SCF ENCYCLOPEDIA ENTRY

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)

SCF APC TUMOR-SUPPRESSOR FAILURE & COLORECTAL ONCOGENIC SYNCHRONIZATION COLLAPSE DOSSIER

I. OFFICIAL DISEASE CLASSIFICATION

Familial adenomatous polyposis belongs to SCF Clinical Domains C5 (Oncology), C14 (Genetic Medicine), C8 (Gastrointestinal Medicine), C2 (Cellular Signaling Biology), and C13 (Systems Degeneration & Transformation Biology).

II. CLINICAL DEFINITION

Familial adenomatous polyposis is an inherited cancer predisposition syndrome characterized by:

• Hundreds to thousands of colorectal adenomas
• Early-onset colorectal neoplasia
• Progressive malignant transformation
• Gastrointestinal polyposis
• Extracolonic tumor development

Primary affected systems:

• Colonic epithelium
• Intestinal stem-cell compartments
• Wnt signaling pathways
• Gastrointestinal mucosa
• Epithelial growth-regulation systems

Associated conditions:

• Colorectal cancer
• Adenomatous polyp

III. MAJOR CLASSIFICATIONS

A. Classic Familial Adenomatous Polyposis

B. Attenuated FAP (AFAP)

C. Gardner Syndrome

Associated condition:

• Gardner syndrome

D. Turcot Syndrome (APC-associated forms)

Associated condition:

• Turcot syndrome

IV. CORE SCF ETIOPATHOGENIC THESIS

Within the Synergistic Compatibility Framework (SCF), FAP represents a systems-level collapse of:

• Cellular proliferation governance
• Epithelial homeostasis coherence
• Stem-cell differentiation balance
• Tumor-suppressor network integrity
• Oncogenic containment systems

SCF interprets FAP as a decentralized epithelial intelligence disorder in which APC loss destabilizes synchronized growth-control harmonics, producing progressive neoplastic amplification throughout the gastrointestinal tract.

V. APC FOUNDATION

Core Pathophysiologic Mechanisms

VI. MAJOR GENETIC CAUSES

Principal Gene

Secondary Oncogenic Progression Genes

Genetic Characteristics

Associated condition:

• Autosomal dominant disorder

VII. SCF FAULT ARCHITECTURE

VIII. MULTI-OMICS PATHOGENESIS

A. Genomics

Affected pathways:

• APC signaling
• Wnt/β-catenin pathways
• Cell-cycle regulation
• DNA repair systems

B. Transcriptomics

Dysregulated pathways:

• Stem-cell maintenance
• Proliferation signaling
• Differentiation pathways
• Oncogenic transcription programs

C. Proteomics

Observed abnormalities:

• APC deficiency
• β-catenin accumulation
• Cyclin activation
• Growth-factor dysregulation

D. Metabolomics

Key dysfunction:

• Aerobic glycolysis
• Increased anabolic metabolism
• ATP demand elevation
• Oxidative stress
• Tumor-supportive metabolic reprogramming

E. Oncomics (SCF)

Observed abnormalities:

• Clonal expansion
• Adenoma accumulation
• Malignant progression
• Epithelial transformation

IX. SCF PATHOGENESIS FLOW

Stage 1 — APC Mutation

Tumor-suppressor activity declines.

Stage 2 — Wnt Hyperactivation

β-catenin signaling increases.

Stage 3 — Adenoma Formation

Multiple colorectal polyps emerge.

Stage 4 — Clonal Expansion

Progressive neoplastic evolution develops.

Stage 5 — Additional Mutational Events

Cancer-driving pathways accumulate.

Stage 6 — Colorectal Carcinoma

Invasive malignancy develops.

X. SYSTEMIC CONSEQUENCES

Associated conditions:

• Desmoid tumor
• Duodenal adenoma
• Hepatoblastoma

XI. RHENOVA INTERPRETATION

Project RHENOVA interprets FAP as an oncogenic bioenergetic destabilization syndrome.

RHENOVA Dynamics

• Stem-cell amplification loops
• Tumor-growth cascades
• Proliferative synchronization failure
• Metabolic rewiring progression
• Oncogenic network expansion

RHENOVA Biomarkers

XII. DBI INTERPRETATION

The SCF Decentralized Biological Intelligence framework interprets epithelial tissues as synchronized biological communication networks coordinating:

• Controlled proliferation
• Tissue renewal
• Stem-cell regulation
• Tumor suppression
• Mucosal integrity

DBI Failure Features

• Growth-control fragmentation
• Stem-cell communication instability
• Oncogenic amplification loops
• Tumor-suppressor collapse

This transforms coordinated epithelial renewal into uncontrolled neoplastic growth.

