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Related Concept Videos

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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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...

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Related Experiment Video

Updated: May 15, 2026

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
11:15

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

IDH1 Mutations Are Associated with Favorable Outcomes in Prostate Cancer.

Luka Cavka1, Subhiksha Nandakumar2, Qingqing Wu1

  • 1Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.

European Urology
|May 13, 2026
PubMed
Summary
This summary is machine-generated.

Prostate cancer with isocitrate dehydrogenase (IDH) mutations is a distinct subtype. Despite high stage and grade, IDH-mutant prostate cancer shows significantly improved survival outcomes compared to wild-type.

Keywords:
Cancer genomicsIDH mutationsProstate cancer

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Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation
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Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation

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Related Experiment Videos

Last Updated: May 15, 2026

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
11:15

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation
07:17

Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation

Published on: August 23, 2024

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Isocitrate dehydrogenase 1 (IDH1) or isocitrate dehydrogenase 2 (IDH2) mutations define a unique molecular subclass of prostate cancer.
  • Clinical features associated with IDH1/IDH2 mutations in prostate cancer remain largely undescribed.

Purpose of the Study:

  • To investigate the clinical and molecular characteristics of prostate cancer harboring IDH1 or IDH2 mutations.
  • To compare the outcomes of IDH-mutant prostate cancer with IDH1/IDH2 wild-type cases.

Main Methods:

  • Retrospective analysis of clinical and molecular data from 111 prostate cancer cases with IDH1/IDH2 mutations (99 IDH1, 12 IDH2).
  • Creation of a matched IDH1/IDH2 wild-type control cohort.
  • Comparative analysis of survival endpoints and molecular alterations.

Main Results:

  • IDH-mutant prostate cancer cases often presented with localized disease but exhibited high tumor stage (42% T3) and grade (54% grade group 5).
  • Patients with IDH1 mutations demonstrated significantly longer overall survival (HR 0.16), metastasis-free survival (HR 0.22), and progression-free survival on hormonal therapy (HR 0.35) compared to controls.
  • IDH1-mutant cases showed enrichment for FOXA1 and CTNNB1 mutations and a depletion of TMPRSS2-ERG fusions, SPOP, and RB1 alterations, alongside global transcriptional repression and metabolic reprogramming.

Conclusions:

  • IDH-mutant prostate cancer represents a distinct subtype with characteristic molecular alterations.
  • Despite potential for high stage and grade at presentation, IDH-mutant prostate cancer is associated with favorable clinical outcomes and improved survival.