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Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Related Experiment Video

Updated: Jul 15, 2026

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Identification of key processes underlying cancer phenotypes using biologic pathway analysis.

Sol Efroni1, Carl F Schaefer, Kenneth H Buetow

  • 1National Cancer Institute Center for Bioinformatics, Rockville, Maryland, United States of America.

Plos One
|May 10, 2007
PubMed
Summary

This study identifies key biological pathways linked to cancer development and progression. These pathways accurately predict tumor type, stage, and patient outcomes, offering new insights into gene-based disease mechanisms.

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Area of Science:

  • Genomics
  • Molecular Biology
  • Cancer Research

Background:

  • Cancer is a group of gene-based diseases caused by disruptions in fundamental biological processes.
  • Current methods for linking disease phenotypes to molecular network alterations are indirect and unsystematic.
  • A systematic approach is needed to map biological pathways to clinical features in cancer.

Purpose of the Study:

  • To objectively identify biological pathways associated with malignancy, staging, and outcome in cancer.
  • To systematically evaluate differences in pathway activity and interaction consistency.
  • To develop a method for mapping genome-wide data to clinical features.

Main Methods:

  • Analysis of large collections of publicly accessible genome-wide gene expression data.
  • Systematic evaluation of differences in activity and consistency of interactions within canonical biological processes.
  • Application of an analytic approach to identify pathways distinguishing tumor types, grades, and phenotypes.

Main Results:

  • Identified small, common sets of pathways (Trka Receptor, Apoptosis response to DNA Damage, Ceramide, Telomerase, CD40L, Calcineurin) that robustly distinguish tumor types from normal samples.
  • These pathways accurately predict tumor grade and phenotypes like estrogen receptor status and p53 mutation state.
  • Identified pathways demonstrated equal or superior performance compared to existing phenotypes in predicting cancer outcomes.

Conclusions:

  • The identified pathways provide robust biomarkers for cancer classification and prognostication.
  • This approach enables the use of genome-wide data to link key biological processes to critical clinical features in cancer.
  • The findings offer a systematic means to understand the molecular underpinnings of cancer heterogeneity and progression.