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Atypical Adenomatous Hyperplasia

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David G Bostwick – 1st expert on this subject based on the ideXlab platform

  • Atypical Adenomatous Hyperplasia adenosis of the prostate dna ploidy analysis and immunophenotype
    International Journal of Surgical Pathology, 2005
    Co-Authors: Antonio Lopezbeltran, Junqi Qian, Rodolfo Montironi, Rafael J Luque, David G Bostwick

    Abstract:

    Atypical Adenomatous Hyperplasia (AAH) of the prostate is a microscopic proliferation of small acini that may be mistaken for adenocarcinoma. Although some data suggest that AAH is associated with adenocarcinoma arising in the transition zone, the clinical significance of this lesion is uncertain. Therefore we studied the DNA ploidy pattern and immunophenotype of AAH as compared with nodular Hyperplasia and well-differentiated adenocarcinoma in 23 formalin-fixed, paraffin-embedded, whole-mounted retropubic prostatectomies. Representative sections were immunostained for keratin 34β-E12, chromogranin, bcl-2, c-erbB-2, ki67-MIB1, and factor VIII (microvessel density). DNA ploidy was determined by image analysis and Feul gen-stained sections. There were rare scattered immunoreactive cells for chromogranin, bcl-2, and c-erbB-2 in nodular Hyperplasia and AAH (mainly in the basal cell compartment) and in carcinoma. The ki67-MIB1 labeling index was different between nodular Hyperplasia and AAH (p<0.001) and carci...

  • Atypical Adenomatous Hyperplasia of the prostate a premalignant lesion
    Cancer Research, 1998
    Co-Authors: Liang Cheng, Junqi Qian, Ailin Shan, John C Cheville, David G Bostwick

    Abstract:

    Abstract To better understand genetic alterations in Atypical Adenomatous Hyperplasia (AAH) of the prostate, we examined the prevalence of allelic imbalance at 5 microsatellite polymorphic markers on chromosomes 7q31–35, 8p12–21, 8p22, 8q22.2, and 18q12.2 from 15 patients with AAH. DNA samples were obtained from formalin-fixed paraffin-embedded sections using tissue microdissection. We found allelic imbalance in 7 of 15 (47%) cases of AAH. Genetic changes that commonly occur in early prostatic carcinogenesis and prostate carcinoma are found in AAH. Current data provide evidence of a genetic link between some cases of AAH and carcinoma.

  • relationship between Atypical Adenomatous Hyperplasia aah prostatic intraepithelial neoplasia pin and prostatic adenocarcinoma
    Pathologica, 1997
    Co-Authors: B Helpap, H Bonkhoff, A Cockett, R Montironi, Patricia Troncoso, D Waters, David G Bostwick

    Abstract:

    : Two histopathologic lesions are considered putative precursors of prostate cancer, but the supportive evidence for one (prostatic intraepithelial neoplasia, or PIN) is much greater than the other (Atypical Adenomatous Hyperplasia, or AAH). High grade PIN is the most likely precursor of carcinoma, arising in the peripheral zone, but probably does not account for well-differentiated cancer arising in the transition zone. The biological significance of Atypical Adenomatous Hyperplasia of the prostate (AAH) is inconclusive at the time. The histological and cytological features of AAH are intermediate between BPH and low grade carcinoma, suggesting that AAH may be a precursor of well differentiated transition; zone carcinoma. In the recent time new findings on morphogenetic aspects of normal and abnormal prostatic growth i.e. stem cell models are discussed and topics about grading and proliferative activities, frequency and histological changes associated with aging as well as clinical relevance of PIN and AAH. This paper reviews the results and discussion at the second international consultation meeting on PIN in Mayo Clinic, Rochester, Nov. 3-4 th. 1995, following the first international consultation meeting of AAH and PIN and origin of the prostatic carcinoma in Ancona, Sept. 11-12 th 1994.

Kenji Suzuki – 2nd expert on this subject based on the ideXlab platform

  • association of cyp19a1 polymorphisms with risks for Atypical Adenomatous Hyperplasia and bronchioloalveolar carcinoma in the lungs
    Carcinogenesis, 2010
    Co-Authors: Takashi Kohno, Kenji Suzuki, Ryutaro Kakinuma, Motoki Iwasaki, Taiki Yamaji, Hideo Kunitoh, Yoko Shimada, Kouya Shiraishi, Yoshio Kasuga, Gerson Shigeaki Hamada

    Abstract:

