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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...
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...

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Correction: Kim et al. Identification of <i>GREM-1</i> and <i>GAS6</i> as Specific Biomarkers for Cancer-Associated Fibroblasts Derived from Patients with Non-Small-Cell Lung Cancer. <i>Cancers</i> 2025, <i>17</i>, 2858.

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Pan-Cancer Single-Cell RNA Sequencing Analysis Refines Multi-Origin Monocyte and Macrophage Lineages.

Truc Do Thanh Nguyen1,2, Andrew J Lee3, Hyun Jung Park1,4

  • 1Translational Genomics Center, Samsung Medical Center, Seoul, Republic of Korea.

Cancer Immunology Research
|November 13, 2025
PubMed
Summary
This summary is machine-generated.

Tumor-associated macrophages (TAMs) have diverse origins, influencing cancer progression. Identifying TAM subtypes offers new therapeutic strategies for better patient outcomes and immunotherapy response.

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Area of Science:

  • Immunology
  • Oncology
  • Genomics

Background:

  • Tumor-associated macrophages (TAMs) are key regulators of the tumor microenvironment, impacting cancer progression, immune evasion, and blood vessel formation.
  • Understanding TAM heterogeneity is crucial for developing effective cancer therapies.

Purpose of the Study:

  • To create a comprehensive myeloid cell atlas in healthy and cancer tissues using single-cell transcriptomics.
  • To investigate the origins and functional roles of distinct TAM subsets.
  • To explore the implications of TAM heterogeneity for patient prognosis and immunotherapy response.

Main Methods:

  • Single-cell transcriptomics analysis of myeloid cell populations.
  • Comparative analysis across healthy and pan-cancer tissues.
  • Identification and characterization of specific TAM and myeloid-derived suppressor cell (MDSC) subtypes.

Main Results:

  • Revealed significant heterogeneity within TAM populations, suggesting dual origins: resident tissue macrophages (C1QC+ TAMs) and circulating monocytes (SPP1+ TAMs, ISG15+ TAMs).
  • Identified THBS1+ MDSCs and their SPP1+ TAM descendants as critical drivers of tumor progression, immunosuppression, and angiogenesis.
  • Established a dichotomous TAM model: C1QC+ TAMs correlate with better outcomes, while the THBS1+ MDSCs-SPP1+ TAMs lineage is linked to poorer survival and immunotherapy resistance.

Conclusions:

  • TAMs exhibit distinct origins and functional states, influencing cancer dynamics.
  • The THBS1+ MDSCs-SPP1+ TAMs axis represents a pro-tumorigenic pathway.
  • Targeting specific TAM subsets holds promise for improving cancer treatment strategies and immunotherapy efficacy.