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Adaptive Mechanisms in Cancer Cells02:53

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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 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...
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Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
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Are rapidly growing cancers more lethal?

Hans-Olov Adami1, Peter Csermely2, Daniel V Veres3

  • 1Clinical Effectiveness Research Group, Institute of Health and Society, University of Oslo, Oslo, Norway; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

European Journal of Cancer (Oxford, England : 1990)
|January 3, 2017
PubMed
Summary
This summary is machine-generated.

Rapidly growing tumors are not more likely to metastasize or be lethal. This study analyzed cancer growth and metastasis, finding no evidence to support the long-held belief, challenging current screening and treatment approaches.

Keywords:
Breast cancerCancer stem-like cellsCervical cancerColorectal cancerDormancyLethalityMetastasisSignalling networksTumour growth

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Area of Science:

  • Oncology
  • Cancer Biology
  • Molecular Biology

Background:

  • The long-standing assumption is that rapid tumor growth correlates with increased metastasis and lethality.
  • This axiomatic view has lacked robust scientific validation for decades.

Purpose of the Study:

  • To investigate the relationship between tumor growth rate and metastatic potential.
  • To challenge the prevailing dogma regarding rapidly growing cancers and their propensity to metastasize.

Main Methods:

  • Conducted an exhaustive system-level analysis of intra- and intercellular signaling networks.
  • Reviewed human evidence from screening interventions, focusing on interval cancers (breast, cervix, large bowel).

Main Results:

  • Analysis indicated rapid growth and metastasis are often distinct outcomes of complex molecular events.
  • Human data from breast, cervix, and large bowel cancers provided no support for the theory that rapid growth increases metastasis.
  • Interval cancers were not found to be more prone to metastasis than non-interval cancers.

Conclusions:

  • The prevailing view linking rapid tumor growth to higher metastatic potential should be reconsidered.
  • The impact of length-biased sampling in cancer screening requires re-evaluation.
  • Current findings do not support more aggressive treatment for interval cancers compared to non-interval cancers.