Student or educator? Sign up with your school email and get 6 months of Pro free.
CoChat
Sign Up
Cited by 83

The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.

p53 at the crossroads of tumor immunity

Efe, Gizem, Rustgi, Anil K., Prives, Carol·2024·Nature Cancer
DOI 10.1038/s43018-024-00796-z
Open this paper in CoChat — free account

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.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/s43018-024-00796-z

Cites

22 of 22 references verified0 citation errors · 0 not checkable

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.

A few free checks a day · papers already verified open instantly · results are public

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?

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

Show all 22 references

Research works printed but not linked: 126

  1. Bouaoun, L. et al. TP53 variations in human cancers: new lessons from the IARC TP53 Database and genomics data. Hum. Mutat. 37, 865–876 (2016). · DOI · Paper page
  2. Kastenhuber, E. R. & Lowe, S. W. Putting p53 in context. Cell 170, 1062–1078 (2017). · DOI · Paper page
  3. Brachmann, R. K., Vidal, M. & Boeke, J. D. Dominant-negative p53 mutations selected in yeast hit cancer hot spots. Proc. Natl Acad. Sci. USA 93, 4091–4095 (1996). · DOI · Paper page
  4. de Vries, A. et al. Targeted point mutations of p53 lead to dominant-negative inhibition of wild-type p53 function. Proc. Natl Acad. Sci. USA 99, 2948–2953 (2002). · DOI · Paper page
  5. Gencel-Augusto, J. & Lozano, G. p53 tetramerization: at the center of the dominant-negative effect of mutant p53. Genes Dev. 34, 1128–1146 (2020). · DOI
  6. Lang, G. A. et al. Gain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndrome. Cell 119, 861–872 (2004). · DOI · Paper page
  7. Freed-Pastor, W. A. & Prives, C. Mutant p53: one name, many proteins. Genes Dev. 26, 1268–1286 (2012). · DOI · Paper page
  8. Tang, Q., Su, Z., Gu, W. & Rustgi, A. K. Mutant p53 on the path to metastasis. Trends Cancer 6, 62–73 (2020). · DOI
  9. Wang, Z. et al. Loss-of-function but not gain-of-function properties of mutant TP53 are critical for the proliferation, survival and metastasis of a broad range of cancer cells. Cancer Discov. 14, 362–379 (2024). · DOI · Paper page
  10. Kim, M. P. & Lozano, G. Mutant p53 partners in crime. Cell Death Differ. 25, 161–168 (2018). · DOI · Paper page
  11. Agupitan, A. D. et al. p53: a guardian of immunity becomes its saboteur through mutation. Int. J. Mol. Sci. 21, 3452 (2020). · DOI
  12. Shatz, M., Menendez, D. & Resnick, M. A. The human TLR innate immune gene family is differentially influenced by DNA stress and p53 status in cancer cells. Cancer Res. 72, 3948–3957 (2012). · DOI · Paper page
  13. Wang, B., Niu, D., Lai, L. & Ren, E. C. p53 increases MHC class I expression by upregulating the endoplasmic reticulum aminopeptidase ERAP1. Nat. Commun. 4, 2359 (2013).
  14. Munoz-Fontela, C. et al. Transcriptional role of p53 in interferon-mediated antiviral immunity. J. Exp. Med. 205, 1929–1938 (2008). · DOI · Paper page
  15. Iannello, A., Thompson, T. W., Ardolino, M., Lowe, S. W. & Raulet, D. H. p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells. J. Exp. Med. 210, 2057–2069 (2013). · DOI · Paper page
  16. Shatz, M., Shats, I., Menendez, D. & Resnick, M. A. p53 amplifies Toll-like receptor 5 response in human primary and cancer cells through interaction with multiple signal transduction pathways. Oncotarget 6, 16963–16980 (2015). · DOI · Paper page
