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Updated: Mar 14, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
Published on: August 25, 2021
Targeted Cancer Therapy: Vital Oncogenes and a New Molecular Genetic Paradigm for Cancer Initiation Progression and
1OncoStem Biotherapeutics LLC, 423 W 127th St., New York, NY 10027, USA. rwillis@oncostembio.com.
Abstract:
It has been declared repeatedly that cancer is a result of molecular genetic abnormalities. However, there has been no working model describing the specific functional consequences of the deranged genomic processes that result in the initiation and propagation of the cancer process during carcinogenesis. We no longer need to question whether or not cancer arises as a result of a molecular genetic defect within the cancer cell. The legitimate questions are: how and why? This article reviews the preeminent data on cancer molecular genetics and subsequently proposes that the sentinel event in cancer initiation is the aberrant production of fused transcription activators with new molecular properties within normal tissue stem cells. This results in the production of vital oncogenes with dysfunctional gene activation transcription properties, which leads to dysfunctional gene regulation, the aberrant activation of transduction pathways, chromosomal breakage, activation of driver oncogenes, reactivation of stem cell transduction pathways and the activation of genes that result in the hallmarks of cancer. Furthermore, a novel holistic molecular genetic model of cancer initiation and progression is presented along with a new paradigm for the approach to personalized targeted cancer therapy, clinical monitoring and cancer diagnosis.
Insights
Cancer initiation stems from fused transcription activators in stem cells, leading to gene dysregulation and cancer hallmarks. This study presents a new molecular model for cancer progression and personalized therapies.
Area of Science:
- Oncology
- Molecular Genetics
- Cancer Biology
Background:
- Cancer is linked to molecular genetic abnormalities, but a functional model of carcinogenesis is lacking.
- Understanding the 'how' and 'why' of cancer initiation requires a detailed molecular genetic perspective.
Purpose of the Study:
- To review key data in cancer molecular genetics.
- To propose a novel molecular genetic model for cancer initiation and progression.
- To introduce a new paradigm for personalized targeted cancer therapy, monitoring, and diagnosis.
Main Methods:
- Review of preeminent data on cancer molecular genetics.
- Proposal of a novel holistic molecular genetic model for cancer initiation and progression.
Main Results:
- Identifies aberrant production of fused transcription activators in stem cells as the sentinel event in cancer initiation.
- Elucidates the downstream consequences: dysfunctional gene regulation, pathway activation, and cancer hallmarks.
- Presents a new model for understanding cancer development and progression.
Conclusions:
- Fused transcription activators are critical in initiating cancer by disrupting normal gene regulation.
- The proposed model offers a framework for personalized targeted cancer therapies.
- This research paves the way for improved cancer diagnosis and clinical monitoring.
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