Relevant bibliographies by topics / Head and Neck Suqamous Cell Carcinoma (HNSCC)

Academic literature on the topic 'Head and Neck Suqamous Cell Carcinoma (HNSCC)'

Author: Grafiati
Published: 9 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Head and Neck Suqamous Cell Carcinoma (HNSCC).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Head and Neck Suqamous Cell Carcinoma (HNSCC)"

1

Romanowska, Kamila, Agnieszka Sobecka, Agnieszka A. Rawłuszko-Wieczorek, Wiktoria M. Suchorska, and Wojciech Golusiński. "Head and Neck Squamous Cell Carcinoma: Epigenetic Landscape." Diagnostics 11, no. 1 (December 27, 2020): 34. http://dx.doi.org/10.3390/diagnostics11010034.

Full text
Abstract:
Head and neck squamous carcinoma (HNSCC) constitutes the sixth most prevalent cancer worldwide. The molecular pathogenesis of HNSCC includes disorders in cell cycle, intercellular signaling, proliferation, squamous cell differentiation and apoptosis. In addition to the genetic mutations, changes in HNSCC are also characterized by the accumulation of epigenetic alterations such as DNA methylation, histone modifications, non-coding RNA activity and RNA methylation. In fact, some of them may promote cancer formation and progression by controlling the gene expression machinery, hence, they could be used as biomarkers in the clinical surveillance of HNSCC or as targets for therapeutic strategies. In this review, we focus on the current knowledge regarding epigenetic modifications observed in HNSCC and its predictive value for cancer development.
APA, Harvard, Vancouver, ISO, and other styles
2

Li, John Zenghong, Wei Gao, Jimmy Yu-Wai Chan, Wai-Kuen Ho, and Thian-Sze Wong. "Hypoxia in Head and Neck Squamous Cell Carcinoma." ISRN Otolaryngology 2012 (October 16, 2012): 1–8. http://dx.doi.org/10.5402/2012/708974.

Full text
Abstract:
Hypoxia is a common feature in most of the solid tumors including head and neck squamous cell carcinoma (HNSCC). Hypoxia reflects the imbalance between oxygen consumption by the rapidly proliferating cancer cells and the insufficient oxygen delivery due to poor vascularization and blood supply. The hypoxic microenvironment in the HNSCC contributes to the development of aggressive carcinoma phenotype with high metastatic rate, resistance to therapeutic agents, and higher tumor recurrence rates, leading to low therapeutic efficiency and poor outcome. To overcome the therapeutic resistance due to hypoxia and improving the prognosis of the HNSCC patients, many approaches have been examined in laboratory studies and clinical trials. In this short paper, we discuss the mechanisms involved in the resistance of radiotherapy and chemotherapy in hypoxic condition. We also exploit the molecular mechanisms employed by the HNSCC cells to adapt the hypoxic condition and their tumorigenic role in head and neck, as well as the strategies to overcome hypoxia-induced therapeutic resistance.
APA, Harvard, Vancouver, ISO, and other styles
3

Fukusumi, T., and J. A. Califano. "The NOTCH Pathway in Head and Neck Squamous Cell Carcinoma." Journal of Dental Research 97, no. 6 (February 28, 2018): 645–53. http://dx.doi.org/10.1177/0022034518760297.

Full text
Abstract:
Comprehensive genomic analyses have been performed for head and neck squamous cell carcinoma (HNSCC), revealing a significant rate of NOTCH1 mutations and identifying NOTCH1 as the second most frequently mutated gene after TP53. Most NOTCH1 mutations are considered inactivating, indicating that NOTCH1 is a tumor suppressor gene. On the other hand, cohorts from Asian populations with HNSCC have shown activating NOTCH1 mutations. HNSCC with NOTCH1 mutations have a worse prognosis than the NOTCH1 wild-type tumors. Additional data on other NOTCH family members have shown that NOTCH promotes HNSCC progression. NOTCH family members, including NOTCH pathway genes, are upregulated in HNSCC compared with normal tissues, and inhibition of the NOTCH pathway decreases cell proliferation and invasion. NOTCH activity in HNSCC is therefore contextual, and NOTCH in HNSCC is considered to have a bimodal role as a tumor suppressor and an oncogene. In this review, recent understandings of NOTCH pathway genes, including NOTCH genes, in HNSCC are described. In addition, the implications of NOTCH pathway alteration for HNSCC-specific NOTCH-targeted cancer therapy are explored.
APA, Harvard, Vancouver, ISO, and other styles
4

Kakurina, G. V., E. S. Kolegova, О. V. Cheremisina, and Е. L. Choinzonov. "Molecular features of head and neck squamous cell carcinoma." Bulletin of Siberian Medicine 17, no. 3 (September 29, 2018): 61–69. http://dx.doi.org/10.20538/1682-0363-2018-3-61-69.

