scholarly journals Detection of human papillomavirus DNA in fine needle aspirates of women with breast cancer

2012 ◽  
Vol 20 (1-2) ◽  
pp. 12-14 ◽  
Author(s):  
Smaroula Divani ◽  
Angeliki Giovani
Keyword(s):  
Breast Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Malignant Tumors ◽  
Transmitted Disease ◽  
Hpv Infection ◽  
Breast Lesions ◽  
Hpv Dna ◽  
Benign Breast Lesions

Background: HPV infection is the most commonly distributed sexually transmitted disease. Human papillomavirus has also been linked to malignant tumors of many human organs. The presence of viral DNA in breast cancer cells is controversial. The aim of the present study was to investigate the presence of HPV-DNA in a group of Greek women with breast carcinoma. Methods: Liquid cytology specimens from 35 malignant breast cases and 35 cases with benign breast lesions were investigated by PCR (clinical arrays technique). In addition, in situ hybridization was performed on all HPV positive cases. Results: HPV-DNA was detected in 17.14% of the carcinoma cases and HPV16 DNA was present in 83.3% of them. All benign breast lesions were negative for HPV-DNA. Conclusion: Our report confirmed the presence of HPV in breast cancer cells while the most prevalent type was HPV16. More studies are necessary in order to elucidate the pathogenesis of HPV and a possible way of prevention of some breast cancers.

scholarly journals FGF18 Enhances Migration and the Epithelial-Mesenchymal Transition in Breast Cancer by Regulating Akt/GSK3β/Β-Catenin Signaling

2018 ◽  
Vol 49 (3) ◽  
pp. 1060-1073 ◽  
Author(s):  
Na Song ◽  
Jiateng Zhong ◽  
Qing Hu ◽  
Tengteng Gu ◽  
Bo Yang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Target Gene ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Gene Promoter ◽  
Hypoxic Condition ◽  
Mesenchymal Transition ◽  
Target Gene Promoter

Background/Aims: Fibroblast growth factors (FGFs) and their high-affinity receptors contribute to autocrine and paracrine growth stimulation in several human malignant tumors, including breast cancer. However, the mechanisms underlying the carcinogenic actions of FGF18 remain unclear. Methods: The transcription level of FGF18 under the hypoxic condition was detected with quantitative PCR (qPCR). A wound-healing assay was performed to assess the role of FGF18 in cell migration. A clonogenicity assay was used to determine whether FGF18 silencing affected cell clonogenicity. Western blotting was performed to investigate Akt/GSK3β/β-catenin pathway protein expression. Binding of β-catenin to the target gene promoter was determined by chromatin immunoprecipitation (ChIP) assays. Results: FGF18 promoted the epithelial-mesenchymal transition (EMT) and migration in breast cancer cells through activation of the Akt/GSK3β/β-catenin pathway. FGF18 increased Akt-Ser473 and -Thr308 phosphorylation, as well as that of GSK3β-Ser9. FGF18 also enhanced the transcription of proliferation-related genes (CDK2, CCND2, Ki67), metastasis-related genes (TGF-β, MMP-2, MMP-9), and EMT markers (Snail-1, Snail-2, N-cadherin, vimentin, TIMP1). β-catenin bound to the target gene promoter on the ChIP assay. Conclusion: FGF18 contributes to the migration and EMT of breast cancer cells following activation of the Akt/GSK3β/β-catenin pathway. FGF18 expression may be a potential prognostic therapeutic marker for breast cancer.

Human Papillomavirus Infections in Children: the Potential Role of Maternal Transmission

2000 ◽  
Vol 11 (2) ◽  
pp. 259-274 ◽  
Author(s):  
Stina Syrjanen ◽  
Mirja Puranen
Keyword(s):  
Human Papillomavirus ◽  
Potential Role ◽  
Malignant Tumors ◽  
Hpv Infection ◽  
In Utero ◽  
Viral Transmission ◽  
Perinatal Infection ◽  
Vaccination Programs ◽  
Hpv Dna ◽  
Ascending Infection

