How Do You Spell ANTINEOPLASTIC AGENT RESISTANCE?

Pronunciation: [ˌantɪnˌiːə͡ʊplˈastɪk ˈe͡ɪd͡ʒənt ɹɪsˈɪstəns] (IPA)

Antineoplastic Agent Resistance is a medical term that refers to the ability of cancer cells to resist the effects of drugs that are typically used to treat cancer. The word is pronounced /æntiˌniəʊˈplæstɪk ˈeɪdʒənt rɪˈzɪstəns/ in IPA phonetic transcription. The spelling of this term is based on its Greek and Latin roots, with 'anti-' meaning against, 'neo-' meaning new or abnormal, and 'plastic' referring to the growth or formation of cells. This complex term is commonly used in cancer research and treatment.

ANTINEOPLASTIC AGENT RESISTANCE Meaning and Definition

1. Antineoplastic agent resistance refers to the ability of cancer cells to develop resistance or insensitivity to the effects of antineoplastic agents, also known as anticancer drugs. Antineoplastic agents are medications used in chemotherapy to kill or inhibit the growth of cancer cells. However, over time, cancer cells can undergo genetic mutations or acquire alterations in their molecular pathways that allow them to evade the effects of these drugs.

   Resistance to antineoplastic agents is a significant challenge in cancer treatment as it can lead to treatment failure and disease progression. There are various mechanisms by which cancer cells can develop resistance to these drugs. One common mechanism is the increased expression or activity of efflux pumps, proteins that actively remove the drugs from the cancer cells, reducing their effectiveness. Other mechanisms involve alterations in drug metabolism or resistance-inducing mutations in specific cellular targets.

   Antineoplastic agent resistance can be inherent (intrinsic), meaning it exists in cancer cells from the start, or acquired, where cancer cells develop resistance after exposure to antineoplastic agents. Acquired resistance is more common and can occur due to the selective pressure imposed by the treatment, leading to the survival and proliferation of resistant cancer cells.

   Understanding the mechanisms underlying antineoplastic agent resistance is crucial for the development of strategies to overcome it. Combination therapies, targeting multiple pathways simultaneously, or the use of alternative drugs with different modes of action are approaches used to combat resistance. Personalized medicine approaches, where treatment is tailored based on individual genetic profiles, may also contribute to circumventing antineoplastic agent resistance in the future.

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