill, 2004).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
What the sources say
- Not checked yetcites Balkwill, 2004 source
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“TNF-α heightens the expression of CXCL1/2 in cancer cells, thus amplifying the CXCL1/2-S100A8/9 loop and causing chemoresistance.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Recent evidence points to tumor microenvironment components as potential participants in the generation of chemoresistance (Denardo et al., 2011; Gilbert and Hemann, 2010; Roodhart et al., 2011; Shaked et al., 2008; Shree et al., 2011).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > INTRODUCTION
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Copy number alterations at 4q21 occur in breast cancer (Beroukhim et al., 2010) and engulf fifteen genes in the amplification peak, including CXCL1-8.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Mediate Mammary Tumor Growth and Lung Metastasis
What the sources say
- Not checked yetcites Beroukhim et al., 2010 source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“CXCR2 receptor is expressed by several stromal cell types such as endothelial and myeloid cells (Murdoch et al., 2008).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Recruit Myeloid Cells to Mammary Tumors
What the sources say
- Not checked yetcites Murdoch et al., 2008 source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Both TLR4 and RAGE are expressed in breast cancer cells (Bos et al., 2009; Hsieh et al., 2003).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Promote Metastasis Through Myeloid Cell-derived S100A8/9
What the sources say
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“S100A8/9 bind to Toll-like receptor 4 (TLR4) and RAGE (receptor for advanced glycation end products), which activate diverse signaling cascades (Gebhardt et al., 2006; Vogl et al., 2007).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Promote Metastasis Through Myeloid Cell-derived S100A8/9
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“S100A8/9 are low molecular weight calcium-binding proteins that are associated with chronic inflammation and cancer (Gebhardt et al., 2006).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Promote Metastasis Through Myeloid Cell-derived S100A8/9
What the sources say
- Not checked yetcites Gebhardt et al., 2006 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
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
“Collectively our results suggest that CXCL1/2 from breast cancer cells recruit myeloid producers of S100A8/9, which in turn promote breast cancer metastasis.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > CXCL1/2 Promote Metastasis Through Myeloid Cell-derived S100A8/9
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
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
“Once initiated, this chemo-protective program could become self-sustaining, leading to the enrichment of residual aggressive clones able to resist chemotherapy and thrive in the lung”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > A Three-Way Paracrine Axis Underlying Chemoresistance and Metastasis
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one. The quote only partly states this claim.
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
“This raises the possibility of clinically targeting this axis both to limit the dissemination of cancer cells and to diminish drug resistance.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > Biological and Clinical Implications
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.
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
“Such pro-inflammatory bursts can boost the CXCL1/2-S100A8/9 survival axis and facilitates the expansion of chemoresistant breast cancer cells.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > RESULTS > Blocking CXCL1 Signaling Increases the Effectiveness of Chemotherapy
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“CD11b+Gr1+ myeloid cells are a heterogeneous group with previously identified roles in tumor angiogenesis and T cell immunosuppression (Gabrilovich and Nagaraj, 2009; Ostrand-Rosenberg and Sinha, 2009; Shojaei et al., 2007).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > Biological and Clinical Implications
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
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
“Our findings argue that although therapy induced inflammation is a predominant feature of the use of chemotherapy, disrupting the CXCL1 driven paracrine axis could improve therapeutic response in existing lesions and also suppress metastasis, even at an advanced stage of tumor progression.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > Biological and Clinical Implications
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Stroma has lower selective pressure for mutations and epigenetic changes than cancer cell genomes.