To date, more than 100 types of human papillomavirus (HPV) have been identified. In the past 20 years, there has been an increasing interest in HPVs because of their potential role in the pathogenesis of malignant tumors. HPV infections are known to affect predominantly adult, sexually active age groups, whereas skin warts, at various anatomic sites, are usually associated with younger individuals. The modes of viral transmission in children remain controversial, including perinatal transmission, auto- and hetero-inoculation, sexual abuse, and, possibly, indirect transmission via fomites. Recent studies on perinatal infection with HPV have been inconclusive. It is still unclear how frequently perinatal infection progresses to clinical lesions, whether genital, laryngeal, or oral. Conflicting reports have been published on the prevalence of HPV infections in children. The current consensus is, however, that newborn babies can be exposed to cervical HPV infection of the mother. The detection rate of HPV DNA in oral swabs of newborn babies varies from 4% to 87%. The concordance of HPV types detected in newborn babies and their mothers is in the range of 57% to 69%, indicating that the infants might acquire the HPV infection post-natally from a variety of sources. HPV antibodies have been detected in 10% to 57% of the children, and there is usually no correlation between seropositivity and the detection of HPV DNA in either the oral or the genital mucosa. There is also evidence that transmission in utero or post-natal acquisition is possible. The mode of in utero transmission remains unknown, but theoretically the virus could be acquired hematogenously, by semen at fertilization, or as an ascending infection in the mother. The understanding of viral transmission routes is important, particularly because several vaccination programs are being planned worldwide. The serologic response to HPV detected in different populations of young women or women at risk of cervical cancer might be due to genital infections, but the possibility that HPV infection has been acquired earlier in life through the oral mucosa or respiratory tract cannot be ruled out.

scholarly journals Cancer Stem Cell-Associated Pathways in the Metabolic Reprogramming of Breast Cancer

2020 ◽  
Vol 21 (23) ◽  
pp. 9125
Author(s):  
Sara El-Sahli ◽  
Lisheng Wang
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Malignant Tumors ◽  
Metabolic Reprogramming ◽  
Metabolic Adaptation ◽  
Metabolic Flexibility ◽  
Tumor Initiating Cells ◽  
Metabolic Adaptations

Metabolic reprogramming of cancer is now considered a hallmark of many malignant tumors, including breast cancer, which remains the most commonly diagnosed cancer in women all over the world. One of the main challenges for the effective treatment of breast cancer emanates from the existence of a subpopulation of tumor-initiating cells, known as cancer stem cells (CSCs). Over the years, several pathways involved in the regulation of CSCs have been identified and characterized. Recent research has also shown that CSCs are capable of adopting a metabolic flexibility to survive under various stressors, contributing to chemo-resistance, metastasis, and disease relapse. This review summarizes the links between the metabolic adaptations of breast cancer cells and CSC-associated pathways. Identification of the drivers capable of the metabolic rewiring in breast cancer cells and CSCs and the signaling pathways contributing to metabolic flexibility may lead to the development of effective therapeutic strategies. This review also covers the role of these metabolic adaptation in conferring drug resistance and metastasis in breast CSCs.

scholarly journals The Role of Ataxia Telangiectasia Mutant and Rad3-Related DNA Damage Response in Pathogenesis of Human Papillomavirus

Pathogens ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 506
Author(s):  
Ying Luo ◽  
Shiyuan Hong
Keyword(s):  
Dna Damage ◽  
Human Papillomavirus ◽  
Dna Damage Response ◽  
Ataxia Telangiectasia ◽  
Malignant Tumors ◽  
Hpv Infection ◽  
Checkpoint Signaling ◽  
Hpv Dna ◽  
Multiple Sensors ◽  
Damage Response

Human papillomavirus (HPV) infection leads to a variety of benign lesions and malignant tumors such as cervical cancer and head and neck squamous cell carcinoma. Several HPV vaccines have been developed that can help to prevent cervical carcinoma, but these vaccines are only effective in individuals with no prior HPV infection. Thus, it is still important to understand the HPV life cycle and in particular the association of HPV with human pathogenesis. HPV production requires activation of the DNA damage response (DDR), which is a complex signaling network composed of multiple sensors, mediators, transducers, and effectors that safeguard cellular DNAs to maintain the host genome integrity. In this review, we focus on the roles of the ataxia telangiectasia mutant and Rad3-related (ATR) DNA damage response in HPV DNA replication. HPV can induce ATR expression and activate the ATR pathway. Inhibition of the ATR pathway results in suppression of HPV genome maintenance and amplification. The mechanisms underlying this could be through various molecular pathways such as checkpoint signaling and transcriptional regulation. In light of these findings, other downstream mechanisms of the ATR pathway need to be further investigated for better understanding HPV pathogenesis and developing novel ATR DDR-related inhibitors against HPV infection.

