Please forward methods of examination of children with DSD error screen to 154. Small cell lung cancer – cytology. Micrograph of a lung primary small cell carcinoma, a type of carcinoma.
Carcinoma is a type of cancer that develops from epithelial cells. Carcinomas occur when the DNA of a cell is damaged or altered and the cell begins to grow uncontrollably and become malignant. As of 2004, no simple and comprehensive classification system has been devised and accepted within the scientific community. They are thus not typically carcinomas.
Cancer occurs when a single progenitor cell accumulates mutations and other changes in the DNA, histones, and other biochemical compounds that make up the cell’s genome. If this process of continuous growth, local invasion, and regional and distant metastasis is not halted via a combination of stimulation of immunological defenses and medical treatment interventions, the end result is that the host suffers a continuously increasing burden of tumor cells throughout the body. Carcinoma is but one form of cancer—one composed of cells that have developed the cytological appearance, histological architecture, or molecular characteristics of epithelial cells. The hallmark of a malignant tumor is its tendency to invade and infiltrate local and adjacent structures and, eventually, spread from the site of its origin to non-adjacent regional and distant sites in the body, a process called metastasis. If unchecked, tumor growth and metastasis eventually creates a tumor burden so great that the host succumbs.
Whole genome sequencing has established the mutation frequency for whole human genomes. Carcinomas, however, have much higher mutation frequencies. The particular frequency depends on tissue type, whether a mis-match DNA repair deficiency is present, and exposure to DNA damaging agents such as components of tobacco smoke. The high mutation frequencies in carcinomas reflect the genome instability characteristic of cancers. The likely major underlying cause of mutations in carcinomas is DNA damage.
The high frequency of mutations in the total genome within carcinomas suggests that, often, an early carcinogenic alteration may be a deficiency in DNA repair. A deficiency in DNA repair, itself, can allow DNA damages to accumulate, and error-prone translesion synthesis past some of those damages may give rise to mutations. In addition, faulty repair of these accumulated DNA damages may give rise to epigenetic alterations or epimutations. In somatic cells, deficiencies in DNA repair sometimes arise by mutations in DNA repair genes, but much more often are due to epigenetic reductions in expression of DNA repair genes. Thus, in a sequence of 113 colorectal carcinomas, only four had somatic missense mutations in the DNA repair gene MGMT, while the majority of these cancers had reduced MGMT protein expression due to methylation of the MGMT promoter region. Microscopic examination by a pathologist is then necessary to identify molecular, cellular, or tissue architectural characteristics of epithelial cells.
Breast: Nearly all breast cancers are ductal carcinoma. Prostate: The most common form of carcinoma of the prostate is adenocarcinoma. Colon and rectum: Nearly all malignancies of the colon and rectum are either adenocarcinoma or squamous cell carcinoma. Pancreas: Pancreatic carcinoma is almost always of the adenocarcinoma type and is highly lethal. Ovaries: One of the most deadly forms due to late detection.
Carcinomas are usually staged with Roman numerals. Stage IV tumors have already metastasized through the blood to distant sites, tissues, or organs. Carcinoma stage is the variable that has been most consistently and tightly linked to the prognosis of the malignancy. The criteria for staging can differ dramatically based upon the organ system in which the tumor arises.