Pathology of neoplasia Flashcards
What is neoplasia
Neoplasia is the uncontrolled and abnormal growth of cells, which can lead to the formation of a tumor. Neoplasia is commonly referred to as cancer, although not all neoplasms are cancerous.
The growth of neoplastic cells is driven by mutations or changes in the DNA of the cells. These mutations can cause the cells to divide and grow uncontrollably, forming a mass of cells known as a tumor.
Neoplasia can be benign or malignant. Benign neoplasms are non-cancerous tumors that do not spread to other parts of the body, while malignant neoplasms are cancerous tumors that can invade nearby tissues and spread to other parts of the body through a process known as metastasis.
Neoplasia can occur in any part of the body and can be caused by a variety of factors, including genetic mutations, exposure to carcinogens, viral infections, and other environmental factors. The diagnosis and treatment of neoplasia typically involve a combination of imaging tests, biopsy, and other diagnostic tests, followed by surgery, radiation therapy, chemotherapy, or a combination of these treatments, depending on the type and stage of the neoplasm.
Cell cycle in cancer cells
Abnormal cell signaling: Cancer cells often have abnormal signaling pathways that allow them to grow and divide uncontrollably. This can be caused by mutations in genes that regulate cell growth and division.
Loss of cell cycle checkpoints: The cell cycle in normal cells is regulated by a series of checkpoints that ensure that the cell is ready to progress to the next stage of the cycle. Cancer cells can bypass these checkpoints, leading to uncontrolled cell division and growth.
DNA damage: Cancer cells often have mutations or damage to their DNA, which can lead to abnormalities in the cell cycle. These mutations can disrupt the normal regulation of the cell cycle and allow cancer cells to continue to divide and grow.
Dysregulation of cell cycle genes: Cancer cells can have mutations or changes in the genes that regulate the cell cycle, such as oncogenes or tumor suppressor genes. These mutations can disrupt the normal regulation of the cell cycle and allow cancer cells to continue to divide and grow.
Mutations in checkpoint genes: Cell cycle checkpoints are regulated by genes that control the progression of cells through the cycle. Cancer cells can have mutations in these genes that disrupt their normal function, allowing cells to bypass the checkpoints and continue to divide.
Dysregulation of cyclins and cyclin-dependent kinases (CDKs): Cyclins and CDKs are proteins that regulate the progression of cells through the cell cycle. In cancer cells, the levels of these proteins may be dysregulated, leading to uncontrolled cell division and bypassing of cell cycle checkpoints.
Inactivation of tumor suppressor genes: Tumor suppressor genes normally act as a brake on cell division, preventing cells from dividing uncontrollably. In cancer cells, these genes can be inactivated, allowing cells to bypass cell cycle checkpoints and continue to divide.
Activation of oncogenes: Oncogenes are genes that promote cell division and growth. In cancer cells, these genes can be activated, allowing cells to bypass cell cycle checkpoints and continue to divide.
Overexpression of anti-apoptotic proteins: Anti-apoptotic proteins are proteins that prevent cells from undergoing programmed cell death (apoptosis). In cancer cells, these proteins may be overexpressed, allowing cells to bypass cell cycle checkpoints and continue to divide.
To describe the enabling characteristics and
emerging hallmarks of cancer
Enabling characteristics:
Self-sufficiency in growth signals: Cancer cells can produce their own growth signals, allowing them to proliferate and survive even in the absence of normal growth signals from the body.
Insensitivity to anti-growth signals: Cancer cells may be insensitive to signals from the body that normally inhibit cell growth, allowing them to continue to divide and proliferate.
Evasion of cell death: Cancer cells can evade programmed cell death (apoptosis), allowing them to survive even when they should be eliminated.
Sustained angiogenesis: Cancer cells can promote the growth of new blood vessels to supply them with nutrients and oxygen, enabling their continued growth and proliferation.
Emerging hallmarks:
Genomic instability and mutation: Cancer cells often have a high rate of mutations and genomic instability, which can drive the evolution of more aggressive cancer cells.
Tumor-promoting inflammation: Chronic inflammation can promote the growth and survival of cancer cells, as well as contributing to the formation of a tumor-supportive microenvironment.
Reprogramming of energy metabolism: Cancer cells often reprogram their metabolism to support their growth and survival, relying on different energy sources than normal cells.
Invasion and metastasis: Cancer cells can invade surrounding tissues and spread to other parts of the body, leading to the formation of metastases.
To understand tumour grading and staging
To understand the concepts of chemotherapy
Alkylating agents: These drugs work by interfering with the DNA in cancer cells, preventing them from dividing and multiplying.
Antimetabolites: These drugs interfere with the normal metabolic processes of cancer cells, preventing them from making the proteins and other substances they need to grow and divide.
Anthracyclines: These drugs work by damaging the DNA in cancer cells, preventing them from replicating.
Taxanes: These drugs interfere with the microtubules in cancer cells, which are necessary for cell division.
Platinum-based drugs: These drugs work by binding to DNA and interfering with its ability to replicate.
