Common critical pathways in embryogenesis and cancer

@article{Kelleher2006CommonCP,
  title={Common critical pathways in embryogenesis and cancer},
  author={Fergal C Kelleher and David William Fennelly and M{\'a}ir{\'i}n Rafferty},
  journal={Acta Oncologica},
  year={2006},
  volume={45},
  pages={375 - 388}
}
Cancer may arise because the developmental programs that create the dramatic alterations in form and structure in embryonic development are potentially corrupted. The cells in our bodies retain memories of these processes and cancer can occur later in life if imperfections occur in the fidelity of these pathways. This article is particularly interested in the phenomenon of epithelial to mesenchymal transition, which occurs in embryogenesis. Also reviewed are the small molecules and pathways… 

Embryonic Programs in Cancer and Metastasis—Insights From the Mammary Gland

  • May Yin Lee
  • Biology
    Frontiers in Cell and Developmental Biology
  • 2022
The study of embryonic development will continue to complement the understanding of the mechanisms of cancer and aid in the discovery of novel therapeutic targets and strategies, given the many overlapping features and similarities of the molecular signatures of normal development and cancer.

Embryogenesis, morphogens and cancer stem cells: putting the puzzle together.

Tumor Reversion Induced by Embryo and Oocyte Extracts

It is observed that molecular factors extracted from Zebrafish embryos during specific developmental phases (20 somites) significantly antagonize proliferation of breast cancer cells, while reversing a number of prominent aspects of malignancy.

LIN28: A Stem Cell Factor with a Key Role in Pediatric Tumor Formation.

It is shown, based on comprehensive literature screen and analysis of published microarray data, that LIN28 expression in pediatric tumors is even more common than in adult tumors, and the possibility that in the case of pediatric cancers, LIN28 acts by preventing normal development/differentiation rather than by...

Similarity in gene-regulatory networks suggests that cancer cells share characteristics of embryonic neural cells

It is shown that inhibition of the epigenetic modification enzyme enhancer of zeste homolog 2 (EZH2), histone deacetylases 1 and 3, lysine demethylase 1A (LSD1), or DNA methyltransferase 1 (DNMT1), which all promote cancer development and progression, leads to postmitotic neuron-like differentiation with loss of malignant features in distinct solid cancer cell lines.

Bone morphogenetic proteins in breast cancer: dual role in tumourigenesis?

This review focuses on the current knowledge of BMP expression, functional roles and involvement in bone metastasis in breast cancer.

Xenopus as a model organism to study heterotrimeric G‐protein pathway during collective cell migration of neural crest

This review aims to provide sufficient evidence supporting how useful Xenopus model with its different tools, such as explants and transplants, paired with improved in vivo imaging techniques, will allow us to tackle the multiple signaling mechanisms involved in neural crest cell migration.

Embryological Basis of Congenital Tumours

If these pathways remain active incessantly and do not obey the normal regulatory mechanisms, cell proliferation becomes independent of the growth stimulus, and this produces a mass—cancer [1–3].

Targeting Hedgehog signaling pathway: Paving the road for cancer therapy

...

References

SHOWING 1-10 OF 121 REFERENCES

Notch and Epithelial-Mesenchyme Transition in Development and Tumor Progression: Another Turn of the Screw

Notch, an ancient cell signaling system that regulates cell fate specification, stem cell maintenance and initiation of differentiation in embryonic and postnatal tissues, may also be involved in the EMT process that occurs during tumor progression and converts polarized epithelial cells into motile, invasive cells.

Notch signaling in development and disease

This review will outline key aspects of Notch signaling and its regulation by endocytosis, glycosylation, and ubiquitination, and overview recent literature elucidating how Notch regulates cell‐lineage decisions in a variety of developmental contexts.

An overview of epithelio-mesenchymal transformation.

  • E. Hay
  • Biology
    Acta anatomica
  • 1995
Interestingly, transfection of either metastatic cells or normal embryonic fibroblasts with the E-cadherin gene converts them to the epithelial phenotype, and it may be possible in the future to manipulate the tissue phenotype of diseased cells to the advantage of the animal.

Hedgehog signalling within airway epithelial progenitors and in small-cell lung cancer

It is proposed that some types of SCLC might recapitulate a critical, Hh-regulated event in airway epithelial differentiation, and a common lethal malignancy that may respond to pharmacological blockade of the Hh signalling pathway is identified.

Notch1 functions as a tumor suppressor in mouse skin

The results indicate that Notch1 functions as a tumor-suppressor gene in mammalian skin and can inhibit β-catenin-mediated signaling.

Epithelium-mesenchyme transition during neural crest development.

The spatiotemporal definability of this system makes it a very useful model for studying EMTs in general, and may act through pathways involving controlled alterations in phosphorylation to effect the complex of responses that make up EMT.

Transformations between epithelium and mesenchyme: normal, pathological, and experimentally induced.

  • E. HayA. Zuk
  • Biology
    American journal of kidney diseases : the official journal of the National Kidney Foundation
  • 1995

Gli and hedgehog in cancer: tumours, embryos and stem cells

Studies in these and other systems suggest that inappropriate function of the Gli transcription factors in stem or precursor cells might lead to the onset of a tumorigenic programme and that these factors are prime targets for anticancer therapies.

Mutations in SUFU predispose to medulloblastoma

It is reported that a subset of children with medulloblastoma carry germline and somatic mutations in SUFU (encoding the human suppressor of fused) of the SHH pathway, accompanied by loss of heterozygosity of the wildtype allele.

Msx2 and Twist cooperatively control the development of the neural crest-derived skeletogenic mesenchyme of the murine skull vault

It is demonstrated that heterozygous loss of Twist function causes a foramen in the skull vault similar to that caused by loss of Msx2 function, and that both the quantity and proliferation of the frontal bone skeletogenic mesenchyme are reduced inMsx2-Twist double mutants compared with individual mutants.
...