L12 Flashcards

1
Q

What are the four main characteristics of cancer cells?

A

Uncontrolled proliferation, loss of differentiation, invasiveness, and the ability to metastasize.

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2
Q

What are the two main genetic changes that lead to cancer?

A

Inactivation of tumor suppressor genes (e.g., p53) and activation of oncogenes.

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3
Q

How do alkylating agents work in cancer chemotherapy?

A

They form covalent bonds with DNA, causing cross-linking and preventing DNA replication, leading to apoptosis (e.g., cyclophosphamide).

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4
Q

What is the mechanism of action of methotrexate?

A

Methotrexate inhibits dihydrofolate reductase, blocking the synthesis of tetrahydrofolate needed for DNA synthesis.

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5
Q

How do plant derivatives like vincristine work in chemotherapy?

A

Vincristine inhibits microtubule polymerization, blocking mitosis and stopping cell division.

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6
Q

What role does trastuzumab (Herceptin) play in cancer therapy?

A

Trastuzumab is a monoclonal antibody that inhibits the Her2/neu receptor, which is overexpressed in some breast cancers.

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7
Q

What are the main drawbacks of current cancer chemotherapy?

A

Non-specific targeting, resistance development, inability to eliminate all malignant cells, and limited effects on invasiveness and metastasis.

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8
Q

How does fluorouracil (5-FU) inhibit cancer cell growth?

A

Fluorouracil inhibits thymidylate synthetase, blocking DNA synthesis without affecting RNA or protein synthesis.

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9
Q

What are the therapeutic applications of glucocorticoids in cancer treatment?

A

Glucocorticoids inhibit lymphocyte proliferation, useful in leukemias and lymphomas.

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10
Q

What are future directions in cancer chemotherapy?

A

Inhibiting oncogene signaling, restoring tumor suppressor genes, targeting angiogenesis, and enhancing the immune response.

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11
Q

Explain the role of tumor suppressor genes and oncogenes in cancer development, with examples.

A

Tumor suppressor genes (e.g., p53) prevent uncontrolled cell division by regulating the cell cycle. Mutations in these genes disable their protective function, allowing cancer growth. Oncogenes are mutated proto-oncogenes that promote excessive cell division (e.g., mutations in growth factor receptors). Together, these genetic changes drive tumor development.

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12
Q

Discuss the mechanisms of action of cytotoxic drugs used in cancer chemotherapy.

A

Cytotoxic drugs include:

  • Alkylating agents: Cross-link DNA to prevent replication (e.g., cyclophosphamide).
  • Antimetabolites: Inhibit enzymes in DNA synthesis (e.g., methotrexate inhibits dihydrofolate reductase; fluorouracil inhibits thymidylate synthetase).
  • Cytotoxic antibiotics: Inhibit topoisomerase II, blocking DNA unwinding (e.g., doxorubicin).
  • Plant derivatives: Disrupt microtubule function, blocking mitosis (e.g., vincristine, paclitaxel).
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13
Q

What are the challenges and future prospects of cancer chemotherapy?

A

Challenges include:

  • Non-specific toxicity to normal cells.
  • Drug resistance development.
  • Limited ability to target metastasis and invasiveness.
  • Incomplete tumor eradication. Future approaches aim to:
  • Target oncogenic pathways.
  • Use gene therapy to restore tumor suppressor function.
  • Develop angiogenesis inhibitors and immune-based therapies.
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14
Q

How do hormone therapies work in cancer treatment, and what are some examples?

A

Hormone therapies target hormone-dependent cancers:

  • Tamoxifen: Competes with estrogen for its receptor, used in hormone-dependent breast cancer.
  • Flutamide: An anti-androgen used for prostate cancer. These therapies inhibit the growth signals driven by hormones in cancer cells.
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15
Q

Describe the mechanism of action and therapeutic use of monoclonal antibodies like trastuzumab in cancer therapy.

A

Trastuzumab targets the Her2/neu receptor, a tyrosine kinase receptor overexpressed in some breast cancers. It inhibits receptor signaling, reducing cell proliferation, and may induce tumor-suppressor pathways (e.g., p53). It is effective in Her2-positive breast cancer patients.

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