    Abstract Estrogen has been indicated to play an etiological role in the development of lung adenocarcinoma (ADC), particularly bronchioloalveolar carcinoma (BAC), a type of ADC that develops from a benign Adenomatous lesion, Atypical Adenomatous Hyperplasia (AAH). Polymorphisms in the CYP19A1 gene cause interindividual differences in estrogen levels. Here, 13 CYP19A1 single-nucleotide polymorphisms (SNPs) were examined for associations with lung AAH risk. AAH is detected as ground-glass opacity (GGO) by computed tomography (CT) examination, and this study consisted of 100 individuals diagnosed with GGO in their lungs among 3088 CT-based cancer screening examinees and 424 without. Minor allele carriers for the rs3764221 SNP showed an elevated risk for GGO [odds ratio (OR) = 1.72, P = 0.017]. Associations of this SNP with risks for lung AAH and BAC in the lungs were next examined using 359 ADC cases whose resected lung lobes were subjected to a histological examination for AAH accompaniment and the presence of BAC components and 330 controls without cancer. The ORs were also increased for lung ADC accompanied by AAH (OR = 1.74, P = 0.029) as well as lung ADC with BAC components (OR = 1.41, P = 0.091). The minor allele was associated with an increased circulating estradiol level (P = 0.079) in a population of 363 postmenopausal women without cancer. These results indicate that CYP19A1 polymorphisms are involved in the risk for lung AAH and BAC in the lungs by causing differences in estrogen levels.

  • loss of heterozygosity on chromosomes 9q and 16p in Atypical Adenomatous Hyperplasia concomitant with adenocarcinoma of the lung
    American Journal of Pathology, 2001
    Co-Authors: Kazuya Takamochi, Tomoyuki Yokose, Kenji Suzuki, Yutaka Nishiwaki, A Ochiai, Kanji Nagai, Tsutomu Ogura, Hidenori Kawasaki, Yukiko Kurashima, Hiroyasu Esumi

    Abstract:

    Atypical Adenomatous Hyperplasia (AAH) has recently been implicated as a precursor to lung adenocarcinoma. We previously reported loss of heterozygosity (LOH) in tuberous sclerosis (TSC) gene-associated regions to frequently be observed in lung adenocarcinoma with multiple AAHs. In this study, we analyzed LOH in four microsatellite loci on 9q, including the TSC1 gene-associated region, and four loci on 16p, including the TSC2 gene-associated region, in both 18 AAHs and 17 concomitant lung adenocarcinomas from 11 patients. Seven of 18 (39%) AAHs and 9 of 17 (53%) adenocarcinomas displayed LOH on 9q. Five (28%) AAHs and seven (41%) adenocarcinomas harbored LOH at loci adjacent to the TSC1 gene. Four of 18 (22%) AAHs and 6 of 17 (35%) adenocarcinomas displayed LOH on 16p. One (6%) AAH and five (29%) adenocarcinomas harbored LOH at loci adjacent to the TSC2 gene. These findings may indicate a causal relationship of LOH on 9q and 16p in a fraction of AAH lesions and adenocarcinomas of the lung. Especially, the frequencies of LOH on 9q and at the TSC1 gene-associated region were high. The TSC1 gene or another neighboring tumor suppressor gene on 9q might be involved in an early stage of the pathogenesis of lung adenocarcinoma.

  • monoclonality of Atypical Adenomatous Hyperplasia of the lung
    American Journal of Pathology, 1999
    Co-Authors: Seiji Niho, Tomoyuki Yokose, Kenji Suzuki, Tetsuro Kodama, Yutaka Nishiwaki, Kiyoshi Mukai

    Abstract:

    Atypical Adenomatous Hyperplasia (AAH) of the lung has been postulated as a possible precursor lesion of bronchioloalveolar carcinoma (BAC). The clonality of AAHs from seven female patients was analyzed to determine whether AAH is a monoclonal expansion. All AAHs were identified in lungs surgically resected for BAC. The clonality of the BAC and bronchiolar metaplasia in each case was also analyzed. Approximately 500 cells in each lesion were precisely microdissected from methanol-fixed sections. Adjacent normal lung tissue was collected as a normal control. DNA was extracted for clonal analysis based on an X-chromosome-linked polymorphic marker, the human androgen receptor gene (HUMARA). HUMARA was found to be amplified with or without previous digestion by the methylation-sensitive restriction endonuclease HpaII. Five cases were informative. All 10 AAHs and 7 BACs obtained from the informative cases showed monoclonality, whereas the control cells showed polyclonality. Three different AAH lesions in a single case showed both possible patterns of monoclonality. BAC and contiguous AAH showed identical monoclonality in two cases. Two lesions of bronchiolar metaplasia, which was considered reactive, were polyclonal. Our results demonstrated the monoclonal nature of AAH, and this finding suggests that AAH is a precursor of BAC or a preneoplastic condition.

