The Ultrastructure And Pathobiology Of Urinary Bladder Cancer
George T. Bryan, Samuel M. Cohen in The Pathology of Bladder Cancer, 2017
Atypical hyperplasia and its more severe form, dysplasia, differ from simple hyperplasia in that there are significant nuclear atypicalities. Atypical hyperplasia is usually subclassified as mild, moderate, or severe based upon the degree of cellular atypicality and the proportion of atypical cells.2,3,145,170,171 The atypical cells have altered nuclear/cytoplasmic ratios, demonstrate pleomorphism, and frequently show loss of cell polarity. Thus, they exhibit some of the morphological changes of malignant cells. The nuclei vary from small round shapes with extensive chromatin clumping, to large hyperchromatic nuclei with evenly dispersed chromatin and large, often multiple nucleoli.171 As seen in scanning electron micrographs, the superficial layer of umbrella cells in normal bladder epithelium is partially preserved in dysplasia, although the cobblestone-like surface pattern is often interrupted by foci of small, spheroid cells.145,171 While cells in the cobblestone areas are covered by microridges, the small spheroid cells are covered by numerous pleomorphic microvilli. Except for these nuclear alterations, the cytoarchitecture of the cells in dysplasia is similar to that of the cells in simple hyperplasia. In dysplasia, mitotic activity is increased in both the basal cell layer and the intermediate cell layer.
Breast Cancer
Mary J. Marian, Gerard E. Mullin in Integrating Nutrition Into Practice, 2017
There are several risk factors for breast cancer including age, family history, and prior breast biopsy, especially when atypical hyperplasia is identified. Estrogen exposure is a well-established risk factor for breast cancer given its profound influence on epithelial cell growth.3 Cumulative, excessive estrogen exposure over the course of a lifetime contributes to breast cancer risk and may be a cause of this disease. Early menarche, late menopause, low parity, or delayed parity all increase a woman’s breast cancer risk.8 Greater estrogen exposure over a women’s life course can have direct genotoxic effects by increasing breast cell proliferation and random genetic errors affecting cellular differentiation and gene expression. The mechanisms of carcinogenesis include the metabolism of estrogen to mutagenic, genotoxic metabolites and the stimulation of tissue growth. These processes cause initiation, promotion, and progression of breast cancer.
The effects of selective estrogen receptor modulators on the endometrium
A. R. Genazzani in Hormone Replacement Therapy and Cancer, 2020
In summary, tamoxifen results in an increase in endometrial proliferation, polyp formation, hyperplasia and carcinoma in postmenopausal women, whether used for breast cancer therapy or prevention. It appears not to have that effect in premenopausal women. Furthermore, at least in some patients, it produces an unusual ultrasound appearance that makes simple transvaginal ultrasound without fluid enhancement less reliable. The high incidence of focal abnormalities also makes blind endometrial sampling with suction piston devices less reliable. Finally, there appear to be high- and low-risk groups for the development of atypical hyperplasia based on the presence or absence of endometrial lesions prior to tamoxifen therapy. Raloxifene appears to act differently from tamoxifen in experimental animals and in clinical trials. However, one short-coming of the Raloxifene Endometrial Safety Study is that women with pre-existing endometrial lesions, a high-risk group for tamoxifen therapy, were excluded from the study. Still, real-world data from the MORE trial compared with data from the BCPT clearly show that raloxifene is not like tamoxifen in its effects on the postmenopausal endometrium. This author believes that patients embarking on tamoxifen therapy should have pretreatment screening to assess whether they are at high risk for developing atypical hyperplasia.
Preliminary dynamic observation of wound healing after low-temperature plasma radiofrequency ablation for laryngeal leukoplakia
Published in Acta Oto-Laryngologica, 2022
Fang Hao, Liyan Yue, Xiaoyan Yin, Chunguang Shan
Currently, the 2005 WHO histopathologic classification is the most widely used classification of precancerous lesions [2]. The WHO classification is based on the degree or extent of epithelial dysplasia, as follows [2]: hyperplasia; mild dysplasia; moderate dysplasia; severe dysplasia hyperplasia; and carcinoma in situ. Among the epithelial dysplasias, atypical hyperplasia is the intermediate between benign and malignant change, and is the key point from quantitative to qualitative change, including abnormal tissue structure and cytologic abnormality. Atypical hyperplasia is divided into three levels: mild; moderate; and severe. Mild atypical hyperplasia is characterized by a small number of atypical cells, small cellular atypia, and the tissue structure is disordered and confined to one-third of the epithelial layer. The tissue structure disorder does not exceed two-thirds of the epithelial cell in moderate atypical hyperplasia. Severe atypical hyperplasia is characterized by a change in cellular atypia and the tissue structure disorder is greater than two-thirds of the epithelial cell. The malignant transformation rate of precancerous lesions increases with the severity of dysplasia [2].
A menopause survey of women with benign breast disease history in northwest China
Published in Climacteric, 2019
W.J. Gou, J.Z. Zhao, R. Zhang, T. Yang, L.Y. Wang, X.H. Zhang
Based on the degree of cellular proliferation and atypia, benign breast lesions can histologically fall into three types: non-proliferative, proliferative without atypia, and atypical hyperplasia. The proliferative without atypia and atypical hyperplasia types may increase the patient’s future risk of developing breast cancer, whereas no increased risk was found in women with no family history and non-proliferative findings5–7. Most lesions that occur in the breast are benign. The non-proliferative breast lesion is the most common category and most women suffering benign disease are not at increased risk of cancer6,7. However, many studies have been made on women who have MPS with a breast cancer history, yet those with a history of benign breast disease have been rarely reported in a menopause survey.
Presidential reflections: how we got here, where we might go
Published in Climacteric, 2023
I get introduced to the North American Menopause Society (NAMS). Lila Nachtigall gets credit for that. I got on one of their committees, I got on their board, I became the treasurer. Eventually, I became the president. But I continued my work in ultrasound in midlife women. Some of my work follows: in 1994, I published the paper ‘Postmenopausal Endometrial Fluid Collections Revisited: Look at the Doughnut Rather than The Hole’ [14]. Roy Pitkin was editor of the Green Journal. He said: ‘Are you sure you want this referenced for keywords, doughnut and hole?’ I said: ‘Well, if you can think of a better way to express it’. He could not. In the 1980s, the literature had suggested a 75% association between endometrial fluid and postmenopausal women in gynecologic cancers. My first nine patients looked like the image in Figure 9. I struggled to get tissue and all nine of them were inactive and atrophic. I thought ‘75% cancer, and I have nine in a row that are negative. I should go to Monte Carlo and place my mortgage money on the roulette wheel’. Until the 10th patient came in. She looked like the image shown in Figure 10. I realized it is not the fluid, but rather the tissue surrounding the fluid that is significant. This woman had complex atypical hyperplasia. We went back and looked at the original nine, they all had a thin lining. ‘Look at the doughnut, not at the hole’.
Related Knowledge Centers
- Atypical Ductal Hyperplasia
- Microscope
- Hyperplasia
- Malignancy
- Atypia
- Invasive Carcinoma of No Special Type