What are oncogenes and tumor suppressor genes?

Oncogenes promote cell growth, while tumor suppressor genes inhibit uncontrolled division.

How does the G1 to S transition regulate cell division?

The G1 to S transition is controlled by key regulators like the G1 cyclin and transcription factor E2F.

Retinoblastoma is a rare childhood eye tumor originating from retinal tissue.

Loss of heterozygosity can occur through various mechanisms, promoting cancer progression.

The APC gene functions as a brake on Wnt signaling, regulating cell behavior in the colon.

Mutations in oncogenes promote uncontrolled cell growth, while tumor suppressor genes inhibit growth, maintaining cellular stability and preventing cancer development.
Understanding the genetic basis of diseases like retinoblastoma and colon cancer is essential for assessing cancer risk and developing targeted treatments that can effectively inhibit specific pathways involved in tumorigenesis.

What are oncogenes and tumor suppressor genes?
Oncogenes promote cell growth, while tumor suppressor genes inhibit uncontrolled division.
How does the G1 to S transition regulate cell division?
The G1 to S transition is controlled by key regulators like the G1 cyclin and transcription factor E2F.
What is retinoblastoma and how does it manifest?
Retinoblastoma is a rare childhood eye tumor originating from retinal tissue.
How does loss of heterozygosity contribute to cancer development?
Loss of heterozygosity can occur through various mechanisms, promoting cancer progression.
What is the role of APC gene in colon cancer development?
The APC gene functions as a brake on Wnt signaling, regulating cell behavior in the colon.

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Cell division is regulated at the single-cell level, while tissue regeneration is mediated at the tissue level.
When these processes go awry, it leads to various diseases, commonly known as cancer.
Cancer is characterized by a stepwise degeneration of normal cell behavior due to mutations.
Oncogenes are mutated genes that promote cell growth, while proto-oncogenes regulate growth in a controlled manner.
Tumor suppressor genes inhibit growth or promote cell death, preventing uncontrolled cell division.
Caretaker genes maintain genomic integrity by repairing DNA and ensuring chromosome stability.
Loss of function mutations in caretaker genes can drive cancer development.
The G1 to S transition in the cell cycle is crucial for cell division, with the G1 cyclin being a key regulator.
The G1 cyclin is activated by the transcription factor E2F, which is inhibited by Rb in early G1.
Rb, growth inhibitors, E2F, G1 cyclin, and CDK are key players in the cell cycle pathway, with Rb and growth inhibitors classified as tumor suppressors and CDK and E2F as proto-oncogenes.

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Rb gene stands for retinoblastoma, a tumor suppressor gene, involved in a rare childhood eye tumor.
Retinoblastoma manifests in the eye with tumors originating from retinal tissue.
Two forms of retinoblastoma exist: sporadic (arising without family history) and familial (inherited).
Sporadic retinoblastoma usually affects one eye and can be treated without increased cancer risk later.
Familial retinoblastoma affects both eyes and increases the risk of other organ tumors later in life.
Inheritance of retinoblastoma is autosomal dominant, with a predisposition to the disease.
Heterozygosity for the Rb gene predisposes individuals to retinoblastoma.
Loss of heterozygosity in retinoblastoma cells can occur through point mutations, chromosome loss, or promoter methylation.
Retinoblastoma appears dominant at the organismal level due to the predisposition to the disease.
Understanding the dual nature of retinoblastoma inheritance is crucial for assessing cancer risk.

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The mechanism of cancer at the cellular level involves tumor suppressors like BRCA1, p53, and APC.
Colon cancer is used as an example to explain the process at the tissue level, focusing on the stem cell niche and cell renewal in the crypts.
To form a tumor in the colon, cells must overcome the barrier of shedding off into the lumen, allowing them to accumulate mutations and undergo tumorigenesis.
Dysregulation of the Wnt signaling pathway, involving the APC gene, is a crucial step in colon cancer development.
Familial adenomatous polyposis is associated with APC gene mutations, leading to the formation of benign polyps in the colon.
APC functions as a brake on Wnt signaling, inhibiting beta-catenin and regulating cell behavior in the colon.
Targeted treatments like Gleevec inhibit the ABL tyrosine kinase in chronic myelogenous leukemia, resulting in effective treatment and improved prognosis for patients.