scholarly journals Case of HER2neu+ Invasive Pleomorphic Lobular Carcinoma With Response to Conventional Neoadjuvant Chemotherapy: A Viable Option for an Exceedingly Rare Breast Cancer Type

Cureus ◽  
2020 ◽  
Author(s):  
Blessie Nelson ◽  
Ashley M Brizendine ◽  
Rachelle Gietzen ◽  
Rohit Venkatesan
2012 ◽  
Vol 61 (3) ◽  
pp. 365-377 ◽  
Author(s):  
Laketa Monhollen ◽  
Carl Morrison ◽  
Foluso O Ademuyiwa ◽  
Rameela Chandrasekhar ◽  
Thaer Khoury

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Kazem Nejati ◽  
Sedigheh Fekri Aval ◽  
Mohammadreza Alivand ◽  
Abolfazl Akbarzadeh ◽  
AmirAhmad Arabzadeh

Context: Breast cancer (BC) is the most common cancer in women worldwide. Hereditary susceptibility created by mutations in autosomal dominant genes is responsible for 5 to 10% of all BC cases in women. Recent studies have identified genes associated with increased risk for aggressive BC, providing the basis for better risk management. Evidence Acquisition: The latest information in National Center for Biotechnology Information (NCBI), Google Scholar, ScienceDirect, and Scopus were the main databases for finding articles. A combination of keywords of ‘metastasis’, ‘invasion’, ‘aggressive breast cancer’, ‘prognostic factor’, ‘mutation’, and ‘cancer treatment’ was searched in the databases to identify related articles. Titles and abstracts of the articles were studied to choose the right articles. Results: Mutations in breast cancer type 1 susceptibility protein (BRCA1) and breast cancer type 2 susceptibility protein (BRCA2) genes are two central players related to the high risk of BC. Mutation in tumor protein p53 (TP53) is another important mutation that leads to triple-negative BC. Although the majority of BC types are not associated with high-throughput mutant genes such as BRCA1, BRCA2, and TP53, they are associated with low-throughput genes, including DNA repair protein Rad50 (RAD50), Nijmegen breakage syndrome gene (NBS1), checkpoint kinase 2 (CHEK2), BRCA1-interacting protein 1 (BRIP1), E-cadherin gene (CDH1) and PALB2, UCHL1, aldehydedehydrogenase1A3 (ALDH1A3), androgen receptor (AR), 5-bisphosphate 3-kinase (PIK3CA), phosphatidylinositol-4, and luminal gene expression that are generally mutated in the global population. High tumor mutational burden (TMB) was associated with improved progression-free survival. Conclusions: The lymph node status, early tumor size, ER, PR, human epidermal growth factor receptor-2 (HER2), and Ki-67 are conventional prognostic factors for BC. However, these factors cannot exactly predict the aggressive behavior of BC. Hence, in this review, we discussed new prognostic factors of aggressive BCs that are useful for the treatment of patients with BC.


2019 ◽  
Vol 77 (1) ◽  
pp. 3-18 ◽  
Author(s):  
Yueru Sun ◽  
Thomas J. McCorvie ◽  
Luke A. Yates ◽  
Xiaodong Zhang

AbstractHomologous recombination (HR) is a pathway to faithfully repair DNA double-strand breaks (DSBs). At the core of this pathway is a DNA recombinase, which, as a nucleoprotein filament on ssDNA, pairs with homologous DNA as a template to repair the damaged site. In eukaryotes Rad51 is the recombinase capable of carrying out essential steps including strand invasion, homology search on the sister chromatid and strand exchange. Importantly, a tightly regulated process involving many protein factors has evolved to ensure proper localisation of this DNA repair machinery and its correct timing within the cell cycle. Dysregulation of any of the proteins involved can result in unchecked DNA damage, leading to uncontrolled cell division and cancer. Indeed, many are tumour suppressors and are key targets in the development of new cancer therapies. Over the past 40 years, our structural and mechanistic understanding of homologous recombination has steadily increased with notable recent advancements due to the advances in single particle cryo electron microscopy. These have resulted in higher resolution structural models of the signalling proteins ATM (ataxia telangiectasia mutated), and ATR (ataxia telangiectasia and Rad3-related protein), along with various structures of Rad51. However, structural information of the other major players involved, such as BRCA1 (breast cancer type 1 susceptibility protein) and BRCA2 (breast cancer type 2 susceptibility protein), has been limited to crystal structures of isolated domains and low-resolution electron microscopy reconstructions of the full-length proteins. Here we summarise the current structural understanding of homologous recombination, focusing on key proteins in recruitment and signalling events as well as the mediators for the Rad51 recombinase.


