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OBJECTIVE. To examine the oral microbiome in the context of oral cavity squamous cell carcinoma. STUDY DESIGN. Basic science research. SETTING. Academic medical center. METHODS. Oral swabs were collected from patients presenting to the operating room for management of oral cavity squamous cell carcinoma and from age- and sex-matched control patients receiving surgery for unrelated benign conditions. 16S ribosomal RNA (rRNA) sequencing was performed on genetic material obtained from swabs. A bacterial rRNA gene library was created and sequence reads were sorted into taxonomic units. RESULTS. Thirty-one control patients (17 males) and 35 cancer patients (21 males) were enrolled. Ages ranged from 23 to 89 (median 63) for control patients and 35 to 86 (median 66) for cancer patients. Sixty-one percent of control patients and 63% of cancer patients were smokers. 16S analyses demonstrated a significant decrease in Streptococcus genera in oral cancer patients (34.11% vs 21.74% of the population, p = .04). Increases in Fusobacterium, Peptostreptococcus, Parvimonas, and Neisseria were also found. The abundance of these bacteria correlated with tumor T-stage. CONCLUSION. 16S rRNA sequencing demonstrated changes in bacterial populations in oral cavity cancer and its progression compared to noncancer controls. We found increases in bacteria genera that correspond with tumor stage—Fusobacteria, Peptostreptococcus, Parvimonas, Neisseria, and Treponema. These data suggest that oral cancer creates an environment to facilitate foreign bacterial growth, rather than implicating a specific bacterial species in carcinogenesis. These bacteria can be employed as a potential marker for tumor progression or interrogated to better characterize the tumor microenvironment.

Група експертів, скликана Радою з наукових питань Американської стоматологічної асоціації (ADA) та Центром доказової стоматології, провела систематичний огляд і сформулювала клінічні рекомендації для інформування лікарів первинної ланки про потенційне використання допоміжних засобів як інструментів сортування для оцінки уражень, у тому числі потенційно злоякісних, ротової порожнини. Типи розглянутих досліджень. Це оновлення рекомендацій ADA 2010 року щодо ранньої діагностики OPSCC та плоскоклітинного раку порожнини рота. Автори провели систематичний пошук літератури в MEDLINE та Embase через Ovid та Кокранівський центральний реєстр контрольованих випробувань для виявлення рандомізованих контрольованих випробувань та досліджень точності діагностичних тестів. Автори використовували підхід «оцінка, розробка та оцінка рекомендацій» для оцінки впевненості у доказах та переходу від доказів до рішень. Результати. Група експертів сформулювала 1 заяву про передову практику та 6 клінічних рекомендацій, у яких дійшла висновку про те, що жоден з доступних допоміжних засобів не продемонстрував достатню точність діагностичних тестів, щоб підтримувати їх рутинне використання як інструментів сортування при оцінці уражень у порожнині рота. Щодо пацієнтів, які звертаються по допомогу з приводу підозрілих уражень, негайне виконання біопсії або направлення до фахівця залишається єдиною найважливішою рекомендацією для клінічної практики. У виняткових випадках, коли пацієнти відмовляються від біопсії або мешкають у сільській місцевості з обмеженим доступом до медичної допомоги, група експертів запропонувала використовувати цитологічне дослідження для ініціації діагностичного процесу до проведення біопсії (умовна рекомендація, докази низької якості). Висновки та практичні рекомендації. Автори закликають клініцистів зберігати пильність і застосовувати додаткові методи дослідження при виявленні підозрілих уражень. Автори наголошують на необхідності консультування, оскільки пацієнти можуть відкладати встановлення діагнозу через занепокоєння та заперечення.

Assessment of programmed death ligand 1 (PD-L1) expression by immunohistochemistry (IHC) has emerged as an important predictive biomarker across multiple tumor types. However, manual quantitation of PD-L1 positivity can be difficult and leads to substantial inter-observer variability. Although the development of artificial intelligence (AI) algorithms may mitigate some of the challenges associated with manual assessment and improve the accuracy of PD-L1 expression scoring, use of AI-based approaches to oncology biomarker scoring and drug development has been sparse, primarily due to the lack of large-scale clinical validation studies across multiple cohorts and tumor types. We developed AI-powered algorithms to evaluate PD-L1 expression on tumor cells by IHC and compared it with manual IHC scoring in urothelial carcinoma, non-small cell lung cancer, melanoma, and squamous cell carcinoma of the head and neck (prospectively determined during the phase II and III CheckMate clinical trials). 1,746 slides were retrospectively analyzed, the largest investigation of digital pathology algorithms on clinical trial datasets performed to date. AI-powered quantification of PD-L1 expression on tumor cells identified more PD-L1-positive samples compared with manual scoring at cutoffs of ≥1% and ≥5% in most tumor types. Additionally, similar improvements in response and survival were observed in patients identified as PD-L1-positive compared with PD-L1-negative using both AI-powered and manual methods, while improved associations with survival were observed in patients with certain tumor types identified as PD-L1-positive using AI-powered scoring only. Our study demonstrates the potential for implementation of digital pathology-based methods in future clinical practice to identify more patients who would benefit from treatment with immuno-oncology therapy compared with current guidelines using manual assessment.