Full text
Abstract:
Relevance.To identify new markers of early diagnosis and prognosis of head and neck squamous cell carcinoma (HNSCC) it is necessary to study the molecular features of this disease.Purpose.The aim of the study was to analyze blood serum protein spectrum in patients with HNSCC and in healthy volunteers using the methods of mass spectrometry and to evaluate the selected serum protein markers as candidates for early detection of HNSCC.Materials and Methods: The blood serum of HNSCC patients before therapy with metastases, without metastases and healthy volunteers was studied by proteomic methods. Validation of the results of proteomic analysis was carried out by ELISA in serum of 52 patients with HNSCC (T1-4N0-3M0), 10 patients with chronic hyperplastic laryngitis, dysplasia DII-DIII and 10 healthy volunteers. The statistical analysis was carried out using Statistica 6.0. Software package.Results.Blood serum proteome of HNSCC patients with metastases, without metastases and healthy volunteers are different and contain proteins of different classes. Adenylyl cyclase-associated protein 1 (CAP1) and protein phosphatase 1B (PPM1B) were selected to validate the obtained results. It was shown that the serum level of CAP1 and PPM1B differed in control and dysplasia groups and dysplasia and cancer groups (p ≤ 0,05). In patients with HNSCC (T1N0M0) the serum CAP1 and PPM1B levels were higher than in patients with dysplasia and healthy individuals (p ≤ 0,05). It was noted the positive correlation of the CAP1 level in the serum with the presence of metastases and the PPM1B level.Conclusion.Candidates for serum markers of HNSCC prognosis were identified. The difference in serum levels of CAP1 and PPM1B depending on the prevalence of primary tumors and the difference in serum level of CAP1 depending on the presence of regional metastases was shown. Determination of CAP1 level in the serum can be useful for early diagnosis and prognosis of HNSCC.
APA, Harvard, Vancouver, ISO, and other styles
5

Shah, Pooja A., Chenfei Huang, Qiuli Li, Sawad A. Kazi, Lauren A. Byers, Jing Wang, Faye M. Johnson, and Mitchell J. Frederick. "NOTCH1 Signaling in Head and Neck Squamous Cell Carcinoma." Cells 9, no. 12 (December 12, 2020): 2677. http://dx.doi.org/10.3390/cells9122677.

Full text
Abstract:
Biomarker-driven targeted therapies are lacking for head and neck squamous cell carcinoma (HNSCC), which is common and lethal. Efforts to develop such therapies are hindered by a genomic landscape dominated by the loss of tumor suppressor function, including NOTCH1 that is frequently mutated in HNSCC. Clearer understanding of NOTCH1 signaling in HNSCCs is crucial to clinically targeting this pathway. Structural characterization of NOTCH1 mutations in HNSCC demonstrates that most are predicted to cause loss of function, in agreement with NOTCH1’s role as a tumor suppressor in this cancer. Experimental manipulation of NOTCH1 signaling in HNSCC cell lines harboring either mutant or wild-type NOTCH1 further supports a tumor suppressor function. Additionally, the loss of NOTCH1 signaling can drive HNSCC tumorigenesis and clinical aggressiveness. Our recent data suggest that NOTCH1 controls genes involved in early differentiation that could have different phenotypic consequences depending on the cancer’s genetic background, including acquisition of pseudo-stem cell-like properties. The presence of NOTCH1 mutations may predict response to treatment with an immune checkpoint or phosphatidylinositol 3-kinase inhibitors. The latter is being tested in a clinical trial, and if validated, it may lead to the development of the first biomarker-driven targeted therapy for HNSCC.
APA, Harvard, Vancouver, ISO, and other styles
6

Boschert, Verena, Jonas Teusch, Urs D. A. Müller-Richter, Roman C. Brands, and Stefan Hartmann. "PKM2 Modulation in Head and Neck Squamous Cell Carcinoma." International Journal of Molecular Sciences 23, no. 2 (January 11, 2022): 775. http://dx.doi.org/10.3390/ijms23020775.

Full text
Abstract:
The enzyme pyruvate kinase M2 (PKM2) plays a major role in the switch of tumor cells from oxidative phosphorylation to aerobic glycolysis, one of the hallmarks of cancer. Different allosteric inhibitors or activators and several posttranslational modifications regulate its activity. Head and neck squamous cell carcinoma (HNSCC) is a common disease with a high rate of recurrence. To find out more about PKM2 and its modulation in HNSCC, we examined a panel of HNSCC cells using real-time cell metabolic analysis and Western blotting with an emphasis on phosphorylation variant Tyr105 and two reagents known to impair PKM2 activity. Our results show that in HNSCC, PKM2 is commonly phosphorylated at Tyrosine 105. Its levels depended on tyrosine kinase activity, emphasizing the importance of growth factors such as EGF (epidermal growth factor) on HNSCC metabolism. Furthermore, its correlation with the expression of CD44 indicates a role in cancer stemness. Cells generally reacted with higher glycolysis to PKM2 activator DASA-58 and lower glycolysis to PKM2 inhibitor Compound 3k, but some were more susceptible to activation and others to inhibition. Our findings emphasize the need to further investigate the role of PKM2 in HNSCC, as it could aid understanding and treatment of the disease.
APA, Harvard, Vancouver, ISO, and other styles
7

Rahman, Sadia, Sandra Kraljević Pavelić, and Elitza Markova-Car. "Circadian (De)regulation in Head and Neck Squamous Cell Carcinoma." International Journal of Molecular Sciences 20, no. 11 (May 30, 2019): 2662. http://dx.doi.org/10.3390/ijms20112662.

