The prenatal origins of cancer
Open accessAbstract
The concept that some childhood malignancies arise from postnatally persistent embryonal cells has a long history. Recent research has strengthened the links between driver mutations and embryonal and early postnatal development. This evidence, coupled with much greater detail on the cell of origin and the initial steps in embryonal cancer initiation, has identified important therapeutic targets and provided renewed interest in strategies for the early detection and prevention of childhood cancer.
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HIF-1α is detected by IHC in most ccRCC cases, and high HIF-1α expression is associated with poor survival, which conflicts with a tumor suppressor role.
“Nevertheless, HIF-1α has been detected by immunohistochemistry (IHC) in most ccRCC cases, and high HIF-1α expression was associated with poor survival in ccRCC, which is again inconsistent with a tumor suppressor role [34].”
From Revisiting the HIF switch in the tumor and its immune microenvironment. (2022) · cites this paper as [34]
The supplied Neuroblastoma and Medulloblastoma passages discuss MYCN and other developmental cancer mechanisms, not HIF-1α in ccRCC. Further searches for HIF-1α, immunohistochemistry, poor survival, and clear-cell renal carcinoma found no passage in our copy addressing the claim. (LLM, conf=0.78)
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References 189 · Cited by 281
- Authors
- Marshall, G. M., Carter, D. R., Cheung, B. B., Liu, T., Mateos, M. K., Meyerowitz, J. G., & Weiss, W. A.
- Affiliations
- UNSW Sydney (AU)
- University of California, San Francisco (US)
- Corresponding author
- Marshall, Glenn M.
- ORCID
- Venue
- Nature Reviews Cancer
- Published
- 2014-03-06
- Volume
- 14
- Issue
- 4
- Pages
- 277-289
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- PMC
- PMC4041218
- OpenAlex
- W2149005023
- Cited by
- 281
- References
- 189
- Citations by year
- 2026: 13 · 2025: 20 · 2024: 17 · 2023: 19 · 2022: 24 · 2021: 31 · 2020: 21 · 2019: 36 · 2018: 26 · 2017: 18 · 2016: 25 · 2015: 25 · 2014: 6
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- UNSWorks (University of New South Wales, Sydney, Australia) (submittedVersion, cc-by-nc-nd)
- UNSWorks (UNSW Sydney) (submittedVersion, cc-by-nc-nd)
- eScholarship (California Digital Library) (submittedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Cancer Institute NSW
- University of New South Wales
- National Institutes of Health
- National Health and Medical Research Council
- Cancer Council NSW
- National Cancer Institute (R01CA148699, P01CA081403, R01CA102321, U01CA176287, F30CA174154, U54CA163155, R01CA133091, R01CA159859)
- National Institute of General Medical Sciences (T32GM007618, T32GM064337)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Acute Lymphoblastic Leukemia research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- childhood cancer, driver mutations, cell of origin, tumor initiation, early cancer detection, cancer prevention, therapeutic target
- MeSH terms
- Animals, B-Lymphocytes, Cerebellar Neoplasms, Child, Down Syndrome, Embryo, Mammalian, Female, Humans, Medulloblastoma, Mutation, Myeloproliferative Disorders, Neural Crest, Neuroblastoma, Pregnancy, Genomic Instability, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Carcinogenesis
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