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Nature

Our medical research library holds 35 studies published in Nature (1961–2025). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 4 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 2 studies PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

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About the journal

  • Publisher: Nature Publishing Group
  • Published: 1869 to the present, England
  • Language: English
  • ISSN: 0028-0836 (print), 1476-4687 (electronic)
  • Its record in the NLM Catalog

2020s

  • Tumour-wide RNA splicing aberrations generate actionable public neoantigens. D.W. Kwok, N.O. Stevers, I. Etxeberria, et al. 2025;639(8054):463-473. PubMed · Publisher · Free full text

    Abstract

    T cell-based immunotherapies hold promise in treating cancer by leveraging the immune system's recognition of cancer-specific antigens1. However, their efficacy is limited in tumours with few somatic mutations and substantial intratumoural heterogeneity2-4. Here we introduce a previously uncharacterized class of tumour-wide public neoantigens originating from RNA splicing aberrations in diverse cancer types. We identified T cell receptor clones capable of recognizing and targeting neoantigens derived from aberrant splicing in GNAS and RPL22. In cases with multi-site biopsies, we detected the tumour-wide expression of the GNAS neojunction in glioma, mesothelioma, prostate cancer and liver cancer. These neoantigens are endogenously generated and presented by tumour cells under physiologic conditions and are sufficient to trigger cancer cell eradication by neoantigen-specific CD8+ T cells. Moreover, our study highlights a role for dysregulated splicing factor expression in specific cancer types, leading to recurrent patterns of neojunction upregulation. These findings establish a molecular basis for T cell-based immunotherapies addressing the challenges of intratumoural heterogeneity.

    © 2025. The Author(s).

2010s

  • Intercellular interaction dictates cancer cell ferroptosis via NF2-YAP signalling. J. Wu, A.M. Minikes, M. Gao, et al. 2019;572(7769):402-406. PubMed · Publisher · Free full text

    Abstract

    Ferroptosis, a cell death process driven by cellular metabolism and iron-dependent lipid peroxidation, has been implicated in diseases such as ischaemic organ damage and cancer1,2. The enzyme glutathione peroxidase 4 (GPX4) is a central regulator of ferroptosis, and protects cells by neutralizing lipid peroxides, which are by-products of cellular metabolism. The direct inhibition of GPX4, or indirect inhibition by depletion of its substrate glutathione or the building blocks of glutathione (such as cysteine), can trigger ferroptosis3. Ferroptosis contributes to the antitumour function of several tumour suppressors such as p53, BAP1 and fumarase4-7. Counterintuitively, mesenchymal cancer cells-which are prone to metastasis, and often resistant to various treatments-are highly susceptible to ferroptosis8,9. Here we show that ferroptosis can be regulated non-cell-autonomously by cadherin-mediated intercellular interactions. In epithelial cells, such interactions mediated by E-cadherin suppress ferroptosis by activating the intracellular NF2 (also known as merlin) and Hippo signalling pathway. Antagonizing this signalling axis allows the proto-oncogenic transcriptional co-activator YAP to promote ferroptosis by upregulating several ferroptosis modulators, including ACSL4 and TFRC. This finding provides mechanistic insights into the observations that cancer cells with mesenchymal or metastatic property are highly sensitive to ferroptosis8. Notably, a similar mechanism also modulates ferroptosis in some non-epithelial cells. Finally, genetic inactivation of the tumour suppressor NF2, a frequent tumorigenic event in mesothelioma10,11, rendered cancer cells more sensitive to ferroptosis in an orthotopic mouse model of malignant mesothelioma. Our results demonstrate the role of intercellular interactions and intracellular NF2-YAP signalling in dictating ferroptotic death, and also suggest that malignant mutations in NF2-YAP signalling could predict the responsiveness of cancer cells to future ferroptosis-inducing therapies.

  • BAP1 regulates IP3R3-mediated Ca2+ flux to mitochondria suppressing cell transformation. A. Bononi, C. Giorgi, S. Patergnani, et al. 2017;546(7659):549-553. PubMed · Publisher · Free full text

    Abstract

    BRCA1-associated protein 1 (BAP1) is a potent tumour suppressor gene that modulates environmental carcinogenesis. All carriers of inherited heterozygous germline BAP1-inactivating mutations (BAP1+/-) developed one and often several BAP1-/- malignancies in their lifetime, mostly malignant mesothelioma, uveal melanoma, and so on. Moreover, BAP1-acquired biallelic mutations are frequent in human cancers. BAP1 tumour suppressor activity has been attributed to its nuclear localization, where it helps to maintain genome integrity. The possible activity of BAP1 in the cytoplasm is unknown. Cells with reduced levels of BAP1 exhibit chromosomal abnormalities and decreased DNA repair by homologous recombination, indicating that BAP1 dosage is critical. Cells with extensive DNA damage should die and not grow into malignancies. Here we discover that BAP1 localizes at the endoplasmic reticulum. Here, it binds, deubiquitylates, and stabilizes type 3 inositol-1,4,5-trisphosphate receptor (IP3R3), modulating calcium (Ca2+) release from the endoplasmic reticulum into the cytosol and mitochondria, promoting apoptosis. Reduced levels of BAP1 in BAP1+/- carriers cause reduction both of IP3R3 levels and of Ca2+ flux, preventing BAP1+/- cells that accumulate DNA damage from executing apoptosis. A higher fraction of cells exposed to either ionizing or ultraviolet radiation, or to asbestos, survive genotoxic stress, resulting in a higher rate of cellular transformation. We propose that the high incidence of cancers in BAP1+/- carriers results from the combined reduced nuclear and cytoplasmic activities of BAP1. Our data provide a mechanistic rationale for the powerful ability of BAP1 to regulate gene-environment interaction in human carcinogenesis.