Full text
Abstract:
Head and neck cancer encompass different malignancies that develop in and around the throat, larynx, nose, sinuses and mouth. Most head and neck cancers are squamous cell carcinomas (HNSCC) that arise in the flat squamous cells that makeup the thin layer of tissue on the surface of anatomical structures in the head and neck. Each year, HNSCC is diagnosed in more than 600,000 people worldwide, with about 50,000 new cases. HNSCC is considered extremely curable if detected early. But the problem remains in treatment of inoperable cases, residues or late stages. Circadian rhythm regulation has a big role in developing various carcinomas, and head and neck tumors are no exception. A number of studies have reported that alteration in clock gene expression is associated with several cancers, including HNSCC. Analyses on circadian clock genes and their association with HNSCC have shown that expression of PER1, PER2, PER3, CRY1, CRY2, CKIε, TIM, and BMAL1 are deregulated in HNSCC tissues. This review paper comprehensively presents data on deregulation of circadian genes in HNSCC and critically evaluates their potential diagnostics and prognostics role in this type of pathology.
APA, Harvard, Vancouver, ISO, and other styles
8

Nair, Sindhu, James A. Bonner, and Markus Bredel. "EGFR Mutations in Head and Neck Squamous Cell Carcinoma." International Journal of Molecular Sciences 23, no. 7 (March 30, 2022): 3818. http://dx.doi.org/10.3390/ijms23073818.

Full text
Abstract:
EGFR is a prototypical receptor tyrosine kinase that is overexpressed in multiple cancers including head and neck squamous cell carcinoma (HNSCC). The standard of care for HNSCC remains largely unchanged despite decades of research. While EGFR blockade is an attractive target in HNSCC patients and anti-EGFR strategies including monoclonal antibodies and kinase inhibitors have shown some clinical benefit, efficacy is often due to the eventual development of resistance. In this review, we discuss how the acquisition of mutations in various domains of the EGFR gene not only alter drug binding dynamics giving rise to resistance, but also how mutations can impact radiation response and overall survival in HNSCC patients. A better understanding of the EGFR mutational landscape and its dynamic effects on treatment resistance hold the potential to better stratify patients for targeted therapies in order to maximize therapeutic benefits.
APA, Harvard, Vancouver, ISO, and other styles
9

Mazumder, Tarikul, Sayantan Nath, Nibendu Nath, and Munish Kumar. "Head and Neck Squamous Cell Carcinoma: Prognosis using molecular approach." Open Life Sciences 9, no. 6 (June 1, 2014): 593–613. http://dx.doi.org/10.2478/s11535-014-0292-3.

Full text
Abstract:
AbstractHead and neck squamous cell carcinoma (HNSCC) is the fifth most prevalent cancer worldwide. Apart from various known clinicopathogical factors, it is still a major concern as many genetic and epigenetic alterations bring about the possibility of this deadly disease. The aim of this review is to explore the possible role of DNA repair pathways and the polymorphic status of DNA repair genes (XPA, XPC, XPD, XRCC1 and XRCC3) in the onset of HNSCC, along with sequence variations in genes such as Glutathione S-transferases (GSTT1, M1 and P1) that are significantly associated with HNSCC risk. We also focus on the p53 gene mutation induced by various etiological agents and threat factors with its implications towards HNSCC, and emphasise the current therapeutic interventions in treating HNSCC.
APA, Harvard, Vancouver, ISO, and other styles
10

Bais, M. V. "Impact of Epigenetic Regulation on Head and Neck Squamous Cell Carcinoma." Journal of Dental Research 98, no. 3 (January 7, 2019): 268–76. http://dx.doi.org/10.1177/0022034518816947.

Full text
Abstract:
The most common type of head and neck cancer, head and neck squamous cell carcinoma (HNSCC), can develop therapeutic resistance that complicates its treatment. The 5-y survival rate for HNSCC remains at ~50%, and improving these outcomes requires a better understanding of the pathogenesis of HNSCC. Studies of HNSCC using in vitro, ex vivo, and in vivo approaches provide a novel conceptual framework based on epigenetic mechanisms for developing future clinical applications. Normal oral tissues are influenced by environmental factors that induce pathological changes affecting the network of epigenetic enzymes and signaling pathways to induce HNSCC growth and metastasis. Although various epigenetic regulator families, such as DNA methyltransferases, ten-eleven translocation proteins, histone acetyltransferases, histone deacetylases, BET bromodomain proteins, protein arginine methyltransferases, histone lysine methyltransferases, and histone lysine demethylases, have a role in diverse cancers, specific members have a function in HNSCC. Recently, lysine-specific demethylases have been identified as a potential, attractive, and novel target of HNSCC. Lysine-specific demethylase 1 (LSD1) expression is inappropriately upregulated in HNSCC and an orthotopic HNSCC mouse model. LSD1 can demethylate lysine at specific histone positions to repress gene expression or stimulate transcription, indicating a dual and context-dependent role in transcriptional regulation. Our study showed that LSD1 promotes HNSCC growth and metastasis. Pharmacological attenuation of LSD1 inhibits orthotopic and patient-derived HNSCC xenograft growth-specific target genes and signaling pathways. This review provides recent evidence demonstrating the function of epigenetic regulator enzymes in HNSCC progression, including potential therapeutic applications for such enzymes in combination and immunotherapy.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Head and Neck Suqamous Cell Carcinoma (HNSCC)"

1

GHIANI, LAVINIA. "THE HISTONE POST-TRANSLATIONAL MODIFICATION LANDSCAPE IN HPV+ AND HPV- HEAD AND NECK SQUAMOUS CELL CARCINOMA: CHARACTERIZING THE ONCOGENIC ROLE OF THE H3K36ME2 METHYLTRANSFERASE NSD2." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/820678.

