Related Experiment Video

Updated: Apr 11, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

18.9K

PIK3CA Amplification Is Common in Left Side-Tubular Adenomas but Uncommon Sessile Serrated Adenomas Exclusively with

Hyunsu Lee1, Jae-Ho Lee1, Dae-Kwang Kim2

  • 11. Department of Anatomy, Keimyung University School of Medicine;

International Journal of Medical Sciences
|May 29, 2015
PubMed

Insights

PIK3CA amplification is an early event in colorectal cancer development, particularly in left-sided tubular adenomas (TAs). This genetic change appears to drive TA growth independently of KRAS mutations.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gastroenterology

Background:

  • Colorectal cancer (CRC) is a complex disease with distinct precancerous pathways, including tubular adenomas (TAs) and sessile serrated adenomas (SSAs).
  • Understanding the molecular drivers of these early lesions is crucial for targeted prevention and treatment strategies.

Purpose of the Study:

  • To investigate the frequency and significance of PIK3CA amplification in colorectal precancerous lesions (TAs and SSAs).
  • To determine the relationship between PIK3CA amplification and common mutations (KRAS, BRAF) in these adenomas.

Main Methods:

  • DNA analysis of paired normal and tumoral tissues from 64 TAs and 32 SSAs.
  • Real-time PCR and pyrosequencing were used to detect PIK3CA amplification, KRAS mutations, and BRAF mutations.

Main Results:

  • PIK3CA amplification was detected in 25% of TAs and 9.4% of SSAs.
  • KRAS and BRAF mutations were mutually exclusive in both adenoma types.
  • In TAs, PIK3CA amplification was associated with left-sided lesions and was mutually exclusive with KRAS mutations.

Conclusions:

  • PIK3CA amplification represents an early and potentially significant event in colorectal carcinogenesis.
  • This amplification may independently drive the development of left-sided TAs, distinct from KRAS mutation pathways.
Keywords:
colorectal cancermitochondriapolymorphismsessile serrated adenomastubular adenomas

More Related Videos

A Multiplexed Luciferase-based Screening Platform for Interrogating Cancer-associated Signal Transduction in Cultured Cells10:13

A Multiplexed Luciferase-based Screening Platform for Interrogating Cancer-associated Signal Transduction in Cultured Cells

Published on: July 3, 2013

11.8K
A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

10.1K

Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
7.5K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.1K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.4K
Tumor Progression02:07

Tumor Progression

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...
7.9K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.4K