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Related Concept Videos

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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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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Tumor Immunotherapy01:27

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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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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.
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Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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Related Experiment Video

Updated: Mar 24, 2026

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
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Potential Therapy for Refractory Colon Cancer.

Mitch Leslie

    Cancer Discovery
    |March 2, 2016
    PubMed
    Summary

    The new drug MM-1151 shows promise in treating colorectal cancer by overcoming resistance to existing therapies like cetuximab. Clinical trials indicate it can slow tumor growth and shrink tumors in patients with specific EGFR mutations.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Drug Discovery

    Background:

    • Cetuximab and panitumumab are standard treatments for metastatic colorectal cancer (mCRC) that target the epidermal growth factor receptor (EGFR).
    • Resistance to these therapies, often driven by mutations in the extracellular domain of EGFR, limits their effectiveness in a subset of patients.
    • Developing novel agents that can overcome or circumvent this resistance is a critical unmet need in mCRC treatment.

    Discussion:

    • MM-1151 demonstrates potential to overcome resistance mechanisms associated with specific EGFR extracellular domain mutations.
    • The drug exhibited efficacy in preclinical models, including a colorectal cancer cell line with relevant mutations and patient-derived cells from a resistant tumor.
    • These findings suggest MM-1151 could offer a new therapeutic option for patients who have progressed on or are resistant to current anti-EGFR therapies.

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    Key Insights:

    • MM-1151 effectively slowed disease progression in a colorectal cancer cell line harboring EGFR mutations associated with cetuximab resistance.
    • The drug inhibited the growth of tumor cells derived from a cetuximab-resistant patient, highlighting its potential to overcome acquired resistance.
    • A Phase I clinical trial showed tumor shrinkage or stabilization in patients with EGFR mutations treated with MM-1151.

    Outlook:

    • Further clinical trials are warranted to establish the safety and efficacy of MM-1151 in a broader patient population with mCRC and specific EGFR mutations.
    • MM-1151 may represent a valuable addition to the therapeutic armamentarium against refractory or resistant colorectal cancer.
    • Investigating the precise molecular mechanisms by which MM-1151 overcomes EGFR inhibitor resistance could guide future drug development.