In the paper
“The major impediments to cure advanced breast cancer are the emergence of pan-resistance to all known chemotherapy drugs and the development of widely metastatic disease, two phenomena that are closely linked clinically (Gonzalez-Angulo et al., 2007).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > A Three-Way Paracrine Axis Underlying Chemoresistance and Metastasis
What the sources say
- Not checked yetcites Gonzalez-Angulo et al., 2007 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The critical role of the microenvironment in tumor progression and response to therapy is being increasingly recognized (Condeelis and Pollard, 2006; Denardo et al., 2011; Gilbert and Hemann, 2010; Shree et al., 2011; Tan et al., 2011).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > A Three-Way Paracrine Axis Underlying Chemoresistance and Metastasis
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Recent reports (Denardo et al., 2011; Gilbert and Hemann, 2010) and the present work show that chemotherapy induces a storm of cytokines and chemokines in the tumor microenvironment many of which might be linked to chemoresistance.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > A Three-Way Paracrine Axis Underlying Chemoresistance and Metastasis
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“CXCR2 receptor antagonists are in clinical trials for chronic inflammatory diseases (Chapman et al., 2009)”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > Biological and Clinical Implications
What the sources say
- Not checked yetcites Chapman et al., 2009 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
“These findings accentuate the clinical relevance of CD11b+Gr1+ in rendering chemotherapy ineffective and promoting metastasis.”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > DISCUSSION > Biological and Clinical Implications
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“All experiments using animals were done in accordance to a protocol approved by MSKCC Institutional Animal Care and Use Committee (IACUC).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > EXPERIMENTAL PROCEDURES > Animal studies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
“Paraffin embedded tissue microarrays and sections from lung metastases and primary breast tumor cores before and after chemotherapy treatment were acquired from the MSKCC Department of Pathology in compliance with protocols approved by the MSKCC Institutional Review Board (IRB).”
§ A CXCL1 paracrine network links cancer chemoresistance and metastasis > EXPERIMENTAL PROCEDURES > Patient samples
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
An integrated understanding of acquired drug resistance in the context of inputs from tumor and its microenvironment is lacking.
“However, an integrated understanding of acquired drug resistance in the context of inputs from tumor and its microenvironment is lacking.”
The paper relies on this without support.
A very small fraction of cells exposed to genotoxic stress can survive and outgrow under repeated cycles of chemotherapy.
“Similarly, a very small fraction of cells exposed to genotoxic stress can survive and outgrow under repeated cycles of chemotherapy.”
The paper relies on this without support.
CXCR2 is the primary receptor for CXCL1/2.
“we utilized antagonists of CXCR2, the primary receptor for CXCL1/2”
The paper relies on this without support.
Stroma has lower selective pressure for mutations and epigenetic changes than cancer cell genomes.
“targeting the immune microenvironment would be an attractive option because of the potentially low selective pressure for mutations and epigenetic changes on the stroma compared to the cancer cell genomes.”
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
“Notably, data from various mouse models indicate that disrupting the CXCR1/2–MDSC axis in tumours is therapeutically efficacious across a wide variety of solid cancers166–172.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [166]
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Metadata
- Authors
- Acharyya, S., Oskarsson, T., Vanharanta, S., Malladi, S., Kim, J., Morris, P. G., Manova-Todorova, K., Leversha, M., Hogg, N., Seshan, V. E., Norton, L., Brogi, E., & Massagué, J.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Cancer Research UK (GB)
- Corresponding author
- Massagué, Joan
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-07
- Volume
- 150
- Issue
- 1
- Pages
- 165-178
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3528019
- OpenAlex
- W2151832198
- Semantic Scholar
- 925990be27c66128df282d0f18c8f2ac8b6b6953
- Cited by
- 1,085
- References
- 51
- Citations by year
- 2026: 32 · 2025: 45 · 2024: 81 · 2023: 81 · 2022: 81 · 2021: 139 · 2020: 99 · 2019: 68 · 2018: 71 · 2017: 75 · 2016: 77 · 2015: 78 · 2014: 69 · 2013: 77 · 2012: 12
- FWCI
- 37.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense
- Howard Hughes Medical Institute
- National Institutes of Health
- National Cancer Institute (R37CA034610, P01CA094060, U54CA163167, CA94060, P30CA008748)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- CXCL1, CXCL2, chemoresistance, metastasis, breast cancer, paracrine signaling, myeloid cells, endothelial cells, S100A8/S100A9, TNF-α, NF-kB, CXCR2, tumor microenvironment, chemotherapy
- MeSH terms
- Animals, Breast Neoplasms, Carcinoma, Disease Models, Animal, Female, Humans, Lung Neoplasms, Lymph Nodes, Lymphatic Metastasis, Mice, Inbred C57BL, Neoplasm Metastasis, Neoplasm Transplantation, Transplantation, Heterologous, Drug Resistance, Neoplasm, Paracrine Communication, Myeloid Cells, Calgranulin A, Calgranulin B, Endothelial Cells, Mice, Chemokine CXCL1, Gene Knockdown Techniques
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