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Related Concept Videos

Nucleotide Excision Repair01:38

Nucleotide Excision Repair

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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Cancer Prevention02:59

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Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
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Base Excision Repair01:54

Base Excision Repair

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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Base-pairing and DNA Repair02:27

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Mismatch Repair01:20

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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DNA Damage can Stall the Cell Cycle02:37

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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...
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Updated: Jun 28, 2025

gDNA Enrichment by a Transposase-based Technology for NGS Analysis of the Whole Sequence of BRCA1, BRCA2, and 9 Genes Involved in DNA Damage Repair
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Association Between Polymorphisms in DNA Damage Repair Pathway Genes and Female Breast Cancer Risk.

Ying Wang1,2, Yalan Sun1,2, Mingjuan Tan2

  • 1School of Basic-Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, China.

DNA and Cell Biology
|April 18, 2024
PubMed
Summary
This summary is machine-generated.

This study investigated genetic variations in DNA repair genes and their association with breast cancer risk in Chinese women. Specific single nucleotide polymorphisms (SNPs) in PALB2, ATR, ATM, and Ku70 were found to be linked to altered breast cancer susceptibility.

Keywords:
DDRDNA damageSNPbreast cancerpolymorphismrisk

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Area of Science:

  • Genetics and Genomics
  • Cancer Research
  • Molecular Biology

Background:

  • Breast cancer risk is influenced by genetic predispositions and DNA damage repair mechanisms.
  • Single nucleotide polymorphisms (SNPs) in DNA repair genes may play a role in cancer development.
  • Understanding these genetic factors is crucial for assessing female breast cancer risk.

Purpose of the Study:

  • To evaluate the association between specific DNA damage repair gene SNPs and breast cancer risk in the Chinese population.
  • To investigate the influence of estrogen receptor (ER), progesterone receptor (PR), and HER-2 expression on these associations.
  • To explore potential interactions with reproductive factors like menstrual status and age of menarche.

Main Methods:

  • A case-control study involving 400 breast cancer patients and 400 healthy controls.
  • Genotyping was performed using the MassARRAY method.
  • Tumor tissue analysis included immunohistochemistry for ER, PR, and HER-2 expression.

Main Results:

  • The ATR rs13091637 polymorphism was associated with decreased breast cancer risk, particularly in tumors with specific ER/PR expression patterns.
  • The PALB2 rs16940342 SNP showed an increased risk of breast cancer, influenced by menstrual status and age of menarche.
  • ATM rs611646 and Ku70 rs132793 polymorphisms were linked to a reduced risk of breast cancer, with a notable association with menarche.

Conclusions:

  • Specific SNPs in DNA damage repair genes (PALB2, ATR, ATM, Ku70) are significantly associated with breast cancer risk in the studied Chinese population.
  • These genetic variations may interact with clinical factors such as hormone receptor status and reproductive history.
  • Further research is warranted to elucidate the precise mechanisms underlying these gene-environment interactions in breast cancer etiology.