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Carcinogens are substances that can cause cancer. They may induce DNA damage directly or create a biological environment that promotes carcinogenesis.

Cyclical hypoxia refers to variable oxygen tension within a tumor. This environment can promote tumor progression and resistance to therapy by selecting for cells adapted to these conditions.

Cancer risk factors include genetic predispositions, lifestyle choices (such as smoking), environmental exposures, and certain infections, all of which can contribute to the development of cancer.

Cancer stem cells are a subpopulation of cells within a tumor that possess the ability to self-renew and reproduce the tumor. They are believed to contribute to cancer recurrence and resistance to therapy.

Metastasis refers to the spread of cancer cells from the primary tumor to distant organs. It is a complex process that involves changes in cell adhesion, invasion, and migration.

Epigenetic changes involve modifications in gene expression without altering the DNA sequence. These changes can silence tumor suppressor genes or activate oncogenes, affecting cancer development.

MicroRNAs are small non-coding RNAs that regulate gene expression post-transcriptionally. Dysregulation of miRNAs can contribute to cancer by affecting oncogenes and tumor suppressor genes.

Oncogenes are genes that when mutated or expressed at high levels, contribute to converting a normal cell into a cancer cell. They are often involved in promoting cell growth and proliferation.

Tumor heterogeneity refers to the presence of diverse cell populations within a tumor. This diversity can stem from genetic, epigenetic, and microenvironmental differences, affecting treatment response.

The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. These include sustaining proliferative signaling, evading growth suppressors, activating invasion and metastasis, enabling replicative immortality, inducing angiogenesis, and resisting cell death.

Angiogenesis is the formation of new blood vessels. Tumors need to induce angiogenesis to secure a blood supply for nutrients and oxygen, which supports their growth and survival.

Tumor suppressor genes are involved in controlling cell growth and division. When they are inactivated or lost, cells can grow uncontrollably, which can lead to cancer.

Chemical carcinogenesis refers to the process by which chemicals cause cancer. It often involves direct damage to DNA or the promotion of a proliferative, tumor-friendly environment.

Immune surveillance is the concept that the immune system regularly checks for and eliminates tumor cells. Escape from immune surveillance is an important step in cancer development.

The Warburg effect describes cancer cells' tendency to favor glycolysis for energy production, even in the presence of oxygen. This metabolic switch supports rapid cell growth and is associated with cancer.

EMT is a process where epithelial cells lose their cell-cell adhesion properties and gain migratory and invasive capabilities to become mesenchymal stem cells. It is an important step in tumor metastasis.

Proto-oncogenes are normal genes whose functions are to regulate cell growth and differentiation. Mutations or increased expression of these genes can convert them into oncogenes.

Apoptosis is programmed cell death, a mechanism to eliminate damaged or unneeded cells. Evasion of apoptosis is a hallmark of cancer, allowing cancer cells to survive and proliferate.

Chronic inflammation can contribute to carcinogenesis by providing bioactive molecules that can damage DNA and stimulate cell proliferation. It serves as a tumor promoter in various cancer types.

Signal transduction pathways control cell growth, differentiation, and survival. Mutations in signaling molecules can lead to aberrant signaling, promoting cancer.

DNA repair genes are responsible for correcting DNA damage. Defects in these genes can lead to a high mutation rate, which is known as 'mutator phenotype' and contributes to carcinogenesis.

Anoikis is a form of apoptosis that occurs when cells detach from the extracellular matrix. Cancer cells that resist anoikis can survive after detaching, facilitating metastasis.

Oncoviruses are viruses that can cause cancer. They can do so by integrating their genetic material into the host genome, leading to the disruption of normal cellular regulation.

Telomerase is an enzyme that extends the telomeres at the ends of chromosomes, which normally shorten with each cell division. Cancer cells often reactivate telomerase to allow unlimited replication.