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Related Concept Videos

Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

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Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
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Cells and tissues must meticulously coordinate their activities for the normal functioning of the human body. Therefore, they exhibit socially responsible behavior - resting, growing, dividing, differentiating, or dying - for the organism’s benefit. Cancer arises when cells divide uncontrollably and invade other tissues or organs.
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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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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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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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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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Cancer Cell Models for the Development of Anti-Cancer Drugs.

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Cancer development involves multiple factors, including chemical carcinogens, viruses, and genetic mutations. Early genetic events like oncogene activation and tumor suppressor gene inactivation are crucial in organ-site cancers.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Organ-site cancer etiology is multi-factorial, involving chemical carcinogens, oncogenic viruses, and genetic alterations.
  • Early genetic events are critical in cancer development, preceding later stages.

Discussion:

  • Activation of oncogenes (RAS, Myc, HER-2) and inactivation of tumor suppressor genes (TP53, RB, APC) are key early genetic events.
  • These genetic changes disrupt normal cellular functions, promoting uncontrolled cell growth.

Key Insights:

  • Understanding these early genetic events is fundamental to comprehending cancer initiation.
  • The interplay between oncogenes and tumor suppressor genes dictates cancer progression.

Outlook:

  • Targeting these early genetic events may offer novel therapeutic strategies.
  • Further research into the precise mechanisms of these genetic alterations can advance cancer prevention and treatment.