IU Indianapolis ScholarWorks :: Browsing by Subject "Squamous cell carcinoma"

Browsing by Subject "Squamous cell carcinoma"

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Age at Diagnosis as a Relative Contraindication for Intervention in Facial Nonmelanoma Skin Cancer
(American Medical Association, 2018-04-01) Chauhan, Ruvi; Munger, Brook N.; Chu, Michael W.; Munshi, Imtiaz; Cohen, Adam C.; Wooden, William A.; Tholpady, Sunil S.; Surgery, School of Medicine
Facial nonmelanoma skin cancers (fNMSCs), consisting of basal cell carcinoma and squamous cell carcinoma, are the most common cancers diagnosed worldwide and increase with age. Standard treatment for fNMSCs requires biopsy for pathological confirmation, followed by excision. Excision can lead to a pathological diagnosis of no residual carcinoma (NRC) due to no identifiable carcinoma within the excisional specimen. This situation can occur owing to wound healing in the specimen clearing the carcinoma or to the original biopsy shaving off the entire lesion. This study assesses the utility of excising fNMSCs according to age, with the hypothesis that the indolent nature of fNMSCs and the high NRC rate, coupled with increasing age-related all-cause mortality, should cause the surgeon to counsel patients differently. Such counseling may prevent surgery among elderly patients (>90 years) who may never see a benefit from fNMSC excision.
Alcohol intake is associated with increased risk of squamous cell carcinoma of the skin: three US prospective cohort studies
(Taylor & Francis, 2016-05) Siiskonen, Satu; Han, Jiali; Li, Tricia; Cho, Eunyoung; Nijsten, Tamar; Qureshi, Abrar; Department of Epidemiology, School of Public Health
The association between alcohol intake and cutaneous squamous cell carcinoma (cSCC) is unclear. We studied the association between alcohol intake and incident invasive cSCC in three cohorts of women and men with repeated assessments of alcohol intake in the US. Information on alcohol intake was collected repeatedly during follow-up. Cumulative average of alcohol intakes was used. Multivariable Cox proportional hazards models with time-dependent exposure were used to estimate relative risks (RRs) and 95% confidence intervals, followed by a meta-analysis. During a follow-up of 4,234,416 person-years, 2,938 cSCC were identified. Alcohol intake was associated with an increased risk of cSCC with a dose-response relationship. Each additional drink (12.8 gram of alcohol) per day was associated with a 22% increased risk of cSCC (RR 1.22, 95% confidence interval: 1.13-1.31). White wine consumption of ≥5 times/wk was associated with an increased risk of cSCC (RR 1.31, 95% confidence interval: 1.09-1.59). We found no increased risk of cSCC with other alcoholic beverages. The population-attributable risk associated with alcohol intake of ≥20 grams/d was 3% of cSCCs. In conclusion, alcohol intake was associated with an elevated risk of cSCC. Among alcoholic beverages, white wine was associated with cSCC.
Cigarette Smoke and Decreased DNA Repair by Xeroderma Pigmentosum Group C Use a Double Hit Mechanism for Epithelial Cell Lung Carcinogenesis
(bioRxiv, 2025-02-27) Al Nasrallah, Nawar; Lee, Bowa; Wiese, Benjamin M.; Karam, Marie N.; Mickler, Elizabeth A.; Zhou, Huaxin; Paolelli, Nicki; Stearman, Robert S.; Geraci, Mark W.; Sears, Catherine R.; Medicine, School of Medicine
Emerging evidence suggests a complex interplay of environmental and genetic factors in non-small cell lung cancer (NSCLC) development. Among these factors, compromised DNA repair plays a critical but incompletely understood role in lung tumorigenesis and concurrent lung diseases, such as chronic obstructive lung disease (COPD). In this study, we investigated the interplay between cigarette smoke, DNA damage and repair, focusing on the Nucleotide Excision Repair (NER) protein Xeroderma Pigmentosum Group C (XPC). We found decreased XPC mRNA expression in most NSCLCs compared to subject-matched, non-cancerous lung. In non-cancerous bronchial epithelial cells, cigarette smoke decreased NER, increased total DNA damage and resultant apoptosis, each exacerbated by XPC deficiency. In contrast, lung cancer cells exhibit greater resilience to cigarette smoke, requiring higher doses to induce comparable DNA damage and apoptosis, and are less reliant on XPC expression for survival. Importantly, XPC protects against chromosomal instability in benign bronchial epithelial cells, but not in lung cancer cells. Our findings support a "double hit" mechanism wherein early decreased XPC expression and resultant aberrant DNA repair, when combined with cigarette smoke exposure, may lead to loss of non-malignant epithelial cells (as observed in COPD), and contributes to early NSCLC transition through altered DNA damage response.
Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer
(Oxford University Press, 2021-08-30) Besson, Caroline; Moore, Amy; Wu, Wenting; Vajdic, Claire M.; de Sanjose, Silvia; Camp, Nicola J.; Smedby, Karin E.; Shanafelt, Tait D.; Morton, Lindsay M.; Brewer, Jerry D.; Zablotska, Lydia; Engels, Eric A.; Cerhan, James R.; Slager, Susan L.; Han, Jiali; Berndt, Sonja I.; Medical and Molecular Genetics, School of Medicine
Background: Epidemiological studies have demonstrated a positive association between chronic lymphocytic leukaemia (CLL) and non-melanoma skin cancer (NMSC). We hypothesized that shared genetic risk factors between CLL and NMSC could contribute to the association observed between these diseases. Methods: We examined the association between (i) established NMSC susceptibility loci and CLL risk in a meta-analysis including 3100 CLL cases and 7667 controls and (ii) established CLL loci and NMSC risk in a study of 4242 basal cell carcinoma (BCC) cases, 825 squamous cell carcinoma (SCC) cases and 12802 controls. Polygenic risk scores (PRS) for CLL, BCC and SCC were constructed using established loci. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results: Higher CLL-PRS was associated with increased BCC risk (OR4th-quartile-vs-1st-quartile = 1.13, 95% CI: 1.02-1.24, Ptrend = 0.009), even after removing the shared 6p25.3 locus. No association was observed with BCC-PRS and CLL risk (Ptrend = 0.68). These findings support a contributory role for CLL in BCC risk, but not for BCC in CLL risk. Increased CLL risk was observed with higher SCC-PRS (OR4th-quartile-vs-1st-quartile = 1.22, 95% CI: 1.08-1.38, Ptrend = 1.36 × 10-5), which was driven by shared genetic susceptibility at the 6p25.3 locus. Conclusion: These findings highlight the role of pleiotropy regarding the pathogenesis of CLL and NMSC and shows that a single pleiotropic locus, 6p25.3, drives the observed association between genetic susceptibility to SCC and increased CLL risk. The study also provides evidence that genetic susceptibility for CLL increases BCC risk.
Cox-II inhibitors show no preventive effect in the development of skin cancer
(Wiley, 2022) Yen, Hsuan; Yen, Hsi; Drucker, Aaron M.; Han, Jiali; Li, Wen-Qing; Li, Tricia; Qureshi, Abrar; Cho, Eunyoung; Epidemiology, Richard M. Fairbanks School of Public Health
Background: Some clinical trials found that cyclooxygenase-2 (COX-2) inhibitor use lowered the risk of skin cancer in high-risk groups. Patients and methods: To determine whether COX-2 inhibitor use is associated with lower risk of basal cell carcinoma (BCC), cutaneous squamous cell carcinoma (cSCC), and melanoma, we analyzed COX-2 inhibitor use and risk of skin cancer based on three prospective cohort studies, the Nurses' Health Study (NHS), NHS II, and the Health Professionals Follow-up Study, including 153,882 participants. Multivariable hazard ratios (HRs) and 95 % confidence intervals (CIs) for the association of COX-2 inhibitor use with risk of BCC, cSCC, and melanoma were estimated using Cox proportional hazards models. We pooled the results using a fixed effects model. Results: 16,142 BCC, 1,973 cSCC, and 631 melanoma cases were documented. Ever vs. never use of COX-2 inhibitor was associated with a modestly increased risk of BCC (multivariable HR 1.09, 95 % CI 1.05-1.14). The hazard ratio was similar for cSCC (multivariable HR 1.12, 95 % CI 1.00-1.27) and melanoma (multivariable HR 1.10, 95 % CI 0.89-1.38), but was not statistically significant. Conclusions: Ever use of COX-2 inhibitor was not associated with a decreased skin cancer risk but was instead associated with a modest, increased risk of BCC.
Defects in the Fanconi Anemia Pathway in Head and Neck Cancer Cells Stimulate Tumor Cell Invasion through DNA-PK and Rac1 Signaling
(American Association for Cancer Research, 2016-04-15) Romick-Rosendale, Lindsey E.; Hoskins, Elizabeth E.; Privette Vinnedge, Lisa M.; Foglesong, Grant D.; Brusadelli, Marion G.; Potter, S. Steven; Komurov, Kakajan; Brugmann, Samantha A.; Lambert, Paul F.; Kimple, Randall J.; Virts, Elizabeth L.; Hanenberg, Helmut; Gillison, Maura L.; Wells, Susanne I.; Pediatrics, School of Medicine
PURPOSE: Head and neck squamous cell carcinoma (HNSCC) remains a devastating disease, and Fanconi anemia (FA) gene mutations and transcriptional repression are common. Invasive tumor behavior is associated with poor outcome, but relevant pathways triggering invasion are poorly understood. There is a significant need to improve our understanding of genetic pathways and molecular mechanisms driving advanced tumor phenotypes, to develop tailored therapies. Here we sought to investigate the phenotypic and molecular consequences of FA pathway loss in HNSCC cells. EXPERIMENTAL DESIGN: Using sporadic HNSCC cell lines with and without FA gene knockdown, we sought to characterize the phenotypic and molecular consequences of FA deficiency. FA pathway inactivation was confirmed by the detection of classic hallmarks of FA following exposure to DNA cross-linkers. Cells were subjected to RNA sequencing with qRT-PCR validation, followed by cellular adhesion and invasion assays in the presence and absence of DNA-dependent protein kinase (DNA-PK) and Rac1 inhibitors. RESULTS: We demonstrate that FA loss in HNSCC cells leads to cytoskeletal reorganization and invasive tumor cell behavior in the absence of proliferative gains. We further demonstrate that cellular invasion following FA loss is mediated, at least in part, through NHEJ-associated DNA-PK and downstream Rac1 GTPase activity. CONCLUSIONS: These findings demonstrate that FA loss stimulates HNSCC cell motility and invasion, and implicate a targetable DNA-PK/Rac1 signaling axis in advanced tumor phenotypes.
