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Related Concept Videos

Rous Sarcoma Virus (RSV) and Cancer01:03

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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
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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...
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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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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.
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Related Experiment Video

Updated: Jun 7, 2025

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Case Series: EGFR and ROS-1 Co-Occurrence in Advanced Non-Small Cell Lung Cancer.

Turki Alfayea1,2,3, Alaa A Salim4, Mohammad Alkaiyat1,2,3

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Journal of Immunotherapy and Precision Oncology
|November 11, 2024
PubMed
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Co-occurring EGFR mutations and ROS-1 rearrangements in non-small cell lung cancer (NSCLC) are increasingly detected with advanced sequencing. One patient responded well to EGFR therapy, while another showed limited benefit, highlighting the need for personalized treatment strategies.

Keywords:
EGFRROS-1advanced lung adenocarcinomaco-occurrence

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Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Non-small cell lung cancer (NSCLC) is a complex disease with various molecular drivers.
  • Epidermal growth factor receptor (EGFR) mutations and ROS proto-oncogene 1 (ROS-1) rearrangements are common in advanced NSCLC.
  • These alterations are typically mutually exclusive but can co-occur.

Observation:

  • This case series presents two patients with advanced NSCLC and coexisting EGFR and ROS-1 alterations.
  • The first patient, with coexisting alterations, achieved over 3 years of stable disease on osimertinib (an EGFR inhibitor).
  • The second patient experienced a brief response to osimertinib followed by progressive disease, with a poor response to subsequent anti-ROS-1 therapy.

Findings:

  • Co-occurrence of EGFR and ROS-1 alterations in NSCLC is becoming more apparent with advanced genomic sequencing.
  • The presence of these co-alterations may influence treatment response, with potential for long-term benefit from anti-EGFR therapy in some cases.
  • Variant allele frequency may be a critical factor in guiding therapeutic decisions.

Implications:

  • Increased utilization of next-generation sequencing is crucial for identifying co-alterations in NSCLC.
  • Personalized treatment strategies, considering co-mutation status and variant allele frequency, are essential for optimizing patient outcomes.
  • Further research is needed to determine optimal treatment sequencing and combination therapies for NSCLC with co-alterations.