The authors present an interesting case of ganglioneuroblastoma, a tumor of the sympathetic chain, presenting as severe obstructive sleep apnea in a healthy 5-year-old boy. The patient's initial polysomnogram demonstrated an apnea-hypopnea index (AHI) of 86 events/hour. He underwent an adenotonsillectomy at an outside hospital and his repeat AHI was still 62. The patient was nonobese and nonsyndromic appearing, which made his incredibly high AHI perplexing. He underwent sleep endoscopy and direct laryngoscopy for further evaluation, which demonstrated a large mass in the left posterior pharynx. He then underwent surgical excision with a resolution of his obstructive sleep apnea.

Summary of sequence analysis of adenoid cystic carcinoma.

Supplemental Figures and Tables legends

Supplemental Tables 6-11. Supp. Table 6. List of all mutations identified in each of the normal samples. Supp. Table 7. List of the mutations in the unmatched OSCC and leukoplakia samples that were filtered-out as they were present in the normal samples or in the dbSNP. Supp. Table 8. Summary of the number of mutations present in each of the sets of samples and the number that were filtered-out during analysis. Supp. Table 9. Combined list of all mutations identified in Chinese OSCC patients in this study and by Song et. al (16). Supp. Table 10. List of all NOTCH1 mutations identified in Caucasians HNSCC samples. Supp. Table 11. List of all HNSCC samples from Caucasian patients used in this study: including exact site and HPV status.

Supplemental Table 5. List of 108 primer pairs designed by Fluidigm Assay Design Group and used in this study for NOTCH1 amplification. Table summarizes the GC-content, length distribution and location of the Access Array amplicons.

The Notch pathway is frequently altered in head and neck squamous cell carcinomas (HNSCC); however, the clinical significance of NOTCH1 dysregulation is poorly understood. This study was designed to characterize expression of the transcriptionally active NOTCH1 intracellular domain (NICD1) in HNSCCs and evaluate its association with NOTCH1 mutation status and clinical parameters. IHC for NICD1 was performed on 79 previously sequenced archival HNSCCs with known NOTCH1 mutation status. Three distinct immunohistochemical staining patterns were identified: positive/peripheral (47%), positive/nonperipheral (34%), and negative (19%). NICD1 expression was associated with NOTCH1 mutation status (P < 0.001). Most NOTCH1–wild-type tumors were peripheral (55%), whereas mutated NOTCH1 tumors were most commonly negative (47%). Nonperipheral tumors were more likely than peripheral tumors to have extracapsular spread [adjusted odds ratio (aOR), 16.01; 95% confidence interval (CI), 1.92–133.46; P = 0.010] and poor differentiation (aOR, 5.27; 95% CI, 0.90–30.86; P = 0.066). Negative staining tumors tended to be poorly differentiated (aOR, 24.71; 95% CI, 1.53–399.33; P = 0.024) and were less likely to be human papillomavirus (HPV) positive (aOR, 0.043; 95% CI, 0.001–1.59; P = 0.087). NOTCH1 mutagenesis was significantly associated with HPV status, with NOTCH1–wild-type tumors more likely to be HPV positive than NOTCH1-mutated tumors (aOR, 19.06; 95% CI, 1.31–276.15; P = 0.031). TP53 disruptive mutations were not associated with NICD1 expression or NOTCH1 mutation. In conclusion, NICD1 is expressed in three distinct patterns in HNSCC that are significantly associated with high-risk features. These findings further support a dual role for NOTCH1 as both tumor suppressor and oncogene in HNSCC. Further research is necessary to clarify the role of NOTCH1 in HNSCC and understand the clinical and therapeutic implications therein. Cancer Prev Res; 8(4); 287–95. ©2015 AACR.

NFIB fusion genes.