Point-of-Care Ultrasound in the Primary Care Office for Early Detection of Squamous Cell Carcinoma of the Supraglottic Larynx: A Case Report
(Springer Nature, 2024-07-29) Wilcox, James; Kaefer, Samuel L.; Medicine, School of Medicine
Point-of-care ultrasound (PoCUS) in the head and neck region is still in its early stages, despite decades of formal ultrasound use. A literature gap exists as recent studies primarily focus on general techniques, leaving room for exploration in ambulatory primary care, especially regarding neck masses. Our case demonstrates a 61-year-old female who presented for an annual wellness appointment, reporting a cough and alarming neck symptoms. A prompt investigation using PoCUS identified a suspicious neck mass. This mass was evaluated with bedside POCUS, and the mass was determined to be an abnormal lymph node with findings concerning malignancy. Subsequent diagnostic measures confirmed metastatic squamous cell carcinoma in the supraglottic larynx. This case underscores PoCUS's transformative potential in ambulatory primary care for neck mass evaluation, facilitating swift and thorough diagnostic processes. This successful outcome emphasizes PoCUS's promising role in routine clinical practice, urging future research for standardized evaluation protocols to enhance diagnostic efficiency.
Predicting progression of in situ carcinoma in the era of precision genomics
(AME Publishing Company, 2019-06) Cheng, Monica; Hanna, Nasser H.; Davidson, Darrell D.; Gunderman, Richard B.; Radiology and Imaging Sciences, School of Medicine
Pten loss induces autocrine FGF signaling to promote skin tumorigenesis
(Elsevier, 2014) Hertzler-Schaefer, Kristina; Mathew, Grinu; Somani, Ally-Khan; Tholpady, Sunil; Kadakia, Madhavi P.; Chen, Yiping; Spandau, Dan F.; Zhang, Xin; Dermatology, School of Medicine
Inactivation of the Pten tumor suppressor negatively regulates the PI3K-mTOR pathway. In a model of cutaneous squamous cell carcinoma (SCC), we demonstrate that deletion of Pten strongly elevates Fgf10 protein levels without increasing Fgf10 transcription in vitro and in vivo. The translational activation of Fgf10 by Pten deletion is reversed by genetic disruption of the mTORC1 complex, which also prevents skin tumorigenesis in Pten mutants. We further show that ectopic expression of Fgf10 causes skin papillomas, whereas Pten deletion-induced skin tumors are inhibited by epidermal deletion of Fgfr2. Collectively, our data identify autocrine activation of FGF signaling as an essential mechanism in promoting Pten-deficient skin tumors.
Tumor-Infiltrating Immune-Related Long Non-Coding RNAs Indicate Prognoses and Response to PD-1 Blockade in Head and Neck Squamous Cell Carcinoma
(Frontiers Media, 2021-10-19) Ma, Ben; Jiang, Hongyi; Luo, Yi; Liao, Tian; Xu, Weibo; Wang, Xiao; Dong, Chuanpeng; Ji, Qinghai; Wang, Yu; BioHealth Informatics, School of Informatics and Computing
Long non-coding RNAs (lncRNAs) in immune cells play critical roles in tumor cell-immune cell interactions. This study aimed to characterize the landscape of tumor-infiltrating immune-related lncRNAs (Ti-lncRNAs) and reveal their correlations with prognoses and immunotherapy response in head and neck squamous cell carcinoma (HNSCC). We developed a computational model to identify Ti-lncRNAs in HNSCC and analyzed their associations with clinicopathological features, molecular alterations, and immunotherapy response. A signature of nine Ti-lncRNAs demonstrated an independent prognostic factor for both overall survival and disease-free survival among the cohorts from Fudan University Shanghai Cancer Center, The Cancer Genome Atlas, GSE41613, and GSE42743. The Ti-lncRNA signature scores in immune cells showed significant associations with TP53 mutation, CDKN2A mutation, and hypoxia. Inferior signature scores were enriched in patients with high levels of PDCD1 and CTLA4 and high expanded immune gene signature (IGS) scores, who displayed good response to PD-1 blockade in HNSCC. Consistently, superior clinical response emerged in melanoma patients with low signature scores undergoing anti-PD-1 therapy. Moreover, the Ti-lncRNA signature was a prognostic factor independent of PDCD1, CTLA4, and the expanded IGS score. In conclusion, tumor-infiltrating immune profiling identified a prognostic Ti-lncRNA signature indicative of clinical response to PD-1 blockade in HNSCC.

Browsing by Subject "Squamous cell carcinoma"

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