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Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Cancer Prevention02:59

Cancer Prevention

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.
Some...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Pedigree Analysis01:35

Pedigree Analysis

Overview

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Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

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Same author

Endoscopic management of duodenal adenomatosis in familial adenomatous polyposis-A case-based review.

United European gastroenterology journal·2021
Same author

European guidelines from the EHTG and ESCP for Lynch syndrome: an updated third edition of the Mallorca guidelines based on gene and gender.

The British journal of surgery·2021
Same author

Initial experience with taTME in patients undergoing laparoscopic restorative proctocolectomy for familial adenomatous polyposis.

Techniques in coloproctology·2017
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[Gender-specific aspects of Lynch syndrome--an update].

Zeitschrift fur Gastroenterologie·2015
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[Colorectal Carcinoma with Suspected Lynch Syndrome: A Multidisciplinary Algorithm].

Zentralblatt fur Chirurgie·2014
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[Can an online risk assessment tool for identification of hereditary colorectal cancer reach the at-risk population and influence screening compliance?].

Deutsche medizinische Wochenschrift (1946)·2014

Related Experiment Video

Updated: Jun 29, 2026

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

[Hereditary colorectal cancer].

G Möslein1

  • 1Klinik für Allgemein- und Viszeralchirurgie, Koloproktologie, St. Josefs-Hospital Bochum-Linden, Axstr. 35, 44879, Bochum. Gabriela.moeslein@helios-kliniken.de

Der Chirurg; Zeitschrift Fur Alle Gebiete Der Operativen Medizen
|October 15, 2008
PubMed
Summary

Distinguishing between Lynch syndrome, MYH-associated polyposis (MAP), and attenuated familial adenomatous polyposis (FAP) is crucial for managing familial colorectal cancer (CRC) and associated risks.

Area of Science:

  • Genetics and Oncology
  • Molecular Pathology

Context:

  • Familial colorectal cancer (CRC) presents diagnostic challenges due to overlapping genetic syndromes.
  • Effective risk management requires differentiating between hereditary non-polyposis colorectal cancer (HNPCC) and polyposis conditions.

Purpose:

  • To highlight the importance of distinguishing between Lynch syndrome, attenuated familial adenomatous polyposis (FAP), and MYH-associated polyposis (MAP).
  • To inform clinical management strategies for familial CRC based on distinct genetic underpinnings.

Summary:

  • Lynch syndrome, caused by mismatch repair (MMR) gene mutations, predisposes to CRC and other cancers.
  • Familial adenomatous polyposis (FAP) and MYH-associated polyposis (MAP), an autosomal recessive disorder, involve polyposis development.
  • Microsatellite instability (MSI) and immunohistochemistry (IHC) are key prognostic markers in Lynch syndrome.

More Related Videos

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

Related Experiment Videos

Last Updated: Jun 29, 2026

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

Impact:

  • Accurate diagnosis enables tailored surveillance and prophylactic surgery recommendations.
  • Improved differentiation of hereditary CRC syndromes optimizes patient care and outcomes.
  • Understanding genetic causes is vital for personalized risk assessment in familial cancer syndromes.