Related Experiment Video
Updated: Jul 4, 2025

04:57
Establishing a Competing Risk Regression Nomogram Model for Survival Data
Published on: October 23, 2020
10.2K
The Risk Function of Breast and Ovarian Cancers in the Avrami-Dobrzyński Cellular Phase-Transition Model
Anna Zawadzka1, Beata Brzozowska2, Anna Matyjanka3
1Maria Skłodowska-Curie National Research Institute of Oncology (NIO-MSCI), 02-781 Warsaw, Poland.
International Journal of Molecular Sciences
|January 27, 2024
Summary
Cancer development, particularly hereditary predispositions, is modeled using biophysical principles. Genetic mutations, like BRCA1/2, influence cancer onset, with fractal dynamics playing a key role.
Area of Science:
- Biophysics
- Oncology
- Genetics
Background:
- Genetic mutations are critical for understanding hereditary cancer predispositions and developing targeted treatments.
- The relationship between the number of cancerogenic mutations and lifetime cancer probability requires elucidation.
Purpose of the Study:
- To investigate the link between cancerogenic mutations and cancer induction probability over a patient's lifetime.
- To validate the Avrami-Dobrzyński biophysical model for cancer induction using clinical data.
Main Methods:
- Utilized clinical data from breast and ovarian cancer patients.
- Applied the Avrami-Dobrzyński biophysical model, conceptualized as a phase-transition process analogous to neoplastic transformation.
- Analyzed model parameters to confirm fractal dynamics in carcinogenesis.
Main Results:
- Model parameter values derived from clinical data support the hypothesis of fractal dynamics in the carcinogenic process.
- A slight divergence between model predictions and clinical data for patients under 30 suggests a potential cancer protection mechanism.
- Clinical data indicate an earlier onset of breast or ovarian cancers by two years in patients with BRCA1/2 mutations.
Conclusions:
- The Avrami-Dobrzyński model, grounded in biophysics, effectively describes cancer induction, highlighting fractal dynamics.
- Early-onset cancer cases in younger individuals may involve protective biological mechanisms.
- BRCA1/2 mutations are associated with a significantly earlier onset of hereditary breast and ovarian cancers.
Keywords:
Avrami equationbreast cancercancercancer physicscarcinogenesisfractalneoplastic transformationovary cancerphase transitionMore Related Videos
Related Concept Videos
Cancer Survival Analysis
348
Cancer survival analysis focuses on quantifying and interpreting the time from a key starting point, such as diagnosis or the initiation of treatment, to a specific endpoint, such as remission or death. This analysis provides critical insights into treatment effectiveness and factors that influence patient outcomes, helping to shape clinical decisions and guide prognostic evaluations. A cornerstone of oncology research, survival analysis tackles the challenges of skewed, non-normally...
348
Tumor Progression
6.3K
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...
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...
6.3K
Inhibition of Cdk Activity
4.8K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.8K
The Retinoblastoma Gene
4.1K
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 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,...
4.1K
Adaptive Mechanisms in Cancer Cells
5.8K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.8K
Cancer-Critical Genes I: Proto-oncogenes
8.9K
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...
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...
8.9K