scholarly journals Detection of cancer stem cell in invasive ductal carcinoma of breast using CD44marker

2014 ◽  
Vol 8 (3) ◽  
pp. 76-82
Author(s):  
Teeba Khalid Hadi ◽  
Ahmed Rushdi Abdulla
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Stem Cell ◽  
Prognostic Factors ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Breast Lesions ◽  
Positive Expression ◽  
Significant Difference ◽  
Benign Breast Lesions

The breast cancer is the most common non-skin malignancy in women. Prognostic factors are important in predicting disease. Malignant tumors are composed of a small population of distinct cancer cells, termed cancer stem cells (CSCs) possess characteristics of both stem cells and cancer cells, in that they have the properties of self-renewal, asymmetric cell division, resistance to apoptosis, independent growth, tumourigenicity and metastatic potential. Objective of this studythat detect cancer stem cell of breast cancer patients by using CD44 and study the compares between patients with breast cancer and patients with benign breast lesions. This study which included 31 patients with breast cancer and 19 patients with benign breast lesions Prognostic factors were registered including: age, histopathological subtype, degree of differentiation. Results of this was Positive expression ofCD44 was observed in 16 cases, while 15cases were negative expression of CD44 out of 31samplesof breast cancer. In Benign1cases were positive expression, while 18 cases were negative expression. CD44 expression showed high significant difference between malignant breast samples and benign samples (P <0.001).

scholarly journals Triple Isozyme Lactic Acid Dehydrogenase Inhibition in Fully Viable MDA-MB-231 Cells Induces Cytostatic Effects That Are Not Reversed by Exogenous Lactic Acid

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1751
Author(s):  
Elizabeth Mazzio ◽  
Nzinga Mack ◽  
Ramesh B. Badisa ◽  
Karam F. A. Soliman
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Lactic Acid ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Malignant Tumors ◽  
Glycolytic Pathway ◽  
Mitochondrial Potential ◽  
Lactic Acid Dehydrogenase ◽  
Acid Dehydrogenase

A number of aggressive human malignant tumors are characterized by an intensified glycolytic rate, over-expression of lactic acid dehydrogenase A (LDHA), and subsequent lactate accumulation, all of which contribute toward an acidic peri-cellular immunosuppressive tumor microenvironment (TME). While recent focus has been directed at how to inhibit LDHA, it is now becoming clear that multiple isozymes of LDH must be simultaneously inhibited in order to fully suppress lactic acid and halt glycolysis. In this work we explore the biochemical and genomic consequences of an applied triple LDH isozyme inhibitor (A, B, and C) (GNE-140) in MDA-MB-231 triple-negative breast cancer cells (TNBC) cells. The findings confirm that GNE-140 does in fact, fully block the production of lactic acid, which also results in a block of glucose utilization and severe impedance of the glycolytic pathway. Without a fully functional glycolytic pathway, breast cancer cells continue to thrive, sustain viability, produce ample energy, and maintain mitochondrial potential (ΔΨM). The only observable negative consequence of GNE-140 in this work, was the attenuation of cell division, evident in both 2D and 3D cultures and occurring in fully viable cells. Of important note, the cytostatic effects were not reversed by the addition of exogenous (+) lactic acid. While the effects of GNE-140 on the whole transcriptome were mild (12 up-regulated differential expressed genes (DEGs); 77 down-regulated DEGs) out of the 48,226 evaluated, the down-regulated DEGS collectively centered around a loss of genes related to mitosis, cell cycle, GO/G1–G1/S transition, and DNA replication. These data were also observed with digital florescence cytometry and flow cytometry, both corroborating a G0/G1 phase blockage. In conclusion, the findings in this work suggest there is an unknown element linking LDH enzyme activity to cell cycle progression, and this factor is completely independent of lactic acid. The data also establish that complete inhibition of LDH in cancer cells is not a detriment to cell viability or basic production of energy.