Disruption of NOTCH1 signaling was recently discovered in head and neck cancer. This study aims to evaluate NOTCH1 alterations in the progression of oral squamous cell carcinoma (OSCC) and compare the occurrence of these mutations in Chinese and Caucasian populations. We used a high-throughput PCR-based enrichment technology and next-generation sequencing (NGS) to sequence NOTCH1 in 144 samples collected in China. Forty-nine samples were normal oral mucosa from patients undergoing oral surgery, 45 were oral leukoplakia biopsies, and 50 were chemoradiation-naïve OSCC samples with 22 paired-normal tissues from the adjacent unaffected areas. NOTCH1 mutations were found in 54% of primary OSCC and 60% of premalignant lesions. Importantly, almost 60% of patients with leukoplakia with mutated NOTCH1 carried mutations that were also identified in OSCC, indicating an important role of these clonal events in the progression of early neoplasms. We then compared all known NOTCH1 mutations identified in Chinese patients with OSCC with those reported in Caucasians to date. Although we found obvious overlaps in critical regulatory NOTCH1 domains alterations and identified specific mutations shared by both groups, possible gain-of-function mutations were predominantly seen in Chinese population. Our findings demonstrate that premalignant lesions display NOTCH1 mutations at an early stage and are thus bona fide drivers of OSCC progression. Moreover, our results reveal that NOTCH1 promotes distinct tumorigenic mechanisms in patients from different ethnical populations. Cancer Prev Res; 8(4); 277–86. ©2014 AACR.See related perspectives, p. 259 and p. 262

Copy number variations in adenoid cystic carcinoma (N=25).

Supplemental Figure 1. List of all NOTCH1 mutations found in Chinese OSCC patients. A. Mutations identified in 22 tumor-normal pairs. B. Mutations found in 28 OSCC samples without matching normal control.

Supplemental Figure 3. A. Association between tumor stage of OSCC patients and NOTCH1 mutation-status. B. Table demonstrates differences in smoking and alcohol consumption rates between the OSCC and leukoplakia patients. C. Table demonstrates differences in smoking and alcohol consumption rates between the OSCC and leukoplakia lesions with mutated NOTCH1. D. The pattern of NOTCH1 base-pair mutations resulting from exposure to tobacco in OSCC and leukoplakia patients (in blue, base-pair mutations that found in both, smokers and non-smokers).

Supplemental Figure 2. List of all NOTCH1 mutations identified in Chinese patients with oral leukoplakia.

Somatic chromosomal rearrangements in adenoid cystic carcinoma (N=25).

Axonal guidance signaling pathway alterations in adenoid cystic carcinoma.

Supplemental Tables 1-4. Supp. Table 1. A. List of all OSCC samples used in this study and clinical/pathological data. B. List of 22 matched tumor-normal pairs. Supp. Table 2. List of all normal samples used in this study and clinical/pathological data. Supp. Table 3. List of all oral leukoplakia samples used in this study and clinical/pathological data. Supp. Table 4. Summary of clinical characteristics for OSCC, leukoplakia and normal samples used in this study.

Somatic mutations in adenoid cystic carcinoma (N=25 tumors).

Circos plots for chromosomal rearrangements in adenoid cystic carcinoma.

Supplementary Table 1. Clinicopathological characteristics of tumors with NICD1 IHC available compared with unavailable.

Supplementary Table S4 provides information on the spectra of mutations seen in MEC tumors of varying histologic grades.

Figure S1 contains representative images of cells with and without the MECT1-MAML2 translocation, as determined by fluorescence in situ hybridization.

Supplementary Table S1 provides a summary of the whole-exome sequencing analysis for normal and tumor samples.

Purpose: Mucoepidermoid carcinoma (MEC) is the most common salivary gland malignancy. To explore the genetic origins of MEC, we performed systematic genomic analyses of these tumors.Experimental Design: Whole-exome sequencing and gene copy-number analyses were performed for 18 primary cancers with matched normal tissue. FISH was used to determine the presence or absence of the MECT1-MAML2 translocation in 17 tumors.Results: TP53 was the most commonly mutated gene in MEC (28%), and mutations were found only in intermediate- and high-grade tumors. Tumors with TP53 mutations had more mutations overall than tumors without TP53 mutations (P = 0.006). POU6F2 was the second most frequently mutated gene, found in three low-grade MECs with the same in-frame deletion. Somatic alterations in IRAK1, MAP3K9, ITGAL, ERBB4, OTOGL, KMT2C, and OBSCN were identified in at least two of the 18 tumors sequenced. FISH analysis confirmed the presence of the MECT1-MAML2 translocation in 15 of 17 tumors (88%).Conclusions: Through these integrated genomic analyses, MECT1-MAML2 translocation and somatic TP53 and POU6F2 mutations appear to be the main drivers of MEC. Clin Cancer Res; 23(1); 283–8. ©2016 AACR.

