Cancer Chemotherapy Targets
Cancer Chemotherapy Targets - Related Videos
07:42
Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Cited by 28 •
2012
This abstract describes a novel method to assess the development of neurotoxicity in patients receiving chemotherapy treatment. While conventional assessment methods are limited in their ability to detect early changes in nerve function, nerve excitability techniques provide early identification of patients at risk of severe neurotoxicity and insight into pathophysiology.
05:06
Alkaline Single Cell Gel Electrophoresis: A Sensitive Technique for Quantitative Estimation of DNA Damage in Individual Cancer Cells Following Chemotherapy
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2025
In this video, we demonstrate an alkaline single-cell electrophoresis assay to quantify both single- and double-strand DNA breaks in doxorubicin-treated cells. Alkaline conditions disrupt the hydrogen bonds between DNA base pairs, resulting in the complete unwinding and separation of DNA strands. This allows differential migration of undamaged and damaged DNA fragments in agarose gel upon electrophoresis, revealing a comet-shaped structure of slowly migrating undamaged DNA forming the circular...
05:17
Detection of Targetable Alterations in Non-small Cell Lung Cancer using Next-generation Sequencing
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2025
This protocol describes an automated, ISO15189-accredited next-generation sequencing workflow for detecting targetable genomic alterations in non-small cell lung cancer (NSCLC) formalin-fixed paraffin-embedded tissues.
08:41
Modeling Chemotherapy Resistant Leukemia In Vitro
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Cited by 15 •
2016
The current report summarizes a protocol that can be utilized to model the influence of the bone marrow microenvironment niche on leukemic cells with emphasis placed on enrichment of the most chemoresistant subpopulation.
02:57
Targeted Cancer Therapies
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2023
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 specific...
FAQs
Interfering with DNA replication limits a tumor cell’s ability to copy its genetic material, while disrupting DNA repair can leave damage unresolved. These effects can inhibit continued cell growth and complement drugs that act on other cellular systems. The distinction matters because replication blockade and repair disruption represent different target-based mechanisms within chemotherapy.
Nucleotide synthesis supplies the components needed for DNA production, so blocking this process can restrict the resources required for replication. Topoisomerases represent another target class associated with DNA-handling processes. Separating these mechanisms helps explain why chemotherapy drugs can reach similar outcomes, such as inhibited tumor growth, through different cellular disruptions.
Microtubules support chromosome separation during mitosis, the stage of the cell cycle when a cell divides. Drugs that interfere with these structures can prevent proper chromosome separation and interrupt cell-cycle progression. This mechanism is distinct from blocking nucleotide synthesis or damaging DNA, yet it can likewise hinder the expansion of rapidly dividing tumor cells.
Target-based treatment planning can combine drugs that disrupt complementary cellular processes, such as DNA handling, nucleotide synthesis, and chromosome separation. Because these agents act through different mechanisms, a regimen can inhibit tumor growth at more than one point in the cell cycle or replication process. This framework helps explain the rationale for combination regimens.
The same cellular systems targeted in tumors may also be present in healthy tissue, so treatment effects must be considered beyond the tumor alone. Understanding whether a drug disrupts DNA processes, nucleotide production, topoisomerases, or microtubules helps relate its mechanism to potential tissue damage. This supports toxicity assessment while treatment choices are being evaluated.
Target information can guide treatment selection by linking a drug’s mechanism with the biological characteristics of a tumor. It also helps distinguish which cellular process a regimen is expected to disrupt and whether complementary agents may be appropriate. This approach is especially relevant when tumors are biologically distinct and may require more selective therapies.