Tomoyuki Yokose – 3rd expert on this subject based on the ideXlab platform

  • Atypical Adenomatous Hyperplasia of the lung in autopsy cases.
    Lung cancer (Amsterdam Netherlands), 2020
    Co-Authors: Tomoyuki Yokose, Kozo Tanno, Kentaro Yamazaki, A Ochiai

    Abstract:

    Atypical Adenomatous Hyperplasia (AAH) is a possible precursor lesion of adenocarcinoma of the lung, but very few reports of AAH have focused on the autopsy lung.
    We intended to clarify the characteristics of AAH in the general population by using 207 autopsy cases, ranging in age from 0 to 90 years old.
    A total of 179 eligible cases (86.5%) and 1265 tissue slides (7.0 per case) was examined independently by two pathologists. One hundred seventy-nine autopsy cases consisted of 125 males and 54 females, whose median ages were 38 (range 0-90) and 31 (range 0-81) years old, respectively. AAH was microscopically found in five of 179 autopsy cases (2.8%). The male/female ratio was 5/0 and age distribution was 52-63 years of age (median 57). One of five cases with AAH harbored esophageal carcinoma, but the others had no present or previous malignant neoplasm. One of five lesions was high grade and the others were low grade. All five cases showed positive immunoreactivity for proSP-C, a type II pneumocytes marker, but not for p53, Ki-67 or CEA.
    The incidence of AAH was very low in the general autopsy cases, as compared with the previously reported surgically resected lung and senile autopsy cases, and AAH seems to occur after middle age in general.

  • loss of heterozygosity on chromosomes 9q and 16p in Atypical Adenomatous Hyperplasia concomitant with adenocarcinoma of the lung
    American Journal of Pathology, 2001
    Co-Authors: Kazuya Takamochi, Tomoyuki Yokose, Kenji Suzuki, Yutaka Nishiwaki, A Ochiai, Kanji Nagai, Tsutomu Ogura, Hidenori Kawasaki, Yukiko Kurashima, Hiroyasu Esumi

    Abstract:

    Atypical Adenomatous Hyperplasia (AAH) has recently been implicated as a precursor to lung adenocarcinoma. We previously reported loss of heterozygosity (LOH) in tuberous sclerosis (TSC) gene-associated regions to frequently be observed in lung adenocarcinoma with multiple AAHs. In this study, we analyzed LOH in four microsatellite loci on 9q, including the TSC1 gene-associated region, and four loci on 16p, including the TSC2 gene-associated region, in both 18 AAHs and 17 concomitant lung adenocarcinomas from 11 patients. Seven of 18 (39%) AAHs and 9 of 17 (53%) adenocarcinomas displayed LOH on 9q. Five (28%) AAHs and seven (41%) adenocarcinomas harbored LOH at loci adjacent to the TSC1 gene. Four of 18 (22%) AAHs and 6 of 17 (35%) adenocarcinomas displayed LOH on 16p. One (6%) AAH and five (29%) adenocarcinomas harbored LOH at loci adjacent to the TSC2 gene. These findings may indicate a causal relationship of LOH on 9q and 16p in a fraction of AAH lesions and adenocarcinomas of the lung. Especially, the frequencies of LOH on 9q and at the TSC1 gene-associated region were high. The TSC1 gene or another neighboring tumor suppressor gene on 9q might be involved in an early stage of the pathogenesis of lung adenocarcinoma.

  • Atypical Adenomatous Hyperplasia of the lung in autopsy cases
    Lung Cancer, 2001
    Co-Authors: Tomoyuki Yokose, Kozo Tanno, Kentaro Yamazaki, A Ochiai

    Abstract:

    Abstract Background: Atypical Adenomatous Hyperplasia (AAH) is a possible precursor lesion of adenocarcinoma of the lung, but very few reports of AAH have focused on the autopsy lung. Methods: We intended to clarify the characteristics of AAH in the general population by using 207 autopsy cases, ranging in age from 0 to 90 years old. Results: A total of 179 eligible cases (86.5%) and 1265 tissue slides (7.0 per case) was examined independently by two pathologists. One hundred seventy-nine autopsy cases consisted of 125 males and 54 females, whose median ages were 38 (range 0–90) and 31 (range 0–81) years old, respectively. AAH was microscopically found in five of 179 autopsy cases (2.8%). The male/female ratio was 5/0 and age distribution was 52–63 years of age (median 57). One of five cases with AAH harbored esophageal carcinoma, but the others had no present or previous malignant neoplasm. One of five lesions was high grade and the others were low grade. All five cases showed positive immunoreactivity for proSP-C, a type II pneumocytes marker, but not for p53, Ki-67 or CEA. Conclusions: The incidence of AAH was very low in the general autopsy cases, as compared with the previously reported surgically resected lung and senile autopsy cases, and AAH seems to occur after middle age in general.