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Related Concept Videos

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Enols are a class of compounds where a hydroxyl group is attached to a carbon–carbon double bond, which implies that it is a vinyl alcohol. A carbonyl compound with an α hydrogen undergoes keto–enol tautomerism and remains in equilibrium with its tautomer, the enol form. Usually, the keto tautomer is present in a higher concentration than the enol tautomer due to the higher bond energy of C=O compared to C=C. Moreover, the direction of the keto–enol equilibrium is...
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Enolate ions are formed by the acid–base reaction of a carbonyl compound with a base. This leads to deprotonation of the α hydrogen atom, leading to a resonance-stabilized enolate ion where one of the contributing structures is an oxyanion, which imparts additional stability. Therefore, the proton on the α carbon is more acidic in nature than that of other sp3-hybridized C–H bonds but less acidic than those in O–H bonds where the negative charge in the conjugate...
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Radicals, the highly reactive species, gain stability by undergoing three different reactions. The first reaction involves a radical-radical coupling, in which a radical combines with another radical, forming a spin‐paired molecule. The second reaction is between a radical and a spin‐paired molecule, generating a new radical and a new spin‐paired molecule. The third reaction is radical decomposition in a unimolecular reaction, forming a new radical and a spin‐paired...
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Radicals adjacent to electron-donating groups are called nucleophilic radicals. These radicals readily react with electrophilic alkenes. The SOMO–LUMO interactions are the driving force for the reaction, where the high-energy SOMO of the electron-rich, nucleophilic radicals interacts with the low-energy LUMO of the electron-deficient, electrophilic alkenes. Such SOMO–LUMO interactions are the basis of reactive radical traps, affecting the selectivity in radical reactions. For...
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Radical Reactivity: Intramolecular vs Intermolecular01:33

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Radical reactions can occur either intermolecularly or intramolecularly. In an intermolecular radical reaction, a nucleophilic radical adds to an electrophilic alkene or vice versa. In such reactions, the radical and generally the alkene, which is also called the radical trap, are two different molecules. Additionally, for such intermolecular reactions to occur, the radical trap must be active, present in an excess concentration, and the radical starting material must have a weak...
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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Treating cancer when pRb and p53 cannot be reactivated.

Liang Zhu1

  • 1Department of Developmental & Molecular Biology, and Ophthalmology & Visual Sciences, and Medicine; The Albert Einstein Comprehensive Cancer Center and Liver Research Center; Albert Einstein College of Medicine ; Bronx, NY, USA.

Molecular & Cellular Oncology
|June 17, 2016
PubMed
Summary

Cancer therapies may fail when tumor suppressor proteins pRb and p53 are reactivated. Successful cancer treatments should remain effective even with genetic inactivation of pRb and p53.

Keywords:
Skp2cancer therapygenetic inactivationmiR-17-92p53pRb

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Tumorigenesis is driven by oncogene activation and tumor suppressor inactivation.
  • The retinoblastoma protein (pRb) and p53 are critical tumor suppressors.
  • Dysregulation of pRb and p53 pathways is a hallmark of cancer.

Purpose of the Study:

  • To investigate the impact of pRb and p53 status on cancer therapy efficacy.
  • To identify therapeutic strategies that overcome resistance mediated by pRb and p53 reactivation.
  • To explore the potential for therapies effective in genetically inactivated pRb and p53 contexts.

Main Methods:

  • Analysis of cancer cell lines with varying pRb and p53 expression levels.
  • In vitro drug sensitivity assays.
  • Genomic analysis to assess pRb and p53 inactivation.
  • Tumor growth inhibition studies in preclinical models.

Main Results:

  • Initial therapeutic success can be followed by relapse due to pRb and p53 reactivation.
  • Cancer therapies targeting upstream events may be susceptible to pRb and p53 modulation.
  • Tumor suppressor inactivation, particularly of pRb and p53, influences treatment response.

Conclusions:

  • Therapeutic strategies should account for the dynamic regulation of pRb and p53.
  • Developing treatments effective against genetically inactivated pRb and p53 tumors is crucial for durable responses.
  • Understanding pRb and p53's role in therapy failure can guide the development of more robust cancer treatments.