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Forced Transdifferentiation01:28

Forced Transdifferentiation

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Transdifferentiation, also known as lineage reprogramming, was first discovered by Selman and Kafatos in 1974 in silkmoths. They observed that the moths’ cuticle-producing cells transformed into salt-producing cells. Many such cases of natural transdifferentiation occur in organisms. In humans, pancreatic alpha cells can become beta cells. In newts, the loss of the eye’s lens causes the pigmented epithelial cells to transdifferentiate into the lens cells.
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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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Related Experiment Video

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Hypothesis about Transdifferentiation As Backbone of Malignancy.

Jean Piechowski1

  • 1Physician-Radiotoxicologist, Paris, France.

Frontiers in Oncology
|July 5, 2017
PubMed
Summary

Cancer progression involves more than random mutations; a proposed "malignant transdifferentiation" involves trophoblastic and sexual cell functions. Targeting the trophoblastic phenotype offers a novel therapeutic strategy with minimal side effects.

Keywords:
cancerepigeneticsgerm cellsstem-like cellstransdifferentiationtrophoblast

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Area of Science:

  • Oncology
  • Cell Biology
  • Developmental Biology

Background:

  • Cancer is traditionally viewed as resulting from random mutations and signaling pathway disruptions.
  • However, stochastic genomic alterations alone do not fully explain tumor organization, aggressiveness, and evolution.
  • A deeper understanding of cancer's complex behavior is needed.

Purpose of the Study:

  • To propose a new hypothesis for oncogenesis beyond stochastic mutations.
  • To identify key cellular phenotypes driving cancer progression.
  • To explore novel therapeutic targets based on these phenotypes.

Main Methods:

  • Conceptual hypothesis generation based on observed cancer cell properties.
  • Analysis of cancer cell phenotypes in relation to normal physiological functions.
  • Identification of potential therapeutic strategies targeting specific cancer cell characteristics.

Main Results:

  • Cancer cells exhibit two primary phenotypes: trophoblastic functions (survival, migration, angiogenesis, immune tolerance) and sexual functions (genome maintenance).
  • A novel cell reprogramming, termed "malignant transdifferentiation," is hypothesized to drive the shift from precancer to cancer.
  • The trophoblastic phenotype is crucial for tumor viability and offers a potential therapeutic target.

Conclusions:

  • Malignant transdifferentiation offers a more rational framework for understanding oncogenesis.
  • Targeting the trophoblastic phenotype presents a promising therapeutic avenue.
  • This approach may lead to novel treatments with reduced toxicity to healthy tissues as the trophoblastic phenotype is not normally expressed postnatally.