Primary aldosteronism
Demetrius Pertsemlidis, William B. Inabnet III, Michel Gagner in Endocrine Surgery, 2017
Primary aldosteronism (PA) describes a number of conditions, all characterized by excess production of aldosterone. Dr. Jerome Conn described the phenomenon of hypertension and hypokalemia in the 1950s, improving after resection of an adrenocortical adenoma [1]. He suggested that this clinical picture was due to overproduction of aldosterone by the adrenal adenoma. Today, this constellation of findings bears Dr. Conn’s name and is known as Conn’s syndrome. While PA is often due to an adrenal adenoma, other causes have since been identified; aldosterone-producing adrenal hyperplasia, in particular, has been recognized as a genetic disorder and is now divided into three types: familial hyperaldosteronism (FH) types I–III. Genetic causes have also been discovered in the past decade for both adenoma and hyperplasia.
Colorectal cancer
J. K. Cowell in Molecular Genetics of Cancer, 2003
Although the genetic changes which give rise to CRC tumors often occur in a particular sequence, it is the accumulation of mutations together with the temporal sequence which determines the malignant potential of a tumor (Figure 2) (Arends, 2000; Fearon and Vogelstein, 1990). In multipotent stem cells, the accumulation of mutations occurs in a stochastic, stepwise manner with each mutation providing a selective advantage for each cell generation, leading to an expanded population of daughter cells (Bodmer et al., 1994). APC mutations occur early (Powell et al., 1992) and are important for initiation. This explains the severe, young colorectal cancer phenotype of familial adenomatous polyposis. In contrast, ras oncogene mutations usually occur in larger adenomas, being present only in 10% of those smaller than 1 cm. It is thought that such mutations are responsible for the development of a small adenoma into a larger lesion. Similarly, allelic losses on chromosomes 5q, 17p and 18q and other chromosomes are frequently observed in malignant tumors, but rarely in adenomas. Such mutations, occurring later in the cascade of mutational events are unlikely to have major relevance in the search for cancer susceptibility as they are largely somatic mutational events, commencing in a single cell. Nevertheless, it is conceivable that variations which predispose to mutational change in any of these genes could influence the nature and rate of cancer development.
Head and neck cancer
Peter Hoskin, Peter Ostler in Clinical Oncology, 2020
Each year in the United Kingdom there are 500−600 new cases per annum. This usually arises de novo but rarely can develop in a pleomorphic adenoma. Local infiltration may cause a facial nerve palsy, distinct from a benign tumour (Figure 13.7). Variants of carcinoma include: Adenoid cystic carcinoma: Slow-growing carcinoma and has a tendency for invasion along nerves and into the cranial cavityAcinic cell carcinoma arising from serous cellsMucoepidermoid carcinoma arising from mucin cellsAdenocarcinomaSquamous carcinoma: Must be distinguished from a metastasisUndifferentiated carcinoma
Potential for prevention: a cohort study of colonoscopies and removal of adenomas in a FIT-based colorectal cancer screening programme
Published in Scandinavian Journal of Gastroenterology, 2019
Mette Bach Larsen, Sisse Helle Njor, Thomas Møller Jensen, Peter Ingeholm, Berit Andersen
Results of colonoscopies were retrieved from the Danish Pathology Register, which holds information from all pathology departments, using the Danish SNOMED coding system for pathology diagnoses [21]. Localisation of adenomas in colon and rectum was defined by the following two SNOMED codes: T67* (colon) and T68* (rectum). Relevant adenomas were identified by the following SNOMED codes: M8213F (flat adenoma), M82110 (tubular adenoma), M82130 (traditional serrated adenoma), M8213M (sessile serrated lesion with dysplasia) and M82630 (tubulovillous adenoma), M82611 (villous adenoma). Adenomas were classified as high-risk adenomas if one of the following three criteria were met: (1) at least one adenoma ≥20 mm, (2) more than five adenomas regardless of their size, or (3) removal of at least one adenoma using the piecemeal technique. Adenomas were classified as intermediate-risk adenomas if one of the following four criteria were met: (1) ≥3 and ≤4 adenomas, (2) at least one adenoma ≥10 mm and <20 mm, (3) at least one tubulovillous or villous adenoma and (4) at least one adenoma with high-grade neoplasia. Adenomas were classified as low-risk adenomas if none of the above criteria were met [17]. In the following, high- and intermediate-risk adenomas are defined as advanced adenomas and low-risk adenomas are classified as non-advanced adenomas. Adenoma was used as a collective name for both advanced and non-advanced adenomas. If more than one specimen was identified in the Danish Pathology Register per individual within the study period, only the one with the more serious result was included.
Advances in tests for colorectal cancer screening and diagnosis
Published in Expert Review of Molecular Diagnostics, 2022
Sarah Cheuk Hei Chan, Jessie Qiaoyi Liang
Colorectal cancer (CRC) is the third most common type of cancer and the second leading cause of cancer deaths around the world in 2020 [1]. It arises from benign tumors in a process known as the adenoma-carcinoma sequence and has been mainly associated with genetic mutations previously [2,3]. Recent evidence has shown that gut microbiome dysbiosis is associated with colorectal tumorigenesis. Abnormality in the composition of the gut microbiota has been implicated as a potentially important etiological factor in the initiation and progression of CRC [4]. Common risk factors include poor diet, sedentary lifestyle, history of colorectal polyps and family history of CRC or adenoma [5]. Since CRC develops over a long period of time, screening enables early detection and thus a higher chance of treatment. An increased screening rate was associated with a 25.5% reduction in annual CRC incidence and a 52.4% drop in mortality from 2000 to 2015 [6], which highlights the importance of screening.
Correlations between clinical hormone change and pathological features of pituicytoma
Published in British Journal of Neurosurgery, 2018
Ting-Wei Chang, Ching-Yi Lee, Shih-Ming Jung, Hung-Yi Lai, Chun-Ting Chen, Mun-Chun Yeap, Chi-Cheng Chuang, Peng-Wei Hsu, Chen-Nen Chang, Po-Hsun Tu, Shih-Tseng Lee
In the present study, patients’ symptoms at presentation were mostly hormone change. Notably, the sizes of their tumours were relatively small (4–11.9 mm in diameter), and significant serum hormone improvements were observed immediately after surgery. However, serum hormone relapse was observed in two of our patients during follow-up (Table 1), for which there are two possible explanations: either the coexisting pituitary adenoma was not resected, or the residual pituicytoma cells induced local irritation and triggered the recurrence. In both cases, it is clear that resection was insufficient. Because pituicytoma is a benign tumour, the goal of surgical treatment is to reduce the mass effect causing clinical symptoms, rather than total tumour removal2; however, this response appears to be inadequate for patients with pituicytoma and predominant hormone elevation. Therefore, we suggest the following. First, the tumour must be resected as thoroughly as possible. Second, a thorough pathological examination must be performed on specimens of the tumour to confirm the existence or absence of adenoma. Finally, a complete IHC study must be conducted to determine the status of the pituitary gland.
Related Knowledge Centers
- Benign Tumor
- Epithelium
- Gland
- Adrenal Gland
- Pituitary Gland
- Thyroid
- Prostate
- Gardner'S Syndrome
- Malignancy
- Malignant Transformation