Related Experiment Video

Updated: May 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

Roles for KRAS in pancreatic tumor development and progression

Marina Pasca di Magliano1, Craig D Logsdon

  • 1Department of Surgery, University of Michigan, Ann Arbor, Michigan 48109, USA. marinapa@umich.edu

Gastroenterology
|April 30, 2013
PubMed

Insights

The oncogene Kras is frequently mutated in pancreatic cancer, but targeting it proved difficult. Recent research corrects past assumptions, revealing new insights into Kras

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The Kras gene is a key oncogene implicated in most pancreatic tumors.
  • Early therapeutic and diagnostic strategies targeting Kras in pancreatic cancer were unsuccessful.
  • Previous understanding of Kras' role in pancreatic cancer was limited and contained inaccuracies.

Purpose of the Study:

  • To review recent advancements in understanding the role of Kras in pancreatic cancer.
  • To highlight the limitations in current knowledge regarding Kras.
  • To identify critical areas for future research in Kras-driven pancreatic cancer.

Main Methods:

  • Utilizing genetically engineered mouse models for in-depth pancreatic carcinogenesis analysis.
  • Leveraging cancer genome sequencing projects to understand tumor heterogeneity.
  • Integrating data from various studies to reassess Kras' function.

Main Results:

  • New findings indicate that many prior assumptions about Kras in pancreatic cancer were incorrect.
  • Genetically engineered mouse models have provided crucial insights into Kras' function in vivo.
  • Cancer genome sequencing has elucidated tumor heterogeneity and identified key oncogenic drivers.

Conclusions:

  • Our understanding of Kras' role in pancreatic cancer development has significantly evolved.
  • Further research is essential to address the remaining knowledge gaps and develop effective Kras-targeted therapies.
  • Future studies should focus on the complexities of Kras signaling and its interaction with the tumor microenvironment.

More Related Videos

Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models06:57

Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models

Published on: April 7, 2018

Mimicking and Manipulating Pancreatic Acinar-to-Ductal Metaplasia in 3-dimensional Cell Culture08:16

Mimicking and Manipulating Pancreatic Acinar-to-Ductal Metaplasia in 3-dimensional Cell Culture

Published on: February 11, 2019

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 superfamily...
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...
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 rapamycin-insensitive companion...
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...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...