Full text
Abstract:
Background: HNSCC is a heterogeneous group of tumors caused mainly by environmental factors and human papillomavirus (HPV) infections. HPV- and HPV+ HNSCC are considered distinct entities, however, they are still treated with the same therapeutic strategies. HPV-induced tumorigenesis is mainly mediated by the E6/E7 oncoviral proteins, that, among all, alter the epigenetics of the host cells. Nevertheless, epigenetic profiles of HNSCC subtypes have not been clearly profiled. Results and Conclusion: hPTMs super-SILAC analysis of HNSCC cell lines and patients’ tissue samples revealed significant differences in the enrichment levels of some hPTM in HPV+ samples compared to HPV- ones and in tumoral tissues compared to normal ones. We focused on one of these identified hPTM and demonstrated that its levels are regulated by E6 and E7. We identified a histone modifier responsible for this hPTM whose levels are upregulated by E6/E7 and are higher in HPV+ compared to HPV- HNSCC cell lines and patients’ tissue samples, as is for the related hPTM. Silencing this enzyme through shRNA in HNSCC cell lines reduced proliferation and migration rates in both subtypes. It also downregulates the expression levels of some EMT mesenchymal makers and of a crucial oncogene involved in HNSCC. RNA-seq analysis revealed that other programs are instead specifically regulated according to the subtype: immune-response related genes are mainly activated in HPV- cell lines, while genes involved in cell differentiation in the HPV+ ones. Our research paves the way to novel lines of research and identifies a promising novel epigenetic target for HNSCC treatments.
APA, Harvard, Vancouver, ISO, and other styles
2

Bennett, Kristi Lynn. "Methylation in head and neck squamous cell carcinoma." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1194544327.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Wood, S. Matthew. "A Study of Head and Neck Squamous Cell Carcinoma Adhesion Mediated by Glycosphingolipids." Ohio University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1314210756.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Haylock, Anna-Karin. "Targeting molecules for diagnostics of Head and Neck squamous cell carcinoma." Doctoral thesis, Uppsala universitet, Öron-, näs- och halssjukdomar, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-315210.

Full text
Abstract:
To personalize treatment for cancer, correct staging of the primary tumor, nodal disease and metastatic disease is of essence. By targeting tumor specific receptors with radiolabeled antibodies, specificity and accuracy of imaging may be improved. Radio-immunodiagnostics can potentially detect small volume disease, occult metastasis and recurrent cancer in treated tissue. This thesis focuses on evaluation of radio-immunoconjugates directed towards CD44v6, which is a surface receptor overexpressed in many head and neck squamous cell carcinomas. At the outset, the monoclonal chimeric antibody cMab U36 and its cleavage products Fab’ and F(ab’)2 were labeled with 125I and assessed in vitro and in vivo (paper I). The best distribution pattern and tumor to organ ratio was achieved with F(ab’)2. Due to the immunological responses humans can develop towards chimeric antibodies, they are not optimal for clinical use, and subsequently fully human antibody fragments were developed. AbD15179, which is a monovalent fragment, was labeled with 111In and 125I and evaluated in vitro and in mice bearing CD44v6-expressing tumors. Tumor to organ ratios were improved compared to cMab U36 derived fragments, and 111In-AbD15179 displayed a more favorable distribution compared to 125I-AbD15179 (Paper II). A bivalent Fab-dHXL, AbD19384 derived from AbD15179, was then constructed and labeled with 125I and evaluated in cell- and biodistribution studies. Furthermore, an imaging study in a small animal PET was performed with 124I-AbD19384 (Paper III). Uptake in kidneys was reduced and liver uptake increased compared to AbD15179 reflecting the larger molecule. The high CD44v6 expressing tumor was clearly visualized with maximum uptake at 48 hours post injection.In paper IV human single chain fragments towards CD44v6v were selected, and the top candidates A11 and H12 were further evaluated in vitro and in vivo. Single chain fragments are small molecules exhibiting fast clearance and high affinity to the target. The study proved this by demonstrating superior tumor to blood ratios of radiolabeled A11 and H12 compared to previously studied molecules.
APA, Harvard, Vancouver, ISO, and other styles
5

Lee, June Young. "The Role of Noxa/MCL-1 in Head and Neck Squamous Cell Carcinoma (HNSCC) Treatment." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3748.

