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Cancers Originate from Somatic Mutations in a Single Cell

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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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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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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.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...

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Related Experiment Video

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A "Patient-Like" Orthotopic Syngeneic Mouse Model of Hepatocellular Carcinoma Metastasis

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Published on: October 24, 2015

Single-Cell Multi-Omics Reveals B2M-Mediated Myeloid Reprogramming and Constructs a Predictive Model for Early

Zhenyao Tan^1,2, Yezhen Tang³, Bendong Chen^1,2

¹Department of Hepatobiliary Surgery, General Hospital of Ningxia Medical University, Yinchuan, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|December 22, 2025

Summary

Early hepatocellular carcinoma (HCC) recurrence is a challenge. This study used multi-omics to find B2M-related immune changes driving recurrence, offering a predictive tool and potential therapies.

Keywords:

B2M early recurrence hepatocellular carcinoma macrophages predictors

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Area of Science:

Oncology
Immunology
Genomics

Background:

Early recurrence of hepatocellular carcinoma (HCC) poses a significant clinical challenge.
The underlying molecular mechanisms driving early HCC recurrence remain incompletely understood.

Purpose of the Study:

To investigate the molecular drivers of early HCC recurrence (recurrence within 2 years) using an integrative multi-omics approach.
To develop a predictive framework for early HCC recurrence.

Main Methods:

Integration of single-cell RNA sequencing, proteomics, transcriptomics, and clinical data.
Identification of relapse-associated proteins and pathways.
Single-cell immune profiling and functional analysis.
Development and validation of a predictive model using LASSO regression.

Main Results:

Identified 14 relapse-associated proteins (e.g., CD274, B2M, MYC, CASP3).
Transcriptomic analysis revealed enrichment of MYC-TARGETS-V2 and INTERFERON-GAMMA-RESPONSE pathways.
Single-cell analysis showed reduced immune infiltration in recurrent tumors, with myeloid cells (cDC2, macrophages) exhibiting B2M-associated reprogramming (HLA downregulation, altered GAS6/PROS1 signaling).
A predictive model based on cDC2 and macrophage signatures showed moderate performance (AUC > 0.65).

Conclusions:

B2M may play a role in remodeling the immune microenvironment in recurrent HCC.
The study provides insights into early HCC recurrence mechanisms.
An integrative single-cell multi-omics approach offers a preliminary predictive tool with potential therapeutic implications, including targeting B2M-related pathways with drugs like vandetanib.