The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Accumulation of p62/SQSTM 1 is associated with poor prognosis in patients with lung adenocarcinoma
Open accessAbstract
p62/SQSTM 1 is a selective substrate of autophagy, and aberrant accumulation of p62 has been observed in various pathological conditions. To understand the roles p62 plays in non‐small‐cell lung cancer (NSCLC), we carried out immunohistochemical analyses of p62 expression in a cohort of patients with annotated clinicopathological data. As analyses of murine and human hepatocellular carcinomas suggested a correlation between p62 and Nrf2 accumulations, we also examined NRF 2 expression in the same cohort. The expression of NRF 2 and p62 was examined by immunohistochemical methods in 109 NSCLC cases, which included patients with adenocarcinoma (n = 72), squamous cell carcinoma (n = 31), and large cell carcinoma (n = 6). Accumulation of NRF 2 and p62 was detected in 34% and 37% of NSCLC patients, respectively. The accumulations of p62 and NRF 2 did not correlate with each other, but both were associated with worse lung cancer‐specific survival (P = 0.0003 for NRF 2; P = 0.0130 for p62). NRF 2 status had an impact on NSCLC prognosis irrespective of histology types, but p62 status did so particularly in adenocarcinoma (P = 0.037). Multivariate analysis indicated that positive immunoreactivities of NRF 2 and p62 were both independent factors predicting worse lung cancer‐specific survival (P < 0.0001 for NRF 2 and P = 0.04 for p62). This study revealed that both NRF 2 and p62 are independent prognostic factors for NSCLC. The prognostic impact of p62 status was pronounced in adenocarcinoma patients, suggesting that molecular mechanisms underlying cancer evolution differ between adenocarcinoma and squamous cell carcinoma. (Cancer Sci 2012; 103: 760–766)
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Pankiv, S., Clausen, T. H., Lamark, T., Brech, A., Bruun, J.-A., Outzen, H., Øvervatn, A., Bjørkøy, G., & Johansen, T. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m702824200 · Cited by 4,578
Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis
DeNicola, G. M., Karreth, F. A., Humpton, T. J., Gopinathan, A., Wei, C., Frese, K., Mangal, D., Yu, K. H., Yeo, C. J., Calhoun, E. S., et al. (2011) · Nature · doi:10.1038/nature10189 · Cited by 2,277
Autophagy-deficient mice develop multiple liver tumors
Takamura, A., Komatsu, M., Hara, T., Sakamoto, A., Kishi, C., Waguri, S., Eishi, Y., Hino, O., Tanaka, K., & Mizushima, N. (2011) · Genes & Development · doi:10.1101/gad.2016211 · Cited by 1,342
Dysfunctional KEAP1–NRF2 Interaction in Non-Small-Cell Lung Cancer
Singh, A., Misra, V., Thimmulappa, R. K., Lee, H., Ames, S., Hoque, M. O., Herman, J. G., Baylin, S. B., Sidransky, D., Gabrielson, E., et al. (2006) · PLoS Medicine · doi:10.1371/journal.pmed.0030420 · Cited by 1,060
Structural Basis for Sorting Mechanism of p62 in Selective Autophagy
Ichimura, Y., Kumanomidou, T., Sou, Y.-S., Mizushima, T., Ezaki, J., Ueno, T., Kominami, E., Yamane, T., Tanaka, K., & Komatsu, M. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m802182200 · Cited by 803
Direct Interaction between Nrf2 and p21Cip1/WAF1 Upregulates the Nrf2-Mediated Antioxidant Response
Chen, W., Sun, Z., Wang, X.-J., Jiang, T., Huang, Z., Fang, D., & Zhang, D. D. (2009) · Molecular Cell · doi:10.1016/j.molcel.2009.04.029 · Cited by 638
Adam, J., Hatipoglu, E., O'Flaherty, L., Ternette, N., Sahgal, N., Lockstone, H., Baban, D., Nye, E., Stamp, G. W., Wolhuter, K., et al. (2011) · Cancer Cell · doi:10.1016/j.ccr.2011.09.006 · Cited by 585
Mature-onset obesity and insulin resistance in mice deficient in the signaling adapter p62
Rodriguez, A., Durán, A., Selloum, M., Champy, M.-F., Diez-Guerra, F. J., Flores, J. M., Serrano, M., Auwerx, J., Diaz-Meco, M. T., & Moscat, J. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.01.011 · Cited by 290
Kurihara, N., Hiruma, Y., Zhou, H., Subler, M. A., Dempster, D. W., Singer, F. R., Reddy, S. V., Gruber, H. E., Windle, J. J., & Roodman, G. D. (2007) · Journal of Clinical Investigation · doi:10.1172/jci28267 · Cited by 127
Cited by
Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging
Jomova, K., Raptova, R., Alomar, S. Y., Alwasel, S. H., Nepovimova, E., Kuca, K., & Valko, M. (2023) · Archives of Toxicology · doi:10.1007/s00204-023-03562-9 · Cited by 2,638
The KEAP1-NRF2 system: a thiol-based sensor-effector apparatus for maintaining redox homeostasis
Yamamoto, M., Kensler, T. W., & Motohashi, H. (2018) · Physiological Reviews · doi:10.1152/physrev.00023.2017 · Cited by 1,968
Self-citationThe Molecular Mechanisms Regulating the KEAP1-NRF2 Pathway
Baird, L., & Yamamoto, M. (2020) · Molecular and Cellular Biology · doi:10.1128/mcb.00099-20 · Cited by 1,542
Self-citationValencia, T., Kim, J. Y., Abu-Baker, S., Moscat-Pardos, J., Ahn, C. S., Reina-Campos, M., Duran, A., Castilla, E. A., Metallo, C. M., Diaz-Meco, M. T., et al. (2014) · Cancer Cell · doi:10.1016/j.ccr.2014.05.004 · Cited by 304
Dual roles of NRF2 in tumor prevention and progression: Possible implications in cancer treatment
Moon, E. J., & Giaccia, A. (2015) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.11.009 · Cited by 160
Metadata
- Authors
- Inoue, D., Suzuki, T., Mitsuishi, Y., Miki, Y., Suzuki, S., Sugawara, S., Watanabe, M., Sakurada, A., Endo, C., Uruno, A., Sasano, H., Nakagawa, T., Satoh, K., Tanaka, N., Kubo, H., Motohashi, H., & Yamamoto, M.
- Venue
- Cancer Science
- Publisher
- Wiley
- Published
- 2012-02-21
- Volume
- 103
- Issue
- 4
- Pages
- 760-766
- ISSN
- 1347-9032 (ISSN-L)
- 1349-7006
- OpenAlex
- W1977721235
- Cited by
- 204
- References
- 9
- FWCI
- 6.27
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Accumulation of p62/SQSTM 1 is associated with poor prognosis in patients with lung adenocarcinoma. https://app.cochat.ai/papers/10.1111/j.1349-7006.2012.02216.x
- The paper
- Inoue, D., Suzuki, T., Mitsuishi, Y., Miki, Y., Suzuki, S., Sugawara, S., Watanabe, M., Sakurada, A., Endo, C., Uruno, A., Sasano, H., Nakagawa, T., Satoh, K., Tanaka, N., Kubo, H., Motohashi, H., & Yamamoto, M. (2012). Accumulation of p62/SQSTM 1 is associated with poor prognosis in patients with lung adenocarcinoma. Cancer Science. https://doi.org/10.1111/j.1349-7006.2012.02216.x
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.