  17. Wang, H. Q. et al. Inhibition of MDM2 promotes antitumor responses in p53 wild-type cancer cells through their interaction with the immune and stromal microenvironment. Cancer Res. 81, 3079–3091 (2021). · DOI
  18. Zhu, M. et al. Loss of p53 and mutational heterogeneity drives immune resistance in an autochthonous mouse lung cancer model with high tumor mutational burden. Cancer Cell 41, 1731–1748 (2023). · DOI · Paper page
  19. Zhu, K. et al. p53 induces TAP1 and enhances the transport of MHC class I peptides. Oncogene 18, 7740–7747 (1999). · DOI
  20. Sabapathy, K. & Nam, S. Y. Defective MHC class I antigen surface expression promotes cellular survival through elevated ER stress and modulation of p53 function. Cell Death Differ. 15, 1364–1374 (2008). · DOI
  21. Cao, Z. et al. An unexpected role for p53 in regulating cancer cell-intrinsic PD-1 by acetylation. Sci. Adv. 7, eabf4148 (2021). · DOI
  22. Elkon, R. et al. Dissection of a DNA-damage-induced transcriptional network using a combination of microarrays, RNA interference and computational promoter analysis. Genome Biol. 6, R43 (2005). · DOI
  23. Li, L. et al. A unique role for p53 in the regulation of M2 macrophage polarization. Cell Death Differ. 22, 1081–1093 (2015). · DOI · Paper page
  24. Dinavahi, S. S. et al. Targeting WEE1/AKT restores p53-dependent natural killer-cell activation to induce immune checkpoint blockade responses in ‘cold’ melanoma. Cancer Immunol. Res. 10, 757–769 (2022). · DOI
  25. Chen, H. A. et al. Senescence rewires microenvironment sensing to facilitate antitumor immunity. Cancer Discov. 13, 432–453 (2023). · DOI · Paper page
  26. Rufini, A., Tucci, P., Celardo, I. & Melino, G. Senescence and aging: the critical roles of p53. Oncogene 32, 5129–5143 (2013). · DOI · Paper page
  27. Stokes, K. L. et al. Natural killer cells limit the clearance of senescent lung adenocarcinoma cells. Oncogenesis 8, 24 (2019). · DOI · Paper page
  28. Pilley, S., Rodriguez, T. A. & Vousden, K. H. Mutant p53 in cell–cell interactions. Genes Dev. 35, 433–448 (2021). · DOI · Paper page
  29. Balkwill, F. & Mantovani, A. Inflammation and cancer: back to Virchow? Lancet 357, 539–545 (2001). · DOI · Paper page
  30. de Visser, K. E. & Joyce, J. A. The evolving tumor microenvironment: from cancer initiation to metastatic outgrowth. Cancer Cell 41, 374–403 (2023). · DOI · Paper page
  31. Cooks, T. et al. Mutant p53 cancers reprogram macrophages to tumor supporting macrophages via exosomal miR-1246. Nat. Commun. 9, 771 (2018). · DOI · Paper page
  32. Carra, G., Lingua, M. F., Maffeo, B., Taulli, R. & Morotti, A. p53 vs NF-κB: the role of nuclear factor-kappa B in the regulation of p53 activity and vice versa. Cell. Mol. Life Sci. 77, 4449–4458 (2020). · DOI
  33. Liu, G., Park, Y. J., Tsuruta, Y., Lorne, E. & Abraham, E. p53 attenuates lipopolysaccharide-induced NF-κB activation and acute lung injury. J. Immunol. 182, 5063–5071 (2009). · DOI
  34. Ravi, R. et al. p53-mediated repression of nuclear factor-κB RelA via the transcriptional integrator p300. Cancer Res. 58, 4531–4536 (1998).
  35. Wadgaonkar, R. et al. CREB-binding protein is a nuclear integrator of nuclear factor-κB and p53 signaling. J. Biol. Chem. 274, 1879–1882 (1999). · DOI · Paper page
