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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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Cancer02:18

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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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Cancer Stem Cells and Tumor Maintenance02:40

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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Adaptive Mechanisms in Cancer Cells02:53

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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mTOR Signaling and Cancer Progression03:03

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Cancer-Critical Genes I: Proto-oncogenes01:33

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures
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Bourgeoning Cancer Targets.

Priyanka Kriplani1

  • 1Guru Gobind Singh College of Pharmacy, Yamuna Nagar, 1685/17, Huda Jagadhri, Jagadhri, India.

Recent Patents on Anti-Cancer Drug Discovery
|August 5, 2022
PubMed
Summary
This summary is machine-generated.

Cancer genome identification offers insights, but many cancer features extend beyond genes. New strategies focus on non-oncogene deficiencies, revealing broader therapeutic targets than mutated genes for improved cancer treatment.

Keywords:
Cancercheckpointepigenetic.extrinsic targetsintrinsic targetsmetabolic susceptibility

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Area of Science:

  • Genomics and Oncology
  • Cancer Biology
  • Therapeutic Target Discovery

Background:

  • Cancer genome identification has advanced understanding of tumor biology and therapeutic strategies.
  • However, many cancer cell characteristics extend beyond genomic alterations, limiting the clinical impact of tumor genome characterization for numerous patients.
  • There is a need for strategies that elucidate the circuitry and function of cancer genes, addressing both oncogene and non-oncogene deficiencies.

Approach:

  • This review discusses a framework for identifying and categorizing a wide array of cancer targets.
  • It explores emerging techniques that highlight the significance of non-oncogene deficiencies.
  • The review synthesizes current knowledge on diverse therapeutic targets, including synthetic lethal targets, oncogene dependencies, DNA damage responses, tumor suppressor restoration, metabolic vulnerabilities, protein-protein interactions, master regulators, and immunomodulatory approaches.

Key Points:

  • Therapeutic targets derived from non-oncogene deficiencies are potentially more extensive than those from mutated genes.
  • A comprehensive framework is presented, encompassing various cancer target categories.
  • These targets offer innovative prospects for clinical translation in cancer therapy.

Conclusions:

  • Characterizing cancer genomes is crucial but insufficient for treating all patients, as cancer biology encompasses non-genomic features.
  • Focusing on non-oncogene deficiencies and a broader range of targets presents a more expansive therapeutic landscape.
  • The discussed targets hold significant promise for advancing clinical cancer treatment strategies.