The most common type of cancer in men is prostate cancer, and in women, it is breast cancer.
Cervical cancer arises in the epithelium of the cervix and is caused by certain strains of HPV.
The gold standard screening test for colorectal cancer is colonoscopy.
Greater exposure to estrogen and obesity increase a woman's risk of developing breast cancer.
Environmental factors such as smoking, diet, alcohol consumption, and radiation exposure play a much bigger role than genetic factors.
Cyclins are regulatory proteins that activate cyclin-dependent kinases (CDKs) and are specific to each cell cycle phase.
When both alleles are mutated or deleted, it can lead to an early onset of retinoblastoma, as per the 2-Hit hypothesis.
The phases of the cell cycle are G1 (growth), S (synthesis), G2, M (mitosis), and G0.
Poorly differentiated malignant tumors exhibit disorganized growth, nuclear pleomorphism and hyperchromasia, high nuclear to cytoplasmic ratio, high mitotic activity with atypical mitosis, invasion through the basement membrane or into local tissue, and metastatic potential.
CDK inhibitors (CDKI) are endogenous inhibitors of CDKs and CDK/cyclin complexes, playing a role in regulating the cell cycle.
The defining feature of a malignant tumor is its ability to metastasize, or spread to distant sites of the body.
Lung cancer is the deadliest cancer type.
During the M phase, checkpoints ensure that the metaphase plate is aligned and that microtubules are in place.
Mutations affecting the RB gene can include deletions, insertions, and point mutations, which may result in no protein production or a non-functional version of the protein.
Prostate cancer is the most diagnosed cancer in males, followed by lung and colorectal cancers.
Cyclin D - CDK4, cyclin D - CDK6, and cyclin E - CDK2 kinase complexes regulate the G1 to S transition.
Mutated RB is associated with increased susceptibility to other cancers, such as osteosarcoma, neuroblastoma, and some types of brain cancers.
Microtubule-targeting agents activate the spindle assembly checkpoint (SAC) and disrupt microtubule dynamics, inducing prolonged mitotic arrest.
The cyclin B - CDK1 complex regulates the G2 to M phase of the cell cycle.
The goal of screening is to catch dysplasia before it becomes carcinoma and to detect carcinoma before clinical symptoms arise.
During the S phase, checkpoints ensure that DNA is replicated entirely, only once, and check if DNA repair is needed.
CDKs are enzymes activated by cyclins that phosphorylate proteins to drive the cell cycle forward.
Epithelial cancers of the lung include squamous cell carcinoma, which undergoes squamous metaplasia from respiratory epithelium, and adenocarcinoma, which appears glandular.
In the G1 phase, the cell replicates its DNA and checks if proliferation is appropriate and if all machinery is ready for replication.
Cyclin E activates CDK2 and helps complete the G1/S transition.
Neoplastic tissue growth is unregulated, irreversible, and monoclonal.
The most common cancers by incidence are breast/prostate, lung, and colorectal.
Breast cancer is the most diagnosed cancer in females, followed by lung and colorectal cancers.
Cyclins and CDKs are major regulators that activate CDK-cyclin complexes, which phosphorylate and inactivate the Rb protein, driving cell cycle progression.
Endogenous inhibitors of CDKs include P16 (CDKN2A) and P21.
Cancer is a disease of aging, and incidence rates for cancer climb steadily as age increases.
The SAC delays chromosome segregation until all chromosomes are correctly attached to the mitotic spindle.
The G1/S checkpoint ensures there is no DNA damage before replication.
Labile cells are often inside the cell cycle and are found in tissues that require constant cellular production, such as bone marrow, skin, hair, and GI epithelium.
The RB1 gene encodes the retinoblastoma protein (Rb), which prevents cells from entering the S phase by inhibiting the E2F family of transcription factors.
Stable cells are arrested in G0 but can enter the cell cycle when needed, such as parenchymal cells for liver regeneration.
Hyper-phosphorylated Rb can no longer bind E2F, leading to the release of E2F, which activates genes in DNA synthesis during the S phase.
Benign tumors are usually well differentiated and exhibit organized growth, uniform nuclei, low nuclear to cytoplasmic ratio, minimal mitotic activity, lack of invasion, and no metastatic potential.
In the G2 phase, the cell prepares for division by doubling the cytoplasm and organelles, while also checking for sufficient cytoplasm and organelles and performing a final DNA check.
The G2/M checkpoint ensures that all DNA is replicated before mitosis begins.
Neuroendocrine cancers in lung cancer include carcinoid, small cell carcinoma, and large cell carcinoma.
Cyclin A regulates the S phase and G2 phase.
During the M Phase, DNA condenses into chromosomes and separates into two daughter cells, followed by cytokinesis.
Clonality can be determined by G6PD isoforms or androgen receptor isoforms.
Permanent cells do not re-enter the cell cycle and have differentiated, such as neurons and cardiac muscle.
The spindle checkpoint ensures that chromosomes are attached to spindle microtubules before separating.
During prophase, DNA condenses into chromosomes, with sister chromatids linked by centromeres.
Cancer is the second leading cause of death in both adults and children.
Benign tumors remain localized and do not metastasize, while malignant tumors invade locally and have the potential to metastasize.
Metaplasia is the replacement of one cell type by another, often as an adaptation to chronic tissue damage.
Dysplasia is characterized by disordered growth of non-neoplastic epithelial cells, with morphologic changes like pleomorphism and hyperchromatic nuclei.
Both metaplasia and dysplasia are reversible but can precede cancer in some cases.
Carcinoma in situ is severe dysplasia that is (pre)malignant, confined to the region, with no invasion of the basement membrane.
Tumor origins can include epithelial, mesenchymal, lymph node, bone marrow, and melanocytes.