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Related Concept Videos

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...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
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...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...

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Related Experiment Video

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Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells
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Tumour vasculature at single-cell resolution.

Xu Pan1,2,3, Xin Li1,4,5, Liang Dong6

  • 1Clinical Research Center (CRC), Medical Pathology Center (MPC), Cancer Early Detection and Treatment Center (CEDTC) and Translational Medicine Research Center (TMRC), Chongqing University Three Gorges Hospital, Chongqing University, Chongqing, China.

Nature
|July 10, 2024
PubMed
Summary

This study maps tumor vasculature at single-cell resolution, revealing how blood vessels form and suggesting APLN+ Tip cells may predict anti-VEGF therapy response.

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Area of Science:

  • Oncology
  • Vascular Biology
  • Single-cell Genomics

Background:

  • Tumor growth and metastasis depend on blood supply and angiogenesis.
  • Understanding tumor vasculature is crucial for developing anti-angiogenic therapies.

Purpose of the Study:

  • To create a comprehensive single-cell atlas of tumor vasculature across diverse cancer types.
  • To elucidate the cellular dynamics and communication within tumor neovascularization.
  • To identify potential biomarkers for disease progression and therapy response.

Main Methods:

  • Single-cell RNA sequencing of approximately 200,000 cells from 372 donors across 31 cancer types.
  • Trajectory inference to model angiogenic cell differentiation pathways.
  • Intercellular communication analysis to understand microenvironment interactions.

Main Results:

  • Tumor angiogenesis initiates from venous endothelial cells and progresses towards arterialization.
  • APLN+ Tip cells (APLN+ TipSI) and their transition to TipSIII cells involve Notch signaling.
  • Stalk cells differentiate with changes in chemokine and TEK expression.
  • APLN+ TipSI cells correlate with disease progression and predict anti-VEGF therapy response.
  • Distinct lineages of lymphatic endothelial cells were identified for lymphangiogenesis and antigen presentation.
  • Endoplasmic reticulum stress in pericytes is linked to proangiogenic BASP1+ matrix production.
  • Neovascular endothelial cells contribute to an immunosuppressive tumor microenvironment.

Conclusions:

  • This atlas provides unprecedented detail on tumor vasculature complexity at single-cell resolution.
  • APLN+ TipSI cells represent a promising biomarker for predicting anti-VEGF therapy outcomes.
  • The findings have significant implications for the clinical application of anti-angiogenic therapies.