  • Asbestos scandal. 2010;468(7326):868. Editorial PubMed · Publisher

    Summary

    This unsigned Nature editorial argued that policies allowing continued asbestos mining, export and use could cause an epidemic of malignant lung disease. It described how inhaled asbestos fibres penetrate the alveoli and the membranes lining the chest cavity and remain there, and how mesothelioma often kills people less than a year after diagnosis. The editorial stated that malignant mesothelioma was unheard of before widespread industrial use of asbestos began in the late nineteenth century, and that it now causes tens of thousands of deaths worldwide each year. It noted that the link between asbestos exposure and the disease was convincingly made in 1960. It criticized the United States for not banning asbestos. It criticized Canada for plans to expand mining that exports asbestos to India, Indonesia and the Philippines, where people have little or no protection. Asbestos from Canada, Russia, Brazil and Kazakhstan was described as routinely mixed into building materials and consumer products. Because the latency is 30 years or more, the editorial said the resulting epidemic may take decades to peak. It rejected the industry claim that chrysotile is safe when handled properly. It attributed conflicting literature to industry-sponsored studies designed to cast doubt, and stated that all forms of asbestos have been proven carcinogenic in humans. It also mentioned concern about erionite. It called for renewed public awareness of the risks of mineral fibres and some man-made fibres, and for governments to ban the extraction, processing and use of materials that can cause serious disease.

    PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

1990s

1980s

  • Misreading of DNA templates containing 8-hydroxydeoxyguanosine at the modified base and at adjacent residues. Y. Kuchino, F. Mori, H. Kasai, et al. 1987;327(6117):77-9. PubMed · Publisher

    Abstract

    It has been shown previously that deoxyguanosine residues in DNA are hydroxylated at the C-8 position both in vitro and in vivo to produce 8-hydroxydeoxyguanosine (8-OH-dG) by various agents that produce oxygen radicals such as reducing reagents-O2, metal ions-O2, polyphenol-H2O2-Fe3+, asbestos-H2O2 or ionizing radiation. These agents are mostly either mutagenic or carcinogenic; therefore, the formation of 8-OH-dG can also be considered a likely cause of mutation or carcinogenesis by oxygen radicals. It is of interest to know whether the 8-OH-dG residue in DNA is misread during DNA replication. To answer this question, we have examined the effect of the 8-OH-dG residue in DNA on the fidelity of DNA replication using a DNA synthesis system in vitro with Escherichia coli DNA polymerase I (Klenow fragment). The synthetic oligodeoxynucleotides, with or without an 8-OH-dG residue in a specified position, were chemically synthesized and used as templates for DNA synthesis under the conditions of the dideoxy chain termination sequencing method. Surprisingly, in addition to misreading of the 8-OH-dG residue itself, pyrimidines next to the 8-OH-dG residue (G has not yet been tested) were also misread.

  • Asbestos risks: Manville tries to pass the buck. S. Budiansky. 1983;304(5924):299. News PubMed · Publisher

  • Asbestos. Conflicts ahead on UK rules. T. Beardsley. 1983;304(5926):479. News PubMed · Publisher

1970s

1960s

  • Haemolytic activity of asbestos and other mineral dusts. G. Macnab, J.S. Harington. 1967;214(5087):522-3. PubMed · Publisher

  • Leahing of constituents of chrysotile asbestos in vivo. A. Holmes, A. Morgan. 1967;215(5099):441-2. PubMed · Publisher

  • Inhibition of virus growth by a toxic factor from asbestos pad and cellulose acetate membrane filters. F. Brown, B. Cartwright, J.F. Newman. 1965;205:310-1. PubMed · Publisher

    Summary

    This short communication examined whether a toxic factor from filters used to sterilize cell culture media reduced the growth of foot-and-mouth disease virus. House had recently shown that Eagle's tissue culture medium eluted from asbestos pads a factor toxic to baby hamster kidney (BHK 21) cells. The authors had earlier found that filtering a phosphate-low medium through a Seitz E.K. asbestos pad considerably reduced virus yield. Monolayers of pig kidney cells or baby hamster kidney cells (BHK 21, clone 13) were infected with foot-and-mouth disease virus type C (strain 997) or type O (strain 1). They were then incubated at 37° in medium that was unfiltered or had been filtered through a Seitz E.K. or Ford's 'Sterimat' asbestos pad or through a cellulose acetate (Millipore) membrane. Virus yield was measured mainly by complement fixation and in some experiments by infectivity. Filtration of phosphate-low or Eagle's medium through either asbestos pad considerably reduced virus yield in both cell types. Membrane filtration had no effect in baby hamster kidney cells. In pig kidney cells, however, it gave yields as low as or lower than asbestos filtration. Mixing filtered with unfiltered medium reduced yield considerably, whereas dilution with 0.15 M sodium chloride had only a small effect. This indicated a toxic factor rather than loss of a nutrient. Medium passing first through an asbestos pad inhibited virus growth, but later samples did not. The authors did not examine the nature of the factor. They concluded that care must be exercised when filters are used to sterilize cell culture solutions intended for virus growth.

    PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

  • Toxicity of cell culture medium due to filtration through asbestos pads. W. House. 1964;201:1242. PubMed · Publisher

  • Asbestosis in non-experimental animals in South Africa. I. Webster. 1963;197:506. PubMed · Publisher

  • A method of treating asbestos filter pads for virus filtration. N.S. Hyslop. 1961;191:305-7. PubMed · Publisher

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