Full text
Abstract:
Head and neck cancer is the sixth leading type of cancer with 90 percent of head and neck cancer arising from squamous cell lining on the epithelium of the oral and nasal cavity, pharynx, and salivary gland. Even with tremendous achievements on chemotherapeutic drugs and therapies, the long-term prognosis of patients with advanced head and neck squamous cell carcinoma (HNSCC) has shown little improvement over the last three decades. Cisplatin is one of widely used chemotherapeutic drugs for multiple cancers, including head and neck cancer, but the prolonged use of this drug is limited by its toxicity and by the development of resistance. To overcome these major roadblocks to improved prognosis requires mechanism-based therapeutic strategies to maximize the antitumor effect of drugs while limiting their toxicities. Cisplatin exerts anticancer effects via multiple mechanisms, yet its most prominent mode of action involves the generation of DNA lesions followed by the activation of the DNA damage response and the induction of BCL-2 family-dependent mitochondrial apoptosis. DNA damage activates a tumor suppressor p53 to induce apoptosis. One of its functions is to induce the expression of several pro-apoptotic proteins such as Noxa, which binds to an anti-apoptotic BCL-2 family protein, MCL-1 (myeloid leukemia cell-1) to inactivate its pro-survival function and induce apoptosis. We examined Noxa expression and apoptosis induced by cisplatin in p53-wild-type HN30 and HN31, p53-truncated and inactive HN4 and HN12, and p53-deleted HN22 and HN8 HNSCC cell lines. We found that Noxa was induced in HN30 and HN31 cells and down-regulation of Noxa by shRNA (short-hairpin RNA) decreased apoptosis, indicating Noxa contribution to cisplatin-induced apoptosis. Interestingly, cisplatin treatment induced Noxa and apoptosis even in p53-deleted HN22 and HN8 cells, suggesting the existence of the p53-independent pathways for the induction of Noxa. Based on these observations, we hypothesized that modulation of Noxa/MCL-1 axis could mimic cisplatin-induced cell death. We found that Noxa overexpression induced cell death in all cell lines tested regardless of p53 status. This finding could be applicable as a potential therapeutic strategy to treat head and neck cancer.
APA, Harvard, Vancouver, ISO, and other styles
6

Adams, Allie K. "Targeting the DEK oncogene in head and neck squamous cell carcinoma: functional and transcriptional consequences." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1427882536.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Maxim, Nicolas T. Mr. "Tumor-Specific Cell Death Induction by Noxa Overexpression for Head and Neck Squamous Cell Carcinoma (HNSCC) Treatment." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4230.

Full text
Abstract:
The primary focus of this research is the mechanisms of cell death in head and neck squamous cell carcinoma (HNSCC) treatment. These cancers typically originate in squamous cells that line the moist mucosal surfaces of head and neck. HNSCC is commonly treated with a platinum based agent, cisplatin. While the drug does offer strong antitumor effects, its prolonged use often results in tumor-acquired resistance, which limits treatment effectiveness. We have shown that cisplatin treatment induces the expression of a pro-apoptotic BCL-2 family member Noxa, which then initiates caspase- dependent apoptosis through its binding and sequestration of pro-survival protein MCL-1 for its inactivation. Without Noxa induction, cell death is significantly reduced when treating HNSCCs with cisplatin. The objectives of this study are (1) to determine the molecular mechanisms by which Noxa induces cell death in HNSCC cells; (2) to determine the molecular mechanisms of cisplatin-resistance in isogenic HNSCC cell lines. We observed an increase of apoptosis by ectopic expression of Noxa in all HNSCC cell lines tested, but not in immortalized human normal oral keratinocytes (NOK), suggesting that Noxa overexpression is sufficient to induce tumor-specific cell death. Noxa-induced cell death was mediated by BAX and BAK activation. BAK activation was mediated through Noxa binding to MCL-1, but not BCL-XL. Cisplatin- resistant cells induced less Noxa and apoptosis, supporting that Noxa induction is prerequisite for apoptosis induced by cisplatin. Taken together, Noxa induces tumor- specific cell death in HNSCC cells primarily through BAX and BAK activation, which suggests the therapeutic potential of this protein.
APA, Harvard, Vancouver, ISO, and other styles
8

Patel, Dhwani. "Regulation of EPS8 Dependent Pathways By Src in Head and Neck Squamous Cell Carcinoma." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3810.

Full text
Abstract:
Head and neck squamous cell carcinoma (HNSCC) is a type of cancer that begins in the epithelial cells that line the mucosal surfaces of the head and neck, including the oral cavity, pharynx, larynx, paranasal sinuses, nasal cavity, and salivary glands. Head and neck cancer is the sixth most common type of cancer with a 5-year survival rate of 60% for all cases. Over the past few years, a subset of cells with stem-like properties, called cancer stem cells, are believed to have tumor-initiation capabilities and are responsible for maintaining on-going tumor growth. Previous data from our lab suggested that cells grown in suspension, called spheroids, may have stem cell like properties. We employed a model system where a primary HNSCC cell line, HN4, was used to set up spheroids. We found that expression of EPS8 and its downstream targets, FOXM1 and CXCL5, was increased in HN4 spheroids. In addition, we measured the expression of Nanog, as it is a transcription factor involved in the self-renewal of human embryonic stem cells. We also used a metastatic HNSCC cell line, HN12, to see how it compared to spheroids. We wanted to investigate the hypothesis that activation of Src potentiates EPS8 function to deregulate downstream signaling pathways. We used a small molecule tyrosine kinase inhibitor, Dasatinib, on HN4 spheroids and HN12 cells. We found that when Src is inhibited, EPS8 expression is decreased in HN4 spheroids and it also interferes with spheroid formation. The results of the current study were also able to show that the proliferation capability of HN12 cells is greatly diminished when treated with Dasatinib, due to G1 arrest in the cell cycle. When we measured for FOXM1, which is a cell cycle regulator, we found the levels were reduced in Dasatinib treated cells, preventing the cells from completing mitosis. With all of the data taken together, it suggests that Src does in fact play a role in regulating the downstream signaling pathways of EPS8, and its inhibition leads to the loss of cell proliferation. Additional studies need to be performed to discover whether Src inhibition will stop the proliferation of cancer stem cells, which are believed to be more resistant to cytotoxic therapies.
APA, Harvard, Vancouver, ISO, and other styles
9

Espinosa-Cotton, Madelyn. "Interleukin-1 signaling contributes to the anti-tumor efficacy of Cetuximab in head and neck squamous cell carcinoma." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6570.

