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Related Concept Videos

Metastasis02:30

Metastasis

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.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Metastasis02:30

Metastasis

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.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Tumor Progression02:07

Tumor Progression

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.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
Cellular Adaptation IV: Dysplasia and Metaplasia01:24

Cellular Adaptation IV: Dysplasia and Metaplasia

DysplasiaDysplasia refers to abnormal changes in the size, shape, and organization of mature cells, characterized by pleomorphism, nuclear abnormalities, and increased mitotic activity. It commonly affects epithelial tissues, including the cervix, gastrointestinal tract, respiratory mucosa, and endometrium. Although it may occur alongside hyperplasia, dysplasia is not a true adaptive response but a preneoplastic change with potential to progress to cancer.When confined above the basement...

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Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

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Published on: April 7, 2017

Metastasis: inherent vs. acquired phenotype.

Li-jun Zhang1, Hang Li, Li-ying Zhang

  • 1Department of Clinical Laboratory, Tangdu Hospital, Shaanxi, PR China.

Medical Hypotheses
|December 17, 2009
PubMed
Summary
This summary is machine-generated.

Tumor cells may possess inherent metastatic ability from their origin, challenging the acquired trait model. This suggests metastasis is a continuous process driven by stem cell-like features and successful colonization at new sites.

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08:28

Experimental Metastasis Assay

Published on: August 24, 2010

Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Metastasis Research

Background:

  • The origin of tumor cell metastatic ability is debated, with classic models positing it as an acquired trait via gene mutations.
  • The proposed inherent metastasis model suggests metastatic potential is a constitutive feature of cells from which tumors originate.
  • This model is supported by tumor origins in stem/progenitor cells and the inherent migratory capacity of normal stem cells.

Purpose of the Study:

  • To propose and explore an inherent metastasis model for tumor cells.
  • To re-evaluate the mechanisms driving tumor cell migration and spread.
  • To identify new therapeutic targets for preventing and treating cancer metastasis.

Main Methods:

  • Reviewing existing evidence on stem cell migration and tumor development.
  • Analyzing the implications of an inherent metastasis model for tumor progression.
  • Identifying areas for future research to validate the proposed model.

Main Results:

  • The inherent metastasis model implies continuous metastatic dissemination throughout tumor development.
  • Disseminated tumor cells are predicted to largely possess stem cell-like characteristics.
  • Similar molecular pathways are suggested for stem cell and cancer cell migration.
  • Genomic alterations promoting tumor stem cells exacerbate metastasis.
  • Successful metastasis depends on disseminated cell survival and growth at ectopic sites, not just initial travel.

Conclusions:

  • The inherent metastasis model offers a new paradigm for understanding tumor spread.
  • Further research is needed to confirm if normal stem/progenitor cells migrate to ectopic sites.
  • Investigating normal stem cell migration mechanisms could reveal critical insights into cancer metastasis.
  • This understanding may lead to novel strategies for preventing and treating metastatic disease.