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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
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Combination Therapies and Personalized Medicine02:50

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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
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Tumor Immunotherapy01:27

Tumor Immunotherapy

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
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Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Related Experiment Video

Updated: Jul 23, 2025

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
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Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

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Targeting KRAS-Mutated NSCLC: Novel TKIs and Beyond.

David J Cantor1, Charu Aggarwal1,2,3

  • 1Division of Hematology-Oncology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|July 19, 2023
PubMed
Summary

KRAS-mutated non-small cell lung cancer (NSCLC) lacks effective targeted therapies. Past MEK inhibitor and chemotherapy combinations failed, necessitating novel treatment strategies for this common cancer subtype.

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Author Spotlight: Advancements in Molecular Biomarker Testing for Non-Squamous Non-Small Cell Lung Cancer
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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • KRAS-mutated non-small cell lung cancer (NSCLC) represents the most frequent genetically altered form of NSCLC.
  • Despite its prevalence, targeted therapeutic options for KRAS-mutated NSCLC remain limited.
  • Previous research exploring MEK inhibitors in combination with chemotherapy has yielded unsuccessful outcomes.

Purpose of the Study:

  • To review existing studies on MEK inhibitors and chemotherapy combinations in KRAS-mutated NSCLC.
  • To discuss the limitations and failures of these prior therapeutic approaches.
  • To explore and present novel strategies for targeting KRAS-mutated NSCLC.

Main Methods:

  • Literature review of published studies on KRAS-mutated NSCLC treatments.
  • Analysis of clinical trial data for MEK inhibitor and chemotherapy combinations.
  • Discussion of emerging therapeutic targets and approaches for KRAS-mutated NSCLC.

Main Results:

  • Multiple studies combining MEK inhibitors with chemotherapy have not demonstrated success in treating KRAS-mutated NSCLC.
  • The limitations of current targeted therapies underscore the need for innovative treatment modalities.
  • The review highlights the ongoing challenges in effectively targeting KRAS-mutated NSCLC.

Conclusions:

  • Targeted therapy for KRAS-mutated NSCLC is an area of active research with unmet needs.
  • Novel approaches beyond MEK inhibitor/chemotherapy combinations are crucial for improving patient outcomes.
  • Further investigation into alternative strategies is warranted to address this significant clinical challenge.