Carcinoma of unknown primary site
The term carcinoma has also come to encompass malignant tumors composed of transformed cells whose origin or developmental lineage is unknown (see cancer of unknown primary origin; CUP), but that possess certain specific molecular, cellular, and histological characteristics typical of epithelial cells. This may include the production of one or more forms of cytokeratin or other intermediate filaments, intercellular bridge structures, keratin pearls, and/or tissue architectural motifs such as stratification or pseudo-stratification. ICD-10 code
(8010-8045) Epithelial neoplasms, NOS
(8050-8080) Squamous cell neoplasms
(M8070/3) Squamous cell carcinoma, NOS
(8090-8110) Basal cell neoplasms
(M8090/3) Basal cell carcinoma, NOS
(8120-8130) Transitional cell carcinomas
(8140-8380) Adenocarcinomas
(M8140/3) Adenocarcinoma, NOS
(M8142/3) Linitis plastica
(M8155/3) Vipoma
(M8160/3) Cholangiocarcinoma
(M8170/3) Hepatocellular carcinoma, NOS
(M8200/3) Adenoid cystic carcinoma
(M8312/3) Renal cell carcinoma
(M8312/3) Grawitz tumor
(8390-8420) Adnexal and Skin appendage Neoplasms
(8430-8439) Mucoepidermoid Neoplasms
(8440-8490) Cystic, Mucinous and Serous Neoplasms
(8500-8540) Ductal, Lobular and Medullary Neoplasms
(8550-8559) Acinar cell neoplasms
(8560-8580) Complex epithelial neoplasms

Carcinoma In situ
The term carcinoma in situ (or CIS) is a term for cells that are significantly abnormal but not cancer. They are thus not typically carcinomas. Pathogenesis
Cancer occurs when a single progenitor cell accumulates mutations and other changes in the DNA, histones, and other biochemical compounds that make up the cells genome. The cell genome controls the structure of the cells biochemical components, the biochemical reactions that occur within the cell, and the biological interactions of that cell with other cells.
High frequency
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. For instance, mutation rates substantially increase (sometimes by 100-fold) in cells defective in DNA mismatch repairA 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. While a mutation or epimutation in a DNA repair gene, itself, would not confer a selective advantage, such a repair defect may be carried along as a passenger in a cell when the cell acquires an additional mutation/epimutation that does provide a proliferative advantage. Such cells, with both proliferative advantages and one or more DNA repair defects (causing a very high mutation rate), likely give rise to the high frequency of total genome mutations seen in carcinomas. DNA repair
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. Diagnosis
Carcinomas can be definitively diagnosed through biopsy, including fine-needle aspiration (FNA), core biopsy, or subtotal removal of single node,.