  36. Schwitalla, S. et al. Loss of p53 in enterocytes generates an inflammatory microenvironment enabling invasion and lymph node metastasis of carcinogen-induced colorectal tumors. Cancer Cell 23, 93–106 (2013). · DOI · Paper page
  37. Kawauchi, K., Araki, K., Tobiume, K. & Tanaka, N. p53 regulates glucose metabolism through an IKK–NF-κB pathway and inhibits cell transformation. Nat. Cell Biol. 10, 611–618 (2008). · DOI · Paper page
  38. Di Minin, G. et al. Mutant p53 reprograms TNF signaling in cancer cells through interaction with the tumor suppressor DAB2IP. Mol. Cell 56, 617–629 (2014). · DOI · Paper page
  39. Cooks, T. et al. Mutant p53 prolongs NF-κB activation and promotes chronic inflammation and inflammation-associated colorectal cancer. Cancer Cell 23, 634–646 (2013). · DOI · Paper page
  40. Weisz, L. et al. Mutant p53 enhances nuclear factor κB activation by tumor necrosis factor α in cancer cells. Cancer Res. 67, 2396–2401 (2007). · DOI · Paper page
  41. Chollat-Namy, M. et al. The pharmalogical reactivation of p53 function improves breast tumor cell lysis by granzyme B and NK cells through induction of autophagy. Cell Death Dis. 10, 695 (2019). · DOI
  42. Heinemann, A. et al. Tumor suppressive microRNAs miR-34a/c control cancer cell expression of ULBP2, a stress-induced ligand of the natural killer cell receptor NKG2D. Cancer Res. 72, 460–471 (2012). · DOI · Paper page
  43. Wellenstein, M. D. et al. Loss of p53 triggers WNT-dependent systemic inflammation to drive breast cancer metastasis. Nature 572, 538–542 (2019). · DOI · Paper page
  44. Matsumoto, Y. et al. Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium. Nat. Med. 13, 470–476 (2007). · DOI · Paper page
  45. Blagih, J. et al. Cancer-specific loss of p53 leads to a modulation of myeloid and T cell responses. Cell Rep. 30, 481–496 (2020). · DOI · Paper page
  46. Beck, A. H. et al. The macrophage colony-stimulating factor 1 response signature in breast carcinoma. Clin. Cancer Res. 15, 778–787 (2009). · DOI · Paper page
  47. Zhu, Y. et al. CSF1/CSF1R blockade reprograms tumor-infiltrating macrophages and improves response to T-cell checkpoint immunotherapy in pancreatic cancer models. Cancer Res. 74, 5057–5069 (2014). · DOI · Paper page
  48. Efe, G. et al. p53 gain-of-function mutation induces metastasis via BRD4-dependent CSF-1 expression. Cancer Discov. 13, 2632–2651 (2023). · DOI
  49. Bezzi, M. et al. Diverse genetic-driven immune landscapes dictate tumor progression through distinct mechanisms. Nat. Med. 24, 165–175 (2018). · DOI · Paper page
  50. Ghosh, M. et al. Mutant p53 suppresses innate immune signaling to promote tumorigenesis. Cancer Cell 39, 494–508 (2021). · DOI · Paper page
  51. Zhang, W. C. et al. Tumour-initiating cell-specific miR-1246 and miR-1290 expression converge to promote non-small cell lung cancer progression. Nat. Commun. 7, 11702 (2016).
  52. Yoo, S. A. et al. Placental growth factor regulates the generation of TH17 cells to link angiogenesis with autoimmunity. Nat. Immunol. 20, 1348–1359 (2019). · DOI
  53. Zhang, S. et al. Trp53 negatively regulates autoimmunity via the STAT3–TH17 axis. FASEB J. 25, 2387–2398 (2011). · DOI · Paper page
  54. Togashi, Y., Shitara, K. & Nishikawa, H. Regulatory T cells in cancer immunosuppression — implications for anticancer therapy. Nat. Rev. Clin. Oncol. 16, 356–371 (2019). · DOI · Paper page
  55. Fischer, K. et al. Inhibitory effect of tumor cell-derived lactic acid on human T cells. Blood 109, 3812–3819 (2007). · DOI · Paper page