2019 ◽  
Vol 73 (4) ◽  
pp. 191-196 ◽  
Author(s):  
Lorena Alves Teixeira ◽  
Francisco Jose Candido dos Reis

BackgroundLoss of function in either breast cancer type 1 susceptibility protein (BRCA1) or breast cancer type 2 susceptibility protein (BRCA2) is a major risk factor for epithelial ovarian cancer (EOC) development. BRCA1 or BRCA2 deficiencies are associated with short-term prognosis and might have importance for the treatment of women with the disease. However, the screening of all possible mechanisms of dysfunction is expensive, time-consuming and difficult to apply in clinical practice. On the other hand, immunohistochemistry (IHC) is a simple and reliable method to access the expression of several proteins in tumour tissues.Materials and methodsThis systematic review aims to evaluate the current usage of IHC to detect BRCA1 and BRCA2 deficiencies in EOC. We searched and evaluated all primary literature on the use of IHC for evaluating BRCA1 and BRCA2 proteins expression in EOC. The main concepts for the search were: ovarian neoplasms, IHC, BRCA1 and BRCA2.ResultsForty-four studies from 925 unique titles were included. A total of 4206 tumour samples were evaluated for BRCA1 and 1041 for BRCA2 expression. Twelve BRCA1 primary antibodies were used in 41 studies, and the most common was the MS110 clone (75.6%). Seven BRCA2 primary antibodies were used in ten studies. Using the cut-off of 10%, 47.0% of EOCs are associated with loss of BRCA1 and 34.5% with the loss of BRCA2 expression.ConclusionIHC was effective to detect loss of BRCA1 protein expression in EOC; however, data on BRCA2 expression were heterogeneous and difficult to interpret.


2012 ◽  
Vol 30 (27_suppl) ◽  
pp. 177-177
Author(s):  
Marina De Brot ◽  
Shirin Muhsen ◽  
Victor P. Andrade ◽  
Starr Koslow Mautner ◽  
Melissa Murray ◽  
...  

177 Background: Pleomorphic lobular carcinoma in situ (PLCIS) is an increasingly diagnosed variant of lobular carcinoma in situ. Histologically, it resembles ductal carcinoma in situ (DCIS), leading to controversy over proper management. Yet, the natural history of PLCIS is unknown. Here we describe our experience with PLCIS. Methods: Review of pathology reports (1995–2012) identified 233 cases of LCIS variants. Patients with synchronous ipsilateral DCIS or invasive cancer (IC) were excluded leaving 25 cases for review. Consensus review by 3 pathologists further excluded 7; leaving 18 cases, 12 of which were classified as PLCIS and 6 as LCIS with pleomorphic features (LCIS-PF). (Table) PLCIS was defined by cellular dyshesion, nuclear pleomorphism with a 2-3 fold size variation, conspicuous nucleoli, mitoses and abundant cytoplasm; lesions not meeting all parameters were classified as LCIS-PF. Loss of e-cadherin was confirmed; clinical data were obtained from medical records. Results: Mean patient age at diagnosis of PLCIS/LCIS-PF was 57 yrs (42-67 yrs). All cases presented with imaging abnormalities. A previous history of breast cancer was present in 7/18 (39%) pts (3/7, ipsilateral; 4/7, contralateral). Following PLCIS/LCIS-PF diagnosis, 6/18 (33%) pts underwent mastectomy and 12/18 had excision alone, with (n=3) or without chemoprevention (n=9). Margin status was negative in 4/12 pts; close in 3/12 pts and positive in 5/12 pts undergoing excision. At a median follow-up of 27 mos (2-148 mos), 2/12 pts treated with excision developed ipsilateral breast cancer (1 DCIS; 1 IC). Both had close margins at initial excision; median time to cancer, 54 mos. Conclusions: Pure PLCIS is an uncommon lesion. Synchronous malignancy or prior history of breast cancer are often present in patients with PLCIS, contributing to the difficulty in determining the actual risk conferred by this lesion and appropriate management. Efforts to systematically characterize LCIS variants and prospective documentation of outcomes are needed to clarify the significance of these lesions. [Table: see text]


The Breast ◽  
2002 ◽  
Vol 11 (2) ◽  
pp. 151-155
Author(s):  
B. Brancato ◽  
D. Bricolo ◽  
M. Bonzanini ◽  
S. Ciatto ◽  
R. Mariotto ◽  
...  

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