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Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

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Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
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Altered P53 conformation.

P Shekhar1, R Welte, J Christman

  • 1KARMANOS CANC INST,DEPT PATHOL,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DETROIT,MI 48201. UNIV ULM,SCH MED,UNIT PUBL HLTH,D-89081 ULM,GERMANY. UNIV NEBRASKA,MED CTR,UNMC EPPLEY CANC CTR,OMAHA,NE 68198. UNIV NEBRASKA,MED CTR,EPPLEY INST RES CANC,OMAHA,NE 68198.

International Journal of Oncology
|April 30, 2011
PubMed
Summary
This summary is machine-generated.

The p53 protein, crucial in cancer, can be functionally impaired even without mutation. This study shows wild-type p53 can alter breast cancer cell growth and morphology, highlighting a new mechanism in tumor progression.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The p53 protein is a critical tumor suppressor and transcription factor.
  • Mutations in p53 are common in human cancers, leading to loss of function.
  • Understanding early events in breast cancer progression is vital.

Purpose of the Study:

  • To investigate the role of p53 in early breast cancer development using the MCF10AT model.
  • To determine if p53 mutations are necessary for preneoplastic changes in breast cancer.
  • To assess the functional status of wild-type p53 in preneoplastic breast cells.

Main Methods:

  • Utilized the MCF10AT cell line, a model for early human breast cancer.
  • Assessed p53 protein status (mutation and conformation) in MCF10AT cells.
  • Evaluated p53's DNA-binding and transcriptional activation capabilities.

Main Results:

  • p53 protein was found to be unmutated in the MCF10AT model.
  • Despite being wild-type, p53 exhibited a conformationally altered state.
  • This altered p53 showed defective DNA binding and transcriptional activation compared to normal MCF10A cells.

Conclusions:

  • p53 mutations are not essential for alterations in growth and morphology during early breast cancer progression.
  • Conformationally altered, wild-type p53 can contribute to neoplastic progression.
  • Stabilized, functionally impaired wild-type p53 is a potential factor in preneoplastic breast cells.