Hydatidiform moles are intriguing pathologic entities representing abnormal placental villous tissue with unique genetic profiles and a wide spectrum of morphologic features, which makes accurate diagnosis challenging. Overrepresentation of the paternal genome in sporadic hydatidiform moles (purely androgenetic in complete hydatidiform moles and diandric triploid in partial hydatidiform moles) is a fundamental genetic event leading to global alteration of imprinting gene expression in the molar trophoblast. Rare familial biparental hydatidiform moles (due to NLRP7 or KHDC3L mutations) share such global imprinting alterations, implying a common end point of pathogenesis. Despite being the cornerstone of diagnosis, routine morphologic assessment of hydatidiform moles continues to suffer from interobserver diagnostic variability, emphasizing the need for new diagnostic modalities. Analyses of p57 expression by immunohistochemistry and polymerase chain reaction–based DNA genotyping have emerged as powerful diagnostic methods for accurate classification of hydatidiform moles. Algorithmic approaches combining histology and these ancillary techniques provide the best diagnostic practice currently available.

Partial Hydatidiform Mole

10.1146/annurev-pathol-052016-100237

Cite

Citations (117)

[Pathogenesis of endometrial cancer: clinicopathologic implications].

PubMed (2006)

Pei Hui

子宫内膜癌是妇科最常见的侵袭性肿瘤之一.2005年中国大陆新发病患者估计为2万例[1].该病常见于绝经后妇女,诊断平均年龄约60岁.1973-1978年期间,美国子宫内膜癌的发病率有短暂增加,这与此期间普及雌激素替代治疗有关.除雌激素替代治疗因素外,其他危险因素包括:肥胖、高脂饮食、生育因素(未产、初潮提前和绝经延迟)、多囊卵巢综合征、三苯氧胺治疗乳腺癌.随着当今中国人民生活水平的提高和肥胖症增多,子宫内膜癌的发病率也相应提高.总的来说,与其他常见的恶性肿瘤相比,妇科恶性肿瘤的分子研究相对滞后.子宫内膜癌的诊断主要依据传统的组织学方法,分子水平的辅助诊断贡献较少.根据其发病途径不同, 子宫内膜癌可分为两种类型,即所谓二元发病模式.因两型子宫内膜癌的临床预防、早期诊断和治疗措施差异较大,及时了解最新的研究动态有重要的临床和病理实践意义。

Pathogenesis

Source

Cite

Citations (1)

KRAS Mutations are Associated With Specific Morphologic Features in Colon Cancer

Journal of Clinical Gastroenterology (2012)

Armağan Günal Pei Hui Selim Kılıç Ruliang Xu Dhanpat Jain

Mutations in the KRAS gene occur at an early stage in the development of colorectal carcinoma. Importantly, KRAS mutation predicts resistance to anti-epidermal growth factor receptor therapy in stage IV disease.The aim of the current study is to correlate histologic features of colon cancer with the presence of KRAS mutations.Tumor tissue from 145 colon cancer resections was tested for KRAS mutations. KRAS mutation status was correlated with demographic and histologic characteristics. Statistical analysis was performed using the Pearson χ2 test and multivariate analysis.KRAS mutations were present in 55/145 cases (37.9%), consistent with reported rates. KRAS mutations were significantly associated with usual adenocarcinoma morphology (multivariate P=0.014), peritumoral lymphocytic response (χ2, P=0.028; multivariate P=0.017), T3-T4 status (χ2, P=0.012; multivariate P=0.015), right-sided location (multivariate P=0.027), absence of lymphovascular invasion (multivariate P=0.008), and metastases at the time of resection (multivariate P=0.034). No association was found between KRAS mutation status and other factors.Specific morphologic features in colon cancer suggest a higher likelihood of the presence of KRAS mutations. These morphologic features overlap partially with those associated with DNA mismatch repair gene mutations. If confirmed, these results may suggest a paradigm for directed KRAS testing.

Lymphovascular invasion

10.1097/mcg.0b013e3182703030

Cite

Citations (14)

Supplementary Figure 1 from In Vitro and In Vivo Activity of IMGN853, an Antibody–Drug Conjugate Targeting Folate Receptor Alpha Linked to DM4, in Biologically Aggressive Endometrial Cancers

Gary Altwerger Elena Bonazzoli Stefania Bellone Tomomi Egawa‐Takata Gulden Menderes

Immunohistochemistry (IHC) showing expression of FRα endometrioid cancer cell blocks

Folate receptor

Conjugate

Antibody-drug conjugate

Alpha (finance)

10.1158/1535-7163.22504590.v1

Cite

Citations (0)

Supplementary Figure S1 from Randomized Phase II Trial of Imiquimod with or without 9-Valent HPV Vaccine versus Observation in Patients with High-grade Pre-neoplastic Cervical Lesions (NCT02864147)

Sangini S. Sheth Ji Eun Oh Stefania Bellone Eric R. Siegel Michelle Greenman

Representative microscopic images of paired cervical biopsies at enrollment at 6 months follow-up.

Imiquimod

10.1158/1078-0432.25728562

Cite

Citations (0)

Figure S2 from Inhibition of BET Bromodomain Proteins with GS-5829 and GS-626510 in Uterine Serous Carcinoma, a Biologically Aggressive Variant of Endometrial Cancer

Elena Bonazzoli Federica Predolini Emiliano Cocco Stefania Bellone Gary Altwerger

Ex vivo c-Myc expression assessed by IHC on the ARK2 xenograft tumor samples, excised 1 hour, 6 hours and 12 hours after the last dose of GS-5829 at 20, 10 mg/kg, JQ1 at 50 mg/kg and vehicle for oral gavage studies, following 28 days of treatment.

Ex vivo

Serous carcinoma

10.1158/1078-0432.22470239.v1

Cite

Citations (0)

Table S3 from Inhibition of BET Bromodomain Proteins with GS-5829 and GS-626510 in Uterine Serous Carcinoma, a Biologically Aggressive Variant of Endometrial Cancer

Elena Bonazzoli Federica Predolini Emiliano Cocco Stefania Bellone Gary Altwerger

Groups and dosing description of the in vivo drug study on USC-ARK1 xenograft.

10.1158/1078-0432.22470230.v1

Cite

Citations (0)

Table S4 from Inhibition of BET Bromodomain Proteins with GS-5829 and GS-626510 in Uterine Serous Carcinoma, a Biologically Aggressive Variant of Endometrial Cancer

Elena Bonazzoli Federica Predolini Emiliano Cocco Stefania Bellone Gary Altwerger

Average quantitative nuclear histological score associated with the ex vivo c-Myc expression assessed by IHC in the ARK2 xenograft tumor samples, excised 1 hour and 6 hours after a single dose of GS-5829 at 40, 20, 10 mg/kg, GS-626510 at 10 mg/kg and vehicle for oral gavage studies.

Ex vivo

10.1158/1078-0432.22470227

Cite

Citations (0)