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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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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Related Experiment Video

Updated: Jun 12, 2026

Pooled shRNA Screen for Reactivation of MeCP2 on the Inactive X Chromosome
11:15

Pooled shRNA Screen for Reactivation of MeCP2 on the Inactive X Chromosome

Published on: March 2, 2018

Elevated XIAP expression alone does not confer chemoresistance.

J M Seeger1, K Brinkmann, B Yazdanpanah

  • 1Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Goldenfelsstrasse 19-21, 50935 Köln, Germany.

British Journal of Cancer
|May 21, 2010
PubMed
Summary
This summary is machine-generated.

Elevated X-linked inhibitor of apoptosis protein (XIAP) alone does not predict chemoresistance. Chemoresistance requires XIAP overexpression alongside functional XIAP regulatory circuits, like SMAC knockdown.

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Last Updated: Jun 12, 2026

Pooled shRNA Screen for Reactivation of MeCP2 on the Inactive X Chromosome
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A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome
08:27

A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome

Published on: May 22, 2019

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Apoptosis Regulation

Background:

  • Elevated X-linked inhibitor of apoptosis protein (XIAP) is observed in various tumors, often linked to chemoresistance.
  • Conflicting data exist regarding XIAP's prognostic value, with some studies suggesting a favorable outcome with higher XIAP expression.
  • XIAP's anti-apoptotic function is complex and context-dependent, especially concerning its expression levels and regulatory factors.

Purpose of the Study:

  • To investigate the impact of long-term, stable XIAP overexpression on cancer cell chemoresistance.
  • To elucidate the role of mitochondrial proteins, such as Bcl2 and SMAC, in XIAP-mediated chemoresistance.
  • To determine if XIAP alone is sufficient to confer resistance to chemotherapeutic agents.

Main Methods:

  • Generation of cancer cell lines with stable XIAP overexpression.
  • Assessment of chemoresistance following long-term XIAP expression.
  • Examination of mitochondrial involvement via stable Bcl2 expression or SMAC knockdown in conjunction with XIAP modulation.

Main Results:

  • Long-term XIAP overexpression at physiological levels (2-5 fold increase) conferred minimal chemoresistance.
  • Severe chemoresistance was observed only when XIAP overexpression was combined with the stable knockdown of SMAC (second mitochondria-derived activator of caspase).
  • XIAP acts as a potent chemoresistance factor primarily in cells with compromised XIAP regulatory circuits.

Conclusions:

  • Elevated XIAP expression alone is insufficient as a predictive marker for chemoresistance.
  • The functional status and expression levels of XIAP modulators, including SMAC, are critical for predicting XIAP's impact on chemosusceptibility.
  • A comprehensive analysis of XIAP and its regulatory network is necessary for accurate chemoresistance prediction in cancer therapy.