Full text
Abstract:
Despite the incorporation of the epidermal growth factor receptor (EGFR) inhibitor cetuximab into the clinical management of recurrent and metastatic (R/M) head and neck squamous cell carcinoma (HNSCC), only a small subset of patients responds to cetuximab, despite EGFR overexpression in virtually all of their tumors. At this time, there is a lack of validated predictive biomarkers to predict which patients will respond to cetuximab. Our previous work suggests that cetuximab activates the interleukin-1 (IL-1) pathway via tumor release of IL-1 alpha (IL-1α), although the implications of activating this pathway are unclear. The IL-1 pathway plays a central role in immune response and displays both pro-tumor and anti-tumor activities. IL-1 may promote tumor growth by upregulating the secretion of pro-inflammatory mediators involved in angiogenesis and metastasis. On the other hand, IL-1 signaling may promote antitumor immunity via enhancement of natural killer (NK)-cell mediated antibody-dependent cell-mediated cytotoxicity (ADCC) and T cell activity, which are important mechanisms of action of cetuximab. The goal of this work is to determine how modulation of the IL-1 pathway affects HNSCC tumor response to cetuximab and if IL-1 may serve as a predictive biomarker for patient response to cetuximab. Blockade of IL-1 signaling did not enhance the anti-tumor efficacy of cetuximab, while IL-1α overexpression and treatment with recombinant IL-1α and IL-1α nanoparticles increased HNSCC tumor response to cetuximab in immunodeficient and immunocompetent HNSCC mouse models. Mechanistically, these results appear to be due to activation of an anti-tumor NK and T cell-mediated immune response. Additionally, we found that both nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) and inducible nitric oxide synthase (iNOS) activity may be involved in the efficacy of IL-1-induced ADCC against cetuximab-coated HNSCC cells. Altogether, these results suggest that IL-1 signaling is necessary for HNSCC tumor response to cetuximab. Furthermore, we have shown that pre-treatment serum and tumor IL-1 ligands can predict progression-free survival of HNSCC patients treated with standard-of-care cetuximab and chemotherapy, cetuximab combined with other targeted therapies, and cetuximab monotherapy. Overall, we propose that IL-1α warrants further study as a novel therapeutic to enhance response to cetuximab and as a predictive biomarker for HNSCC response to cetuximab.
APA, Harvard, Vancouver, ISO, and other styles
10

Bradburn, Jennifer Elizabeth. "Reactive species promotion of head and neck squamous cell carcinoma." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1166555968.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Head and Neck Suqamous Cell Carcinoma (HNSCC)"

1

Moy, Jennifer, and Robert L. Ferris. "Immunotherapy in Head and Neck Squamous Cell Carcinoma (HNSCC)." In Molecular Determinants of Head and Neck Cancer, 365–96. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78762-6_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Rischin, Danny. "Biomarkers for Immune Modulatory Treatment in Head and Neck Squamous Cell Carcinoma (HNSCC)." In Critical Issues in Head and Neck Oncology, 83–91. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_6.

Full text
Abstract:
AbstractImmune checkpoint inhibitors have changed the standard of care for recurrent/metastatic head and neck squamous cell carcinoma (R/M HNSCC). However, only a minority of patients respond, hence the search for predictive biomarkers. Potential predictive biomarkers for immune checkpoint inhibitors discussed in this chapter include (1) Immune checkpoint ligand expression e.g., PD-L1, (2) biomarkers of a T-cell inflamed tumour microenvironment (TME) such as gene expression profiles of activated T cells, (3) biomarkers of tumour neoepitope burden such as tumour mutation burden (TMB) and (4) multidimensional quantitative techniques. At present only PD-L1 expression has been shown to have clinical utility in head and neck cancer. It enriches for populations more likely to respond, but the false positive predictive value remains high. In the pivotal Keynote−048 trial that established a role for pembrolizumab (anti-PD1) monotherapy and pembrolizumab + chemotherapy as treatment options in first-line R/M HNSCC, primary endpoints included overall survival in defined subgroups based on PD-L1 expression. In this trial the combined positive score (CPS) was used which takes into account PD-L1 expression in tumour and immune cells. Based on this trial regulatory approvals for first-line pembrolizumab in R/M HNSCC require assessment of PD-L1 expression using the CPS. Finally we discuss emerging evidence that locoregionally advanced HPV-associated oropharyngeal cancers that have high expression of CD103 positive CD8 T cells have an excellent prognosis and features that suggest increased probability of responding to anti-PD1/PD-L1, raising the possibility of incorporating these immune therapies as part of a de-escalation trial strategy.
APA, Harvard, Vancouver, ISO, and other styles
3

Huang, Shao Hui, Avinash Pilar, Jishi Li, Zhiyuan Xu, and Brian O’Sullivan. "Contemporary Opportunities in Nonsurgical Management of Locoregionally Advanced Head and Neck Squamous Cell Carcinoma." In Critical Issues in Head and Neck Oncology, 119–37. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_9.