Purpose: To determine if phosphodiesterase 5 (PDE5) inhibitors can augment immune function in patients with head and neck cancer through inhibition of myeloid-derived suppressor cells (MDSC).Experimental Design: We performed a randomized, prospective, double blinded, placebo controlled, phase II clinical trial to determine the in vivo effects of systemic PDE5 inhibition on immune function in patients with head and neck squamous cell carcinoma (HNSCC).Results: Tadalafil augmented immune response, increasing ex vivo T-cell expansion to a mean 2.4-fold increase compared with 1.1-fold in control patients (P = 0.01), reducing peripheral MDSC numbers to mean 0.81-fold change compared with a 1.26-fold change in control patients (P = 0.001), and increasing general immunity as measured by delayed type hypersensitivity response (P = 0.002). Tumor-specific immunity in response to HNSCC tumor lysate was augmented in tadalafil-treated patients (P = 0.04).Conclusions: These findings demonstrate that tadalafil augments general and tumor-specific immunity in patients with HNSCC and has therapeutic potential in HNSCC. Evasion of immune surveillance and suppression of systemic and tumor-specific immunity is a significant feature of head and neck cancer development. This study demonstrates that a PDE5 inhibitor, tadalafil, can reverse tumor-specific immune suppression in patients with head and neck cancer, with potential for therapeutic application. Clin Cancer Res; 21(1); 30–38. ©2015 AACR.

Supplementary Table S2 provides a comprehensive list of somatic mutations identified via whole-exome sequencing in 18 MEC tumor samples.

Supplementary Table S3 contains information on the clinical characteristics and mutational landscapes of MEC tumors of varying histologic grades.

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NOTCH1 mutations have been reported to occur in 10% to 15% of head and neck squamous cell carcinomas (HNSCC). To determine the significance of these mutations, we embarked upon a comprehensive study of NOTCH signaling in a cohort of 44 HNSCC tumors and 25 normal mucosal samples through a set of expression, copy number, methylation, and mutation analyses. Copy number increases were identified in NOTCH pathway genes, including the NOTCH ligand JAG1. Gene set analysis defined a differential expression of the NOTCH signaling pathway in HNSCC relative to normal tissues. Analysis of individual pathway-related genes revealed overexpression of ligands JAG1 and JAG2 and receptor NOTCH3. In 32% of the HNSCC examined, activation of the downstream NOTCH effectors HES1/HEY1 was documented. Notably, exomic sequencing identified 5 novel inactivating NOTCH1 mutations in 4 of the 37 tumors analyzed, with none of these tumors exhibiting HES1/HEY1 overexpression. Our results revealed a bimodal pattern of NOTCH pathway alterations in HNSCC, with a smaller subset exhibiting inactivating NOTCH1 receptor mutations but a larger subset exhibiting other NOTCH1 pathway alterations, including increases in expression or gene copy number of the receptor or ligands as well as downstream pathway activation. Our results imply that therapies that target the NOTCH pathway may be more widely suitable for HNSCC treatment than appreciated currently. Cancer Res; 74(4); 1091–104. ©2013 AACR.

PDF file - 82K, Growth effects of NOTCH1 siRNA inhibition in HNSCC cells with wildtype NOTCH1 status. NOTCH1 was downregulated in UPCI-SCC090 (090, top, NOTCH1 wt) and SCC61 (bottom, NOTCH1 wt) by siRNA as described in methods. The effect of NOTCH1 downregulation on cell proliferation for these two cell lines is shown in the middle. The effect of siNOTCH1 on NOTCH1 expression (left) or expression of its targets (HES1 and HEY1, right) is also shown. The mRNA expression levels were calculated relative to GAPDH and were normalized to 1 in the control experiments with scrambled siRNA sequences. Experiments were performed in pentaplicates, mean plus-minus SEM were shown. *, p-value < 0.05.

PDF file - 73K, Significant overexpression of JAG1 (A) and PSEN1 (B) in the tumors with increased copy number gains in comparison to that in the normal tissues in the cohort of 44 HNSCC tumors and 25 normal mucosa. N, normal mucosa; T, HNSCC tumors; -, without JAG1(A) or PSEN1 (B) copy number gain; +, with JAG1 (A) or PSEN1 (B) copy number gain. Boxes represent the interquartile range (25th-75th percentile) and horizontal lines inside the boxes indicate median. Whiskers indicate the minimum and maximum values. P value was calculated by using t test.

PDF file - 169K, NOTCH pathway activation in HNSCC. A, Immunohistochemical analysis of NOTCH1, HES1 and HEY1 protein expression in HNSCC. Tissue microarray arrays with quadruplicates of samples from each of 56 HNSCC tumor and 11 non-tumor patients were stained with anti-NOTCH1, anti-HES1 or anti-HEY1 antibody, as described in methods. Top, the heat-map of immunohistochemical analysis for tissue microarray slides. Rows, genes; column, each individual sample. The average staining