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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

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Related Experiment Video

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A Modified Sonographic Algorithm for Image Acquisition in Life-Threatening Emergencies in the Critically Ill Newborn
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From CMS to iCMS/IMF: Developing Roadmap to Precision Therapy in Colorectal Cancer.

Sungwon Jung1,2

  • 1Department of Genome Medicine and Science, Gachon University College of Medicine, Incheon 21565, Republic of Korea.

International Journal of Molecular Sciences
|November 27, 2025
PubMed
Summary

The intrinsic subtype-MSI-fibrosis (IMF) system refines colorectal cancer (CRC) classification and treatment strategies. This framework integrates molecular subtypes, MSI status, and fibrosis for precise therapeutic decisions.

Keywords:
CMSIMFcolorectal cancerfibrosisiCMSsingle-cell

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Area of Science:

  • Oncology
  • Molecular Biology
  • Bioinformatics

Background:

  • Colorectal cancer (CRC) classification evolved from Consensus Molecular Subtypes (CMS) to epithelial-intrinsic subtypes (iCMS) and the layered Intrinsic Subtype-MSI-Fibrosis (IMF) system.
  • The IMF system integrates intrinsic molecular states, microsatellite instability (MSI) status, and tumor fibrosis for a comprehensive classification.

Purpose of the Study:

  • To review the biological basis of iCMS/IMF, their connection to tumor microenvironment (TME) crosstalk, and the role of advanced transcriptomics.
  • To explore how single-cell and spatial transcriptomics enhance therapeutic stratification by analyzing TME heterogeneity and fibrosis.
  • To outline prognostic and therapeutic implications, including immunotherapy, targeted therapies, and decision points based on the fibrosis axis.

Main Methods:

  • Review of existing literature on iCMS/IMF, TME crosstalk, and transcriptomic technologies.
  • Analysis of how single-cell and spatial transcriptomics resolve TME heterogeneity and its impact on fibrosis.
  • Integration of pathology, molecular diagnostics, and therapy mapping for precision medicine.

Main Results:

  • The IMF system provides a refined framework for understanding CRC biology and TME interactions.
  • Single-cell and spatial transcriptomics offer deeper insights into TME heterogeneity and its influence on fibrosis.
  • Specific therapeutic strategies are suggested for MSI-high, BRAF-mutant, and RAS wild-type tumors, informed by the IMF system.

Conclusions:

  • The iCMS/IMF framework facilitates reproducible classification and enhances precision medicine in colorectal cancer.
  • Integrating pathology, molecular diagnostics, and therapy mapping with advanced imaging and therapeutics offers a roadmap for future CRC treatment.
  • Future research should focus on biomarker-drug hypotheses for microsatellite-stable iCMS3 and high-fibrosis tumors to advance clinical translation.