  56. Maddalena, M. et al. TP53 missense mutations in PDAC are associated with enhanced fibrosis and an immunosuppressive microenvironment. Proc. Natl Acad. Sci. USA 118, e2025631118 (2021). · DOI
  57. Shah, C. A. et al. Intratumoral T cells, tumor-associated macrophages, and regulatory T cells: association with p53 mutations, circulating tumor DNA and survival in women with ovarian cancer. Gynecol. Oncol. 109, 215–219 (2008). · DOI
  58. Braun, M. W. & Iwakuma, T. Regulation of cytotoxic T-cell responses by p53 in cancer. Transl. Cancer Res. 5, 692–697 (2016). · DOI
  59. Wormann, S. M. et al. Loss of p53 function activates JAK2–STAT3 signaling to promote pancreatic tumor growth, stroma modification, and gemcitabine resistance in mice and is associated with patient survival. Gastroenterology 151, 180–193 (2016). · DOI · Paper page
  60. Siolas, D., Vucic, E., Kurz, E., Hajdu, C. & Bar-Sagi, D. Gain-of-function p53R172H mutation drives accumulation of neutrophils in pancreatic tumors, promoting resistance to immunotherapy. Cell Rep. 36, 109578 (2021). · DOI
  61. Hassin, O. & Oren, M. Drugging p53 in cancer: one protein, many targets. Nat. Rev. Drug Discov. 22, 127–144 (2023). · DOI · Paper page
  62. Uddin, M. B. et al. p53 missense mutant G242A subverts natural killer cells in sheltering mouse breast cancer cells against immune rejection. Exp. Cell Res. 417, 113210 (2022). · DOI
  63. Belkahla, S. et al. The metabolism of cells regulates their sensitivity to NK cells depending on p53 status. Sci. Rep. 12, 3234 (2022). · DOI
  64. Breunig, C. et al. MicroRNA-519a-3p mediates apoptosis resistance in breast cancer cells and their escape from recognition by natural killer cells. Cell Death Dis. 8, e2973 (2017). · DOI
  65. He, X. Y. et al. p53 in the myeloid lineage modulates an inflammatory microenvironment limiting initiation and invasion of intestinal tumors. Cell Rep. 13, 888–897 (2015). · DOI
  66. Sharma, M. D. et al. Activation of p53 in immature myeloid precursor cells controls differentiation into Ly6c+CD103+ monocytic antigen-presenting cells in tumors. Immunity 48, 91–106 (2018). · DOI
  67. Kawashima, H. et al. Tumor suppressor p53 inhibits systemic autoimmune diseases by inducing regulatory T cells. J. Immunol. 191, 3614–3623 (2013). · DOI
  68. Stein, Y., Aloni-Grinstein, R. & Rotter, V. Mutant p53—a potential player in shaping the tumor–stroma crosstalk. J. Mol. Cell Biol. 11, 600–604 (2019). · DOI
  69. Guha, T. & Malkin, D. Inherited TP53 mutations and the Li-Fraumeni syndrome. Cold Spring Harb. Perspect. Med. 7, a026187 (2017). · DOI · Paper page
  70. Yoshii, S. et al. Exosomal microRNAs derived from colon cancer cells promote tumor progression by suppressing fibroblast TP53 expression. Cancer Sci. 110, 2396–2407 (2019). · DOI
  71. Capaci, V. et al. Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome. Nat. Commun. 11, 3945 (2020). · DOI
  72. Ma, S. et al. Gain-of-function p53 protein transferred via small extracellular vesicles promotes conversion of fibroblasts to a cancer-associated phenotype. Cell Rep. 34, 108726 (2021).
  73. Addadi, Y. et al. p53 status in stromal fibroblasts modulates tumor growth in an SDF1-dependent manner. Cancer Res. 70, 9650–9658 (2010). · DOI
  74. Schauer, I. G. et al. Interleukin-1β promotes ovarian tumorigenesis through a p53/NF-κB-mediated inflammatory response in stromal fibroblasts. Neoplasia 15, 409–420 (2013). · DOI
