Journal of Neoplasm

Description

A cancer that grows from epithelial cells is called a carcinoma. Specifically, a carcinoma is a type of cancer that begins in the tissue that lines the inside or outside of the body and is caused by cells that formed during embryogenesis in the endodermal, mesodermal, or ectodermal germ layers. When a cell's DNA is damaged or altered, it begins to grow uncontrollably and develops into a cancer.

DNA Strands

Because they are made up of simpler monomeric units known as nucleotides, the two DNA strands are referred to as polynucleotides. A sugar called deoxyribose, one of the four nitrogen-containing nucleobases (cytosine, guanine, and thymine), and a phosphate group make up each nucleotide. An alternating sugar-phosphate backbone is formed when the sugar of one nucleotide and the phosphate of the next join the nucleotides in a chain through covalent bonds known as the phospho-diester linkage. Double-stranded DNA is formed when the nitrogenous bases of the two distinct polynucleotide strands are joined by hydrogen bonds in accordance with the rules for pairing bases. There are two groups of complementary nitrogenous bases: pyrimidines and purines. Thymine and cytosine are the pyrimidines in DNA; Adenine and guanine are the purines.

The same biological data can be found stored on both double-stranded DNA strands. When the two strands separate, this information is replicated. More than 98% of human DNA is non-coding, which means that it does not serve as a pattern for protein sequences. Antiparallel means that the two DNA strands run in opposite directions from one another. Each sugar has one of four different kinds of nucleobases (or bases) attached to it . Genetic information is encoded by the sequence of these four nucleobases along the backbone. With the exception of Thymine (T), for which RNA substitutes Uracil (U), transcription is the process by which DNA bases are exchanged for their corresponding bases to create RNA strands. In a process known as translation, these RNA strands specify the amino acid sequence of proteins within the genetic code. Ovarian tumor mediastinal metastases are not uncommon, according to autopsy results. Ovarian carcinomas normally spread by transcaelomic, lymphatic or haematogenous dispersal to peritoneum, pelvic and para-aortic lymph hubs, lung and pleura. Ovarian carcinoma mediastinal metastasis is described in a case. A CT scan revealed a mass in the retrosternum, which was then resected using VTC surgery.

Endometrioid carcinomas of the endometrium have been found to frequently carry PTEN mutations. Some connection has been found between PTEN transformations and the presence of Microsatellite Unsteadiness (MU) in EEC, yet no persuading cause-impact relationship for such affiliation has been advertised. Blood, tumor tissue that had been frozen and paraffin-embedded, and tumor tissue from patients with Endometrial Carcinoma (EC) were used to extract DNA. DNA sequencing and Single-Strand Conformation Polymorphism (SSCP) analysis revealed PTEN mutations. Clinicopathologic data and MI status were correlated with the findings. PTEN mutations were found in 17 tumors (44.7%), and endometrioid (51.5%) tumors were more likely to have them than Nonendometrioid Carcinomas (NEEC) tumors (0 of 5, 0%). The spectrum of PTEN mutations in MI+ and MI tumors was distinct. PTEN mutations were found in tumors with MI+ (60%) but only tumors with MI (34.8). PTEN mutations were found in short coding mononucleotide repeats in EC with MI. These findings confirm that PTEN is a crucial target gene in the development of endometrial cancer. The presence of PTEN mutations in short coding mononucleotide repeats in MI-positive tumors provides some explanation for the frequent presence of PTEN mutations in these tumors and suggests that these mutations may be the result of mismatch repair deficiencies.

Adenosquamous Carcinoma

A typical illustration of heterogeneous tumors is adenosquamous carcinoma of the lung, one of the rather uncommon subtypes of lung cancer. This tumor has two distinct components, either adenocarcinomatous or squamous carcinomatous. Adenosquamous carcinoma should only be diagnosed in tumors that clearly demonstrate glandular differentiation in the form of acini, tubules, or papillary structures and squamous differentiation in the form of keratin or intracellular bridges. A minimum of 10% of each component in the entire tumor is required for a definitive diagnosis of lung adenosquamous carcinoma, as stated in the most recent classification of lung tumors established by the World Health Organization. A genetic approach to the clonality of adenosquamous carcinoma has not yet been attempted, despite the fact that both components of the disease have been morphologically characterized. On definitively diagnosed adenosquamous carcinoma tumors that had not been subjected to anti-cancer chemotherapy or irradiation therapy prior to sampling, both topographic genotyping and immunohistochemical analysis were carried out in this study. Comparative DNA sequences of p53, K-ras, and chromosomal analysis at 9p21 and 9q31–32 were carried out on the various components of each tumor as part of topographic genotyping. P53 mutations are thought to be a useful marker for determining the clonality of cancer cells because they are found in approximately half of non-small-cell carcinomas at various points within hot spots. K-ras mutations have been found in 46% of adenocarcinomas of the lung, but fewer or none have been found in squamous cell carcinoma. Squamous cell carcinoma has more abnormal loci than adenocarcinoma of the lung. The p53 mutations that existed between the various components of each tumor were contrasted with the immunolocalization of p53 overexpression. Additionally, statistical differences in immunohistochemical expression of tumor associated antigens, such as Carcino-Embryonic Antigen (CEA), cancer antigen 19-9 (CA19-9) and mucin 1 (MUC1), were examined. These antigens are primarily expressed in adenocarcinomas. Due to its rather restricted expression in squamous cell carcinomas, Squamous Cell Carcinoma-related antigen (SCC) was also investigated. To further define these tumors' two components, the expressions of p21WAF1/Cip1 (WAF1) and Vascular Endothelial Growth Factor (VEGF) Proliferating Cell Nuclear Antigen (PCNA) were also examined. The levels of immunoreactivity were measured by the appropriation of immunoreactive cancer cells among entire growth cells .

The clonality of adenosquamous carcinoma of the lung as a typical model of heterogeneous tumors and the process of carcinogenesis and cancer progression of these tumors were the primary goals of this study. For heterogeneous tumors, such data may point to effective treatments.