Full text
Abstract:
AbstractThe majority of head and neck squamous cell carcinoma (HNSCC) is now classified into two major types: HPV-mediated [HPV(+)] and HPV-negative [HPV(−)]. Within this paradigm, the 8th edition TNM staging system effected modification about what is considered “locally-advanced” HNSCC. Two phase-III trials (RTOG 1016 and De-ESCALATE HPV) disappointingly showed that cetuximab is not as effective in HPV(+) oropharyngeal cancer (OPC) compared to cisplatin with radiotherapy. The recent NRG HN002 de-escalation trial demonstrated the presence of outcome heterogeneity within “low-risk” HPV(+) OPC, some of which continue to benefit from cisplatin combined with reduced-dose radiotherapy. Moreover, distant metastasis (DM) has consolidated its position as the leading cause of death in HPV(+) OPC and strategies to mitigate it are necessary. Unanswered questions and ongoing-emerging concepts exist in both HPV(+) and HPV– diseases. These include understanding the importance of risk under the rubric of extranodal extension (ENE), including degrees of pathological ENE (pENE), and emerging knowledge about radiologic ENE (rENE). Strategies addressing modification of biological phenomena have become paramount and includes hypoxia modification (such as smoking cessation). In addition, contemporary evidence suggests that immunotherapy improves survival in recurrent/metastatic settings, and it is now also being explored in primary disease presentations in combination with (chemo-)radiotherapy. Induction chemotherapy achieves DM reduction in nasopharyngeal cancer but has only been explored minimally in HPV(+) OPC. Evidence that loco-regional management can be de-intensified following a favorable response to induction treatment would provide an attractive option for HPV(+) OPSCC patients while also addressing risk of developing distant disease.
APA, Harvard, Vancouver, ISO, and other styles
4

Demidova, Elena V., Waleed Iqbal, and Sanjeevani Arora. "Molecular Regulation of Cell Cycle and Cell Cycle-Targeted Therapies in Head and Neck Squamous Cell Carcinoma (HNSCC)." In Molecular Determinants of Head and Neck Cancer, 185–227. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78762-6_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Roden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi, and Athanassios Argiris. "New and Promising Targeted Therapies in First and Second-Line Settings." In Critical Issues in Head and Neck Oncology, 277–96. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_18.

Full text
Abstract:
AbstractDeeper understanding of the molecular pathogenesis of malignancies, including head and neck squamous cell carcinoma (HNSCC), has led to the investigation of several novel targeted therapies. These therapeutic approaches may eventually replace or complement existing treatment modalities, such as surgery, radiation therapy, and traditional cytotoxic chemotherapy. Epidermal growth factor receptor (EGFR) inhibitors, and specifically cetuximab, are as of now the only class of targeted agents, excluding immune checkpoint inhibitors, with approval in the treatment of HNSCC. Beyond EGFR inhibition, novel therapies under evaluation are directed against vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR), PI3K/AKT/mTOR pathway, cell cycle regulation (for example, cyclin dependent kinases 4 and 6), HRAS, DNA repair mechanisms, and others. Development of new therapies has to take into consideration the complexity of solid tumors and their heterogeneity. Multitargeted combination therapy approaches may be required in certain cases in order to maximize antitumor effect. Ways to individualize treatment using validated biomarkers are likely to improve outcomes. We review the most relevant molecular targets in HNSCC and provide updates on clinical trial data with promising new targeted agents.
APA, Harvard, Vancouver, ISO, and other styles
6

Rischin, Danny. "Update of Immune Therapies in Recurrent/Metastatic Head and Neck Cancer." In Critical Issues in Head and Neck Oncology, 297–306. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_19.

Full text
Abstract:
AbstractSince the initial reports of activity of pembrolizumab in recurrent/metastatic head and neck squamous cell carcinoma (R/M HNSCC), investigation of the role of immune therapies has been the major focus of clinical trials in R/M HNSCC. Randomised trials initially with nivolumab and later with pembrolizumab established overall survival benefit in patients with R/M HNSCC previously treated with platinum compared to physicians choice of 2nd line therapy, and have led to regulatory approval around the world. More recently the Keynote-048 trial has compared both pembrolizumab monotherapy and pembrolizumab + platinum/5FU to the Extreme regimen of platinum/5FU/cetuximab in the first-line R/M setting. The key findings from this trial are that pembrolizumab monotherapy compared to Extreme improved overall survival in patients with PD-L1 combined positive score (CPS) ≥ 20 and ≥ 1, and that pembro/chemotherapy improved OS in CPS ≥ 20, CPS ≥ 1 and the total population. Relative to Extreme there was less toxicity in the monotherapy arm and comparable toxicity in the pembro/chemo arm. Based on this trial use of pembrolizumab as part of first-line treatment for R/M HNSCC is appropriate for the majority of patients, and represents a new standard of care. The focus has now moved to identifying combinations that may be superior to pembrolizumab monotherapy or to chemotherapy + pembrolizumab. Some of the more promising approaches under investigation in HNSCC are discussed in this chapter. In summary, immune therapies are now the cornerstone of management of R/M HNSCC with the approval of pembrolizumab in the first-line R/M setting.
APA, Harvard, Vancouver, ISO, and other styles
7

