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Preclinical and clinical development of new progesterone receptor antagonists with high receptor specificity for breast cancer treatment
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
J. Hoffmann, H. Hess-Stumpp, R. B. Lichtner, U. Fuhrmann, G. Siemeister, M. R. Schneider
This observation demonstrates that, in the absence of progesterone receptor function, prolactin alone is not sufficient to induce the neoplastic transformation, and that progesterone may activate mitogenic mediators of the prolactin pathway. Under these conditions, the epithelial cells might exhibit a low proliferative index and, at the time of carcinogen administration, be a poor candidate for malignant transformation.
Methods to Study the Vasculature in ADPKD
Published in Jinghua Hu, Yong Yu, Polycystic Kidney Disease, 2019
Patricia Outeda, Terry Watnick
The incorporation of BrdU into proliferating cells can be detected by immunofluorescence. Wash the cells using PBS and fix them with 2% PFA for 20 min and then permeabilize with 1% Triton X-100 in PBS for 5 min. Denature the DNA by incubating the cells with 2 N HCl for min at 37°C, followed by five rinses in PBS. Incubate cells with 3% bovine serum albumin (BSA) in PBS and then probe with a fluorochrome-conjugated anti-BrdU antibody (1:15) in a humidified chamber at 37°C for 60 min. After several washes with PBS, mount the slides using mounting media and DAPI (4′,6-diamidino-2-phenylindole) to stain the nuclei. Image several fields at 40× using an inverted fluorescence microscope (3–4 different fields from each duplicate). The proliferation index can be calculated as the percentage of BrdU positive cells/total number of cells (DAPI-positive). Each experiment should be performed in triplicate and repeated a minimum of 4 to 5 times.
Tumors of the Head and Neck
Published in Victor A. Bernstam, Pocket Guide to GENE LEVEL DIAGNOSTICS in Clinical Practice, 2019
The high percentage of aneuploidy (48%) in squamous cell carcinoma (SCC) of the oral cavity correlates with the size of the tumor, low histological grade, and the presence of lymph node metastases. Likewise, polyploidy is higher in poorly differentiated tumors and in metastases. The proliferative index does not reach statistically significant correlation with tumor size or duration of the disease, although it is inversely correlated with the degree of differentiation.
Phenotypic subtypes predict outcomes in colorectal cancer
Published in Acta Oncologica, 2023
Jussi Kasurinen, Ines Beilmann-Lehtonen, Tuomas Kaprio, Jaana Hagström, Caj Haglund, Camilla Böckelman
The prognosis for CRC patients with a high proliferation index varies between studies [32–34]. One explanation could be that, although highly proliferative tumors are often more aggressive, they are also metabolically more active and might respond better to adjuvant chemotherapy. Interestingly, in our study, the prognosis among patients with canonical tumors who also had a high proliferation index varied substantially in different clinical subgroups. For instance, in patients aged 69 or older and in patients with colon cancer, prognosis among individuals with canonical tumors closely resembled the favorable prognosis accompanying immune tumors. However, in rectal cancer patients and among patients younger than 69, those with canonical tumors exhibited a worst prognosis. Notably, Roseweir et al. [28] used a method similar to ours to classify 1030 stage I–III CRC patients treated with a curative intent according to phenotypic subgroups. As in our study, prognosis among canonical patients with stage I or II disease resembled the favorable prognosis found among immune tumor patients; however, the prognosis among stage III canonical tumor patients was remarkably worse and resembled the mesenchymal tumor subgroup. Thus, it appears that clinicopathological factors greatly influence prognosis among canonical tumor patients. In young patients with rectal tumors and advanced disease in particular, a canonical subtype apparently associates with a poor prognosis.
Is the TCH-P regimen active in early or locally advanced HER2-positive breast cancer? Results of a retrospective study
Published in Acta Oncologica, 2022
Raffaele Longo, Victoire Thiebaut, Pierre-Olivier Legros, Marco Campitiello, Francesca Plastino, Christophe Goetz, Bogdan Margineanu, Julie Pujois, Michel Gunther, Julie Egea, Chloé Wendel
Female patients aged ≥18 years with operable (cT1c-3, N0-1) or locally advanced (T2-3, N2 or N3; T4, any N) HER2+ BC and a primary tumor size >1 cm were eligible. HER2 expression was determined using immunohistochemistry (IHC) and in situ hybridization (fluorescence in situ hybridization [FISH]) by central laboratory testing at our Department of Pathology, according with the current recommendations [12]. FISH positivity was mandatory for IHC 2+ tumors. The status of estrogen (ER) and progesterone (PR) receptors was assessed immunohistochemically by the Allred score [13] using the primary antibody SP1 and 1E2, respectively. A score ≥10% defined HR + tumors for them a hormonal therapy was indicated. The nuclear immunostaining of Ki67 was assessed by counting at least 500–1000 tumor cells per case across 5 high power fields of the section incubated with the primary antibody against Ki67 (MIB-1, 1:100, Dako, Glostrup, Denmark) [14]. The Ki67 proliferative index was scored as high when ≥20% of the tumor cells were positive. To overcome the problem of tumor heterogeneity, two representative tumor foci were marked on slides with hematoxylin and eosin-stained sections from selected paraffin blocks. Two tissue cores of 2 mm were used from each block [14]. Additional inclusion criteria were Eastern Cooperative Oncology Group performance status (ECOG PS) of 0 or 1, and LVEF ≥50% at baseline. All the patients have been informed and gave their consent to treatment, data analysis and publication.
Silencing of TMEM158 Inhibits Tumorigenesis and Multidrug Resistance in Colorectal Cancer
Published in Nutrition and Cancer, 2020
Lihua Liu, Jiantao Zhang, Shiquan Li, Libin Yin, Jiandong Tai
Immunohistochemical analysis was performed as described elsewhere. Briefly, tumor sections were incubated overnight with the primary antibody Ki-67 (1:150) in conjunction with proper controls. The sections were then washed three times with 0.05% Tween, incubated with secondary antibody for 1 h, washed three times with 0.05% Tween in PBS, visualized by 3,3′-diaminobenzidine substrateand counterstained with hematoxylin QS (Vector Lab, Burlingame, CA, USA). The proliferative index was calculated as the percentage of Ki-67-positive cells in 10 randomly selected microscopic fields under light microscopy (Carl Zeiss, Berlin, Germany) and expressed as a percentage of the total cells. TUNEL analysis was performed using the in situ Cell Death Detection Kit (Roche, Indianapolis, IN, USA) according to the manufacturer’s protocol, and 10 randomly selected microscopic fields in each group were used to calculate the relative ratio of TUNEL-positive cells.