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Related Concept Videos

Cancer Stem Cells and Tumor Maintenance02:40

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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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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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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged 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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An In Vitro System to Study Tumor Dormancy and the Switch to Metastatic Growth
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An In Vitro System to Study Tumor Dormancy and the Switch to Metastatic Growth

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Tumor cell dormancy.

Roger R Gomis1, Sylwia Gawrzak2

  • 1Oncology Program, Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08028 Barcelona, Spain; ICREA Institució Catalana de Recerca i Estudis Avançats, 08010 Barcelona, Spain.

Molecular Oncology
|December 27, 2016
PubMed
Summary
This summary is machine-generated.

Metastatic cancer cells can remain dormant for years, evading treatment and treatment detection. Understanding tumor dormancy mechanisms is crucial for developing new therapies to combat cancer spread and improve patient survival.

Keywords:
Breast cancerCancerDormancyLatencyMetastasis

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Area of Science:

  • Oncology
  • Cancer Biology
  • Cellular Biology

Background:

  • Metastasis is the leading cause of cancer-related mortality, with current treatments often failing to achieve lasting results.
  • Tumor dormancy, characterized by dormant disseminated tumor cells (DTCs), poses a significant challenge, as these cells can evade therapy and persist for years before causing overt metastasis.
  • Effective models that accurately replicate metastatic dormancy and colonization of critical tissues like bone are scarce, hindering research and therapeutic development.

Approach:

  • This review synthesizes recent advancements in understanding the factors contributing to metastatic dormancy.
  • It explores both intrinsic genetic properties of DTCs and extrinsic microenvironmental changes that promote their survival and colonization.
  • Focuses on models that recapitulate dormancy and metastasis to clinically relevant tissues, particularly bone.

Key Points:

  • Dormant disseminated tumor cells (DTCs) can evade cancer treatments and persist for extended periods.
  • Both genetic factors within DTCs and the surrounding microenvironment influence their survival and ability to colonize distant sites.
  • The development of improved models is essential for studying metastatic dormancy and bone metastasis.

Conclusions:

  • Further research into the mechanisms of tumor dormancy is vital for improving cancer detection and treatment strategies.
  • Targeting both cell-autonomous and microenvironmental factors may offer novel therapeutic avenues for managing metastatic disease.
  • Innovations in modeling metastatic dormancy are needed to advance our understanding and clinical management of cancer metastasis.