Moskovitz, Jessica M., and Robert L. Ferris. "Tumor Immunology, Immunotherapy and Its Application to Head and Neck Squamous Cell Carcinoma (HNSCC)." In Critical Issues in Head and Neck Oncology, 341–55. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-98854-2_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

De Crevoisier, R. M. D., J. Bourhis, and F. M. D. Eschwéege. "Modified Fractionated Radiotherapy in Head and Neck Squamous Cell Carcinoma (HNSCC) & Re-Irradiation in Recurrent Head and Neck Carcinomas." In Head and Neck Cancer, 199–212. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/0-306-48060-3_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Anandharaj, Arunkumar, Oleksandr Ekshyyan, Tara Moore-Medlin, Vikas Mehta, and Cherie-Ann O. Nathan. "Human Papillomavirus (HPV) Biomarkers in Head and Neck Squamous Cell Carcinoma (HNSCC)." In Biomarkers in Cancer, 1–17. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7744-6_31-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kudinov, Alexander E., and Tim N. Beck. "Transforming Growth Factor Beta (TGF-β) Signaling in Head and Neck Squamous Cell Carcinoma (HNSCC)." In Molecular Determinants of Head and Neck Cancer, 89–115. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78762-6_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Head and Neck Suqamous Cell Carcinoma (HNSCC)"

1

Clark, Cheryl A., Joyce Rong, and Cherie‐Ann O. Nathan. "Abstract A76: Curcumin inhibits head and neck squamous cell carcinoma (HNSCC) migration." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Dec 6–9, 2009; Houston, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-09-a76.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Theodoraki, MN, C. Brunner, and TK Hoffmann. "Modulation of the tumor microenvironment in Head and Neck Squamous Cell Carcinoma (HNSCC)." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686084.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Chaudhary, Ritu, Xuefeng Wang, Biwei Cao, Nicholas T. Gimbrone, Robbert JC Slebos, and Christine H. Chung. "Abstract 1812: LncRNAs as prognostic biomarkers in head and neck squamous cell carcinoma (HNSCC)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1812.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Chaudhary, Ritu, Xuefeng Wang, Biwei Cao, Nicholas T. Gimbrone, Robbert JC Slebos, and Christine H. Chung. "Abstract 1812: LncRNAs as prognostic biomarkers in head and neck squamous cell carcinoma (HNSCC)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1812.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Zaheer, Saad, Sabaoon Zeb, and Faisal F. Khan. "Intelligent analysis of methylation data in Head and Neck Squamous Cell Carcinoma (HNSCC) interactomes." In 2021 International Conference on Artificial Intelligence (ICAI). IEEE, 2021. http://dx.doi.org/10.1109/icai52203.2021.9445265.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bußmann, L., C. Betz, A. Münscher, M. Kriegs, K. Hoffer, AT Vu, S. Brand, C. Petersen, and K. Rothkamm. "Characterization of human head and neck squamous cell carcinoma (HNSCC) on a kinomic level." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685974.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Rozek, Laura, Shama Virani, Emily Bellile, Jeremy Taylor, Maureen Sartor, Alisha Virani, Katie Rentschler, et al. "Abstract 3114: Soy isoflavones modulate global methylation in head and neck squamous cell carcinoma (HNSCC)." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3114.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ngan, Hoi Lam, Yuchen Liu, Peony Hiu Yan Poon, and Vivian Wai Yan Lui. "Abstract 4033:RAC1genomic aberrations as predictive biomarkers for head and neck squamous cell carcinoma (HNSCC)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4033.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ngan, Hoi Lam, Yuchen Liu, Peony Hiu Yan Poon, and Vivian Wai Yan Lui. "Abstract 4033:RAC1genomic aberrations as predictive biomarkers for head and neck squamous cell carcinoma (HNSCC)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4033.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Bußmann, L., K. Hoffer, H. Zech, C. Betz, Chia-Jung Busch, and M. Kriegs. "Kinase activity profiles as prognostic marker for immunotherapy in head and neck squamous cell carcinoma (HNSCC)." In Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1710943.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Head and Neck Suqamous Cell Carcinoma (HNSCC)"

1

Dioguardi, Mario, Diego Sovereto, and Giuseppe Troiano. The Prognostic Role of miR-31 and miR-155 in HNSCC: Protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0119.

Full text
Abstract:
Review question / Objective: the PICO question was formulated , in which the following points are identified: Participants (patients with HNSCC), Intervention (altered expression of miR-31 and miR-155 in HNSCC), Control (patients with HNSCC who have low expression of miR-31 and miR-155), Outcome (difference in prognosis of survival among patients with low and high miR-31 and miR-155 expression in HNSCC The PICO question therefore is as follows: Is there a difference in OS (overall Survival) between HNSCC patients with high miR-31 and miR-155 expression versus those with low expression? Condition being studied: Head and Neck Squamous Cell Carcinoma (HNSCC), altered expression of miR-31 and miR-155 tissue.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Head and Neck Suqamous Cell Carcinoma (HNSCC)' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography