THE CELL ON THE WHEEL 🛞

Introduction 

THE UNPAIRED GENE EITHER DNA mRNA NUCLEOUS NUCLEOTIDE RIBOSOME MITOCONDRIAL PATHWAYS AND VARIOUS GLYCOLYSIS PATHWAY LIKE KREB CYCLE PYARUVATE ADINOSINE PHOSPHATE TYOSINE ADENINE TRY PHOSPHATE WITH INTRUSIVE GENE EXPRESSION AND MUTANT SOME TIME INHERITANCE UPPER MANY GENERATIONS OF FAILURE  INFILTERED CAUSE FOR DIFFERENCIAL CARCINOMA ⚛️

Modern molecular-biology understanding.

1. What is meant by an “unpaired gene” ⚛️

An unpaired gene usually refers to:

Loss of normal allelic balance (one functional copy + one damaged copy)

Or abnormal gene dosage (extra copies, deletions, or silencing)

This can happen due to:

Mutations

Chromosomal instability

Epigenetic silencing

Mitochondrial DNA defects

When genes are no longer properly paired or regulated, cellular homeostasis collapses.

2. DNA → mRNA → Ribosome: where failure begins 🧬

Normal flow (Central Dogma):

DNA (nucleus) → mRNA → Ribosome → Protein

In carcinoma:

DNA mutations (point mutation, deletion, insertion)

Faulty transcription → abnormal mRNA

Faulty translation → abnormal proteins

Key problems:

Oncogene activation (e.g., uncontrolled growth signals)

Tumor suppressor gene loss (e.g., p53, RB)

Stop codon failure or frame-shift errors

Ribosome produces misfolded or hyperactive proteins

Result → uncontrolled cell division

3. Intrusive gene expression & mutant inheritance 🧪

Intrusive gene expression means:

Genes that should be OFF become ON

Embryonic, viral, or silent genes get reactivated

External DNA (virus, transposons) integrates into genome

Inheritance across generations:

Germline mutations (BRCA, TP53, mismatch repair genes)

Epigenetic inheritance (DNA methylation patterns)

Mitochondrial DNA mutations passed from mother

This explains:

Cancer predisposition running in families

“Upper many generations of failure” as you mention

4. Mitochondrial pathway failure 🔥

Mitochondria control:

ATP production

Apoptosis (programmed cell death)

Reactive oxygen species (ROS balance)

In carcinoma:

Mitochondrial DNA mutations

Faulty electron transport chain

Excess ROS → DNA damage

Failure of apoptosis → cancer cells survive

Cancer cells avoid death even when damaged.

5. Glycolysis, Krebs cycle & Warburg effect ⚙️

Normal cells:

Glucose → Pyruvate → Krebs Cycle → ATP (mitochondria)

Cancer cells:

Prefer glycolysis even with oxygen

(Warburg Effect)

This causes:

Excess lactate production

Acidic microenvironment

Rapid biomass synthesis (DNA, lipids, proteins)

Pathways involved:

Glycolysis ↑

Pyruvate diverted away from Krebs cycle

ATP generated inefficiently but rapidly

Supports uncontrolled proliferation

6. ATP, ADP, AMP imbalance ⚡

You mentioned:

Adenosine phosphate system

In cancer:

ATP demand is extremely high

AMPK signaling is altered

Energy checkpoints fail

Cells divide even under stress

This removes normal metabolic brakes.

7. Tyrosine, adenine & signaling failure 🧠

Tyrosine kinase pathways:

EGFR, HER2, BCR-ABL

When mutated → constant “growth ON” signal

Adenine base errors:

DNA replication mismatch

Defective repair enzymes

Accumulation of mutations

Result → genomic instability

8. Why this leads to differential carcinoma 🌱

Different tissues show different carcinoma because:

Each tissue has unique gene expression

Different metabolic dependence

Different mitochondrial density

Different exposure to carcinogens

Thus:

Lung carcinoma ≠ liver carcinoma ≠ breast carcinoma

Same basic failure, different manifestation

9. Unified summary ⚛️

Differential carcinoma arises from:

Unpaired or damaged genes

Abnormal DNA → mRNA → protein flow

Intrusive or inherited mutant gene expression

Mitochondrial dysfunction

Shifted metabolism (Warburg effect)

ATP signaling imbalance

Failure of apoptosis

Accumulation across generations

This creates a self-sustaining malignant system.

#HARGHARVINCA🧬

#HARGHARMADHUVINCA🧬

#TSAC⚛️

#AILIfe⚛️