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Related Concept Videos

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.
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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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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.
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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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Updated: Jul 5, 2025

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
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Folate Receptor Alpha-A Novel Approach to Cancer Therapy.

Teresita Gonzalez1, Meri Muminovic1, Olger Nano1

  • 1Memorial Cancer Institute, Pembroke Pines, FL 33028, USA.

International Journal of Molecular Sciences
|January 23, 2024
PubMed
Summary

Folate receptor alpha (FRα) is overexpressed in cancer cells, making it a key target for new cancer therapies. Its role in tumor growth and its presence across various cancers highlight its importance in precision medicine.

Keywords:
FOLR1antibody drug conjugatefolate receptor alpha

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Analyzing Tumor and Tissue Distribution of Target Antigen Specific Therapeutic Antibody
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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Folate receptor alpha (FRα), a GPI-anchored glycoprotein encoded by the FOLR1 gene, is crucial for DNA synthesis, cell proliferation, and intracellular signaling.
  • FRα is significantly overexpressed in various cancer cells, including ovarian cancer, non-small-cell lung cancer (NSCLC), and colon cancer, compared to normal tissues.

Purpose of the Study:

  • To review the role of Folate receptor alpha (FRα) as a therapeutic target and biomarker in oncology.
  • To highlight the applications of FRα in developing novel cancer treatments and diagnostic tools.

Main Methods:

  • Literature review of studies on Folate receptor alpha (FRα) in cancer.
  • Analysis of FRα's role in tumorigenesis and its expression patterns in different cancer types.
  • Examination of current and emerging therapeutic strategies targeting FRα.

Main Results:

  • FRα is a validated target for oncologic therapeutics due to its cancer-specific overexpression.
  • FRα is utilized in antibody drug conjugates, small-molecule-drug conjugates, and CAR-T cell therapies.
  • FRα serves as a prognostic marker and a predictor of chemotherapy resistance.

Conclusions:

  • FRα is a pivotal target in precision medicine for cancer treatment and diagnosis.
  • Targeting FRα offers a promising avenue for developing effective oncologic therapeutics.
  • Identification of FRα is essential for personalized cancer care strategies.