Presence of human papillomavirus DNA in breast cancer patients: SERUM and tissue analysis.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e12582-e12582
Author(s):  
Sara Ravaioli ◽  
Andrea Rocca ◽  
Francesca Pirini ◽  
Serena De Matteis ◽  
Francesca Fanini ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Papillomavirus ◽  
Pap Smear ◽  
Hpv Infection ◽  
Low Grade ◽  
Breast Cancer Patients ◽  
Hpv Dna ◽  
Viral Spread ◽  
Increased Risk

e12582 Background: It has been demonstrated an increased risk of breast cancer (BC) incidence in patients with previous cervical dysplasia, suggesting a role of human papillomavirus (HPV) of cervical lesions in the development of BC. Although, the origin of HPV spreading to the mammary gland and its mechanism of dissemination is not clear. Methods: Seven serum samples from healthy donors and 58 from early BC patients collected pre-surgery were analyzed for the presence of HPV DNA. For 49/58 patients HPV DNA was analyzed also on the primary tumor tissue. 17 patients had luminal A BC (4 relapsed, 13 non relapsed), 16 had luminal B BC (5 relapsed, 11 non relapsed), 13 had triple-negative BC (6 relapsed, 7 non relapsed), 12 had HER2-positive BC (4 relapsed, 8 non relapsed). Circulating DNA was extracted from 500 μl of serum by Qiamp DNA Mini kit (Qiagen, Milan, Italy) and tumor DNA was extracted from at least four 10-micron sections by QIAamp DNA FFPE Tissue Kit (Qiagen, Milan, Italy). Circulating HPV DNA was amplified by a multiplex PCR with HPV E6 or E7 gene-specific primers and the sequence was assessed by a high-throughput MALDI-TOF mass spectrometry-based method. Results: HPV DNA was detected in only 5 serum of BC patients and in none of the healthy controls. 4/5 BC cases had high-risk HPV DNA (type 39,45,52,59) and 1 had type 73 low-risk HPV DNA. 4/5 HPV DNA-positive patients had previously low-grade cervical intraepithelial neoplasia (CIN I) detected by Pap smear. These 5 patients with circulating HPV DNA did not show HPV positivity in the BC tissue. 2 out of 49 cases were positive for universal HPV DNA sequence in tissue and only 1 case showed HPV type 51. No relation was found between HPV infection and tumor subtype or prognosis, neither for HPV DNA positivity between serum and tissue. Conclusions: Our data support the feasibility of HPV DNA detection by liquid biopsy in BC. The presence of circulating HPV could be due to a viral spread from other organs. More data are needed to establish the role of circulating HPV DNA and its potential association with HPV infection of the breast and/or of the cervix. [Table: see text]

scholarly journals MicroRNA-222 promotes drug resistance to doxorubicin in breast cancer via regulation of miR-222/bim pathway

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Hong Dai ◽  
Ling-yun Xu ◽  
Qi Qian ◽  
Qiu-wei Zhu ◽  
Wei-xian Chen
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Malignant Tumors ◽  
Clinical Problem ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Caspase Pathway ◽  
Resistance To Doxorubicin ◽  
Mcf 7

Abstract Resistance to doxorubicin (DOX) is the most common clinical problem in breast cancer therapy, and the underlying molecular mechanism remains to be investigated. MicroRNAs (miRNAs) exhibit important regulatory functions in various malignant tumors including breast cancer. The aim of the present study was to find the relationship between miR-222 and DOX resistance. We found that miR-222 was highly expressed in patients’ serum and DOX-resistant cell line MCF-7-R and that miR-222 could promote proliferation and migration of breast cancer cells. Our results also showed that inhibition of miR-222 in MCF-7-R significantly increased Bcl-2 interacting mediator (Bim) expression both in mRNA and protein levels by using quantitative real-time PCR (qRT-PCR) and Western blot. MTT and flow cytometry suggested that lower expressed miR-222 enhanced apoptosis and decreased IC50 of MCF-7-R cells. Conversely, in MCF-7 cells transfected with miR-222 mimics, up-regulation of miR-222 was associated with decreased Bim level accompanied by less apoptosis and higher IC50. Moreover, miR-222 inhibitors reversed DOX resistance via miR-222-Bim-caspase pathway. Collectively, these data first elucidated that miR-222 could function as an oncogene and was able to reduce the sensitivity of breast cancer cells to DOX through miR-222-Bim-caspase pathway, which provided a potential target to increase DOX sensitivity in clinical breast cancer treatment.

The proliferation of breast cancer cells are inhibited by the human intrabody targeting cyclinD1

2010 ◽  
Vol 34 (8) ◽  
pp. S49-S49
Author(s):  
Lei Wang ◽  
Xun Zhou ◽  
Lihong Zhou ◽  
Yong Chen ◽  
Xun Zhu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells
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