  75. Narendran, A. et al. Mutant p53 in bone marrow stromal cells increases VEGF expression and supports leukemia cell growth. Exp. Hematol. 31, 693–701 (2003). · DOI
  76. Liu, Q. et al. p53 mutant p53N236S regulates cancer-associated fibroblasts properties through Stat3 pathway. Onco Targets Ther. 13, 1355–1363 (2020). · DOI
  77. Guo, G. et al. Trp53 inactivation in the tumor microenvironment promotes tumor progression by expanding the immunosuppressive lymphoid-like stromal network. Cancer Res. 73, 1668–1675 (2013). · DOI
  78. Ren, G. et al. CCR2-dependent recruitment of macrophages by tumor-educated mesenchymal stromal cells promotes tumor development and is mimicked by TNFα. Cell Stem Cell 11, 812–824 (2012). · DOI · Paper page
  79. Huang, Y. et al. p53 regulates mesenchymal stem cell-mediated tumor suppression in a tumor microenvironment through immune modulation. Oncogene 33, 3830–3838 (2014). · DOI
  80. Butera, G. et al. The mutant p53-driven secretome has oncogenic functions in pancreatic ductal adenocarcinoma cells. Biomolecules 10, 884 (2020). · DOI
  81. Madar, S. et al. Mutant p53 attenuates the anti-tumorigenic activity of fibroblasts-secreted interferon β. PLoS ONE 8, e61353 (2013). · DOI
  82. Ju, Q. et al. Mutant p53 increases exosome-mediated transfer of miR-21-3p and miR-769-3p to promote pulmonary metastasis. Chin. J. Cancer Res. 31, 533–546 (2019). · DOI
  83. Sun, J. & Hemler, M. E. Regulation of MMP-1 and MMP-2 production through CD147/extracellular matrix metalloproteinase inducer interactions. Cancer Res. 61, 2276–2281 (2001).
  84. Zhu, H. et al. A role for p53 in the regulation of extracellular matrix metalloproteinase inducer in human cancer cells. Cancer Biol. Ther. 8, 1722–1728 (2009). · doi:10.4161/cbt.8.18.9207
  85. Amit-Cohen, B. C., Rahat, M. M. & Rahat, M. A. Tumor cell–macrophage interactions increase angiogenesis through secretion of EMMPRIN. Front. Physiol. 4, 178 (2013).
  86. Zheng, H. et al. Pathobiological characteristics of intestinal and diffuse-type gastric carcinoma in Japan: an immunostaining study on the tissue microarray. J. Clin. Pathol. 60, 273–277 (2007). · DOI
  87. Rahnamoun, H. et al. Mutant p53 shapes the enhancer landscape of cancer cells in response to chronic immune signaling. Nat. Commun. 8, 754 (2017). · DOI
  88. Godefroy, E. & Bhardwaj, N. Dysregulation of anti-tumor immunity by the matrix metalloproteinase-2. Oncoimmunology 1, 109–111 (2012). · doi:10.4161/onci.1.1.17994
  89. Owyong, M. et al. MMP9 modulates the metastatic cascade and immune landscape for breast cancer anti-metastatic therapy. Life Sci. Alliance 2, e201800226 (2019). · DOI
  90. Yu, Q. & Stamenkovic, I. Cell surface-localized matrix metalloproteinase-9 proteolytically activates TGF-β and promotes tumor invasion and angiogenesis. Genes Dev. 14, 163–176 (2000). · DOI · Paper page
  91. Yoshida, D., Kim, K., Noha, M. & Teramoto, A. Hypoxia inducible factor 1-α regulates of platelet derived growth factor-B in human glioblastoma cells. J. Neurooncol. 76, 13–21 (2006). · DOI
  92. Bourhis, M., Palle, J., Galy-Fauroux, I. & Terme, M. Direct and indirect modulation of T cells by VEGF-A counteracted by anti-angiogenic treatment. Front. Immunol. 12, 616837 (2021). · DOI · Paper page
  93. Gabrilovich, D. I. et al. Production of vascular endothelial growth factor by human tumors inhibits the functional maturation of dendritic cells. Nat. Med. 2, 1096–1103 (1996). · DOI · Paper page