XIII. CLINICAL MANIFESTATIONS

Gastrointestinal Manifestations

• Hundreds to thousands of adenomatous polyps
• Rectal bleeding
• Anemia
• Abdominal pain
• Diarrhea

Associated condition:

• Iron deficiency anemia

Extracolonic Manifestations

• Osteomas
• Dental abnormalities
• Epidermoid cysts
• Congenital hypertrophy of the retinal pigment epithelium (CHRPE)

Associated conditions:

• Osteoma
• Congenital hypertrophy of retinal pigment epithelium

Neoplastic Manifestations

• Colorectal carcinoma
• Duodenal cancer
• Thyroid cancer
• Desmoid tumors

XIV. DIAGNOSTICS

Diagnostic Hallmarks

Tumor suppressor principle:

APC\ Loss \Rightarrow \beta-Catenin\ Accumulation

Proliferation relationship:

Wnt\ Hyperactivation \Rightarrow Adenoma\ Formation

Cancer progression concept:

Adenoma\ Accumulation \Rightarrow Colorectal\ Carcinoma

XV. SCF SYSTEMIC AXIS INVOLVEMENT

XVI. STANDARD OF CARE

Surveillance

Surgical Management

Pharmacologic Strategies

Examples:

• Sulindac
• Celecoxib

XVII. SCF-PCR THERAPEUTIC ARCHITECTURE

A. Preventative (PCR-P)

Goals:

• Prevent adenoma accumulation
• Suppress oncogenic signaling
• Preserve epithelial integrity

B. Curative (PCR-C)

Goals:

• Restore APC pathway function
• Normalize Wnt signaling
• Eliminate neoplastic clones

C. Restorative (PCR-R)

Goals:

• Restore epithelial homeostasis
• Improve stem-cell regulation
• Reduce oncogenic stress
• Rebuild proliferative synchronization harmonics

XVIII. ETHNOBIOPROSPECTING TARGETS

Traditional Chinese Medicine

• Scutellaria baicalensis
• Salvia miltiorrhiza

Ayurveda

• Curcuma longa
• Withania somnifera

Vietnamese Thuốc Nam

• Centella asiatica
• Phyllanthus amarus

XIX. SCF API DISCOVERY TARGETS

High-Priority Molecular Targets

• APC restoration pathways
• Wnt/β-catenin suppression systems
• Stem-cell regulatory networks
• Anti-fibrotic signaling pathways
• Tumor microenvironment normalization systems
• DNA stability enhancement pathways
• Epithelial synchronization restoration platforms

XX. SCF LAYMAN’S SUMMARY

Familial adenomatous polyposis is a hereditary cancer syndrome caused by mutations in the APC gene. The loss of APC function removes an important brake on cell growth, causing hundreds to thousands of precancerous polyps to form in the colon and rectum. Without treatment, colorectal cancer is almost inevitable. FAP can also affect the stomach, duodenum, thyroid, bones, skin, and connective tissues. SCF interprets FAP as a systems-level epithelial communication disorder involving APC failure, Wnt pathway overactivation, stem-cell dysregulation, oncogenic amplification, and loss of synchronized tissue-growth control.

XXI. STRATEGIC RESEARCH PRIORITIES

1. APC gene-restoration technologies
2. Wnt/β-catenin pathway modulation systems
3. Stem-cell regulatory therapeutics
4. AI-driven adenoma progression forecasting
5. Anti-fibrotic desmoid-targeting therapies
6. Tumor microenvironment normalization systems
7. Epithelial synchronization restoration platforms

MASTER REGISTRY INDEX

SCF-FAP-0001 — Familial Adenomatous Polyposis Master Registry

SCF-FAP-APC-0002 — APC Tumor Suppressor Failure Layer

SCF-FAP-WNT-0003 — Wnt Signaling Dysregulation Layer

SCF-FAP-RHENOVA-0004 — Oncogenic Bioenergetic Destabilization Layer

SCF-FAP-DBI-0005 — Epithelial Communication Failure Layer

SCF-FAP-PCR-0006 — Preventative–Curative–Restorative Layer