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Tumor Progression

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...

Loss of Tumor Suppressor Gene Functions

Loss of Tumor Suppressor Gene Functions

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 Immunotherapy

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

Replicative Cell Senescence

Replicative Cell Senescence

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...

The Retinoblastoma Gene

The Retinoblastoma Gene

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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Cancer-Critical Genes II: Tumor Suppressor Genes

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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Related Experiment Video

Updated: Nov 6, 2025

A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing Neoadjuvant Therapies

A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing Neoadjuvant Therapies

Published on: July 28, 2020

Tumor reversion: a dream or a reality.

Avantika Tripathi¹, Anjali Kashyap², Greesham Tripathi¹

¹Amity Stem Cell Institute, Amity Medical School, Amity University Haryana, Panchgaon, Haryana, Manesar (Gurugram), -122413, India.

Biomarker Research

|May 7, 2021

Summary

Tumor reversion, the process of turning cancer cells back into normal cells, is becoming a reality. Advances in molecular biology and genome editing offer new therapeutic strategies for cancer treatment.

Keywords:

PTMs Phenotype reversion Revertant SIAH1 TCTP1 Tumor reversion

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Last Updated: Nov 6, 2025

A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing Neoadjuvant Therapies

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Published on: July 28, 2020

The Influence of Liver Resection on Intrahepatic Tumor Growth

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Flow Cytometric Detection of Newly-formed Breast Cancer Stem Cell-like Cells After Apoptosis Reversal

Flow Cytometric Detection of Newly-formed Breast Cancer Stem Cell-like Cells After Apoptosis Reversal

Published on: January 26, 2019

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

Tumor reversion, once a theoretical concept, is now approaching clinical feasibility.
Multiple molecular mechanisms, including microRNAs, transcription factors, and advanced editing tools, are implicated in cancer cell phenotype modulation.

Purpose of the Study:

To review current developments in tumor reversion research.
To identify existing challenges and future directions for therapeutic applications of tumor reversion.

Main Methods:

Review of literature on molecular mechanisms and therapeutic approaches.
Analysis of genome-editing techniques, proteomics, and chemical biology strategies.
Evaluation of in vitro and in vivo tumor regression models.

Main Results:

Subtle but definitive evidence supports the manipulation of cancer cells towards a normal phenotype.
Genome-editing and proteomics profiling show early promise in tumor regression models.
Therapeutic compounds are identified that induce normal cell phenotypes in cancer cells.

Conclusions:

Significant progress has been made in understanding and manipulating tumor reversion.
Further refinement of in vitro and in vivo models is crucial for clinical translation.
Tumor reversion holds promise for a new era of cancer therapies impacting clinical practice.