  94. Amelio, I. et al. p53 mutants cooperate with HIF-1 in transcriptional regulation of extracellular matrix components to promote tumor progression. Proc. Natl Acad. Sci. USA 115, E10869–E10878 (2018). · DOI
  95. Pfister, N. T. et al. Mutant p53 cooperates with the SWI/SNF chromatin remodeling complex to regulate VEGFR2 in breast cancer cells. Genes Dev. 29, 1298–1315 (2015). · DOI
  96. Yeudall, W. A. et al. Gain-of-function mutant p53 upregulates CXC chemokines and enhances cell migration. Carcinogenesis 33, 442–451 (2012). · DOI
  97. Novo, D. et al. Mutant p53s generate pro-invasive niches by influencing exosome podocalyxin levels. Nat. Commun. 9, 5069 (2018). · DOI
  98. Liu, Y., Leslie, P. L. & Zhang, Y. Life and death decision-making by p53 and implications for cancer immunotherapy. Trends Cancer 7, 226–239 (2021). · DOI
  99. Assoun, S. et al. Association of TP53 mutations with response and longer survival under immune checkpoint inhibitors in advanced non-small-cell lung cancer. Lung Cancer 132, 65–71 (2019). · DOI · Paper page
  100. Sun, H. et al. Specific TP53 subtype as biomarker for immune checkpoint inhibitors in lung adenocarcinoma. EBioMedicine 60, 102990 (2020). · DOI · Paper page
  101. Cha, Y. J., Kim, H. R., Lee, C. Y., Cho, B. C. & Shim, H. S. Clinicopathological and prognostic significance of programmed cell death ligand-1 expression in lung adenocarcinoma and its relationship with p53 status. Lung Cancer 97, 73–80 (2016). · DOI
  102. Liu, N. et al. Mutant p53 achieved gain-of-function by promoting tumor growth and immune escape through PHLPP2/AKT/PD-L1 pathway. Int. J. Biol. Sci. 18, 2419–2438 (2022). · DOI
  103. Zhou, X. et al. Pharmacologic activation of p53 triggers viral mimicry response thereby abolishing tumor immune evasion and promoting antitumor immunity. Cancer Discov. 11, 3090–3105 (2021). · DOI · Paper page
  104. Zhang, W. W. et al. The first approved gene therapy product for cancer Ad-p53 (Gendicine): 12 years in the clinic. Hum. Gene Ther. 29, 160–179 (2018). · DOI · Paper page
  105. Kim, S. S., Harford, J. B., Moghe, M., Rait, A. & Chang, E. H. Combination with SGT-53 overcomes tumor resistance to a checkpoint inhibitor. Oncoimmunology 7, e1484982 (2018). · DOI
  106. Xiao, Y. et al. Combining p53 mRNA nanotherapy with immune checkpoint blockade reprograms the immune microenvironment for effective cancer therapy. Nat. Commun. 13, 758 (2022).
  107. Chada, S. et al. Tumor suppressor immune gene therapy to reverse immunotherapy resistance. Cancer Gene Ther. 29, 825–834 (2022). · DOI
  108. Ghosh, A. et al. Increased p53 expression induced by APR-246 reprograms tumor-associated macrophages to augment immune checkpoint blockade. J. Clin. Invest. 132, e148141 (2022). · DOI
  109. Martinov, T. & Greenberg, P. D. Targeting driver oncogenes and other public neoantigens using T cell receptor-based cellular therapy. Annu. Rev. Cancer Biol. 7, 331–351 (2023). · DOI
  110. Malekzadeh, P. et al. Neoantigen screening identifies broad TP53 mutant immunogenicity in patients with epithelial cancers. J. Clin. Invest. 129, 1109–1114 (2019). · DOI · Paper page
  111. Lo, W. et al. Immunologic recognition of a shared p53 mutated neoantigen in a patient with metastatic colorectal cancer. Cancer Immunol. Res. 7, 534–543 (2019). · DOI · Paper page
  112. Malekzadeh, P. et al. Antigen experienced T cells from peripheral blood recognize p53 neoantigens. Clin. Cancer Res. 26, 1267–1276 (2020). · DOI
  113. Jayasinghe, R. G. et al. Systematic analysis of splice-site-creating mutations in cancer. Cell Rep. 23, 270–281 (2018). · DOI · Paper page
  114. Ye, C. et al. Altered HLA-A2-restricted TP53 epitope induces specific CTL cytotoxicity against hepatocellular carcinoma. Eur. J. Immunol. 53, e2250054 (2023).
  115. Kim, S. P. et al. Adoptive cellular therapy with autologous tumor-infiltrating lymphocytes and T-cell receptor-engineered T cells targeting common p53 neoantigens in human solid tumors. Cancer Immunol. Res. 10, 932–946 (2022). · DOI · Paper page
  116. DeLeo, A. B. & Whiteside, T. L. Development of multi-epitope vaccines targeting wild-type sequence p53 peptides. Expert Rev. Vaccines 7, 1031–1040 (2008). · DOI
  117. Vermeij, R. et al. Immunological and clinical effects of vaccines targeting p53-overexpressing malignancies. J. Biomed. Biotechnol. 2011, 702146 (2011).
  118. Xue, Y., San Luis, B. & Lane, D. P. Intratumour heterogeneity of p53 expression; causes and consequences. J. Pathol. 249, 274–285 (2019). · DOI
  119. Lauwen, M. M. et al. Self-tolerance does not restrict the CD4+ T-helper response against the p53 tumor antigen. Cancer Res. 68, 893–900 (2008). · DOI
  120. Hernandez, J., Lee, P. P., Davis, M. M. & Sherman, L. A. The use of HLA A2.1/p53 peptide tetramers to visualize the impact of self tolerance on the TCR repertoire. J. Immunol. 164, 596–602 (2000). · DOI
  121. Zwaveling, S. et al. Antitumor efficacy of wild-type p53-specific CD4+ T-helper cells. Cancer Res. 62, 6187–6193 (2002).
  122. Leffers, N. et al. Immunization with a p53 synthetic long peptide vaccine induces p53-specific immune responses in ovarian cancer patients, a phase II trial. Int. J. Cancer 125, 2104–2113 (2009). · DOI
  123. Vermeij, R. et al. Potentiation of a p53-SLP vaccine by cyclophosphamide in ovarian cancer: a single-arm phase II study. Int. J. Cancer 131, E670–E680 (2012). · DOI · Paper page
  124. Speetjens, F. M. et al. Induction of p53-specific immunity by a p53 synthetic long peptide vaccine in patients treated for metastatic colorectal cancer. Clin. Cancer Res. 15, 1086–1095 (2009). · DOI · Paper page
  125. Svane, I. M. et al. Vaccination with p53-peptide-pulsed dendritic cells, of patients with advanced breast cancer: report from a phase I study. Cancer Immunol. Immunother. 53, 633–641 (2004). · DOI
  126. Antonia, S. J. et al. Combination of p53 cancer vaccine with chemotherapy in patients with extensive stage small cell lung cancer. Clin. Cancer Res. 12, 878–887 (2006). · DOI · Paper page

Cited by

See all 83

Metadata

Authors
Efe, G., Rustgi, A. K., & Prives, C.
ORCID
Venue
Nature Cancer
Publisher
Springer Science and Business Media LLC
Published
2024-07-15
Volume
5
Issue
7
Pages
983-995
ISSN
2662-1347
DOI
10.1038/s43018-024-00796-z
Cited by
83
References
22
Language
en
Licence
Funders
U.S. Department of Health & Human Services | NIH | National Cancer Institute (R35CA220526, P30CA013696, F31CA275369-02, P01-CA098101, R01CA272903-01)

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: p53 at the crossroads of tumor immunity. https://app.cochat.ai/papers/10.1038/s43018-024-00796-z
The paper
Efe, G., Rustgi, A. K., & Prives, C. (2024). p53 at the crossroads of tumor immunity. Nature Cancer. https://doi.org/10.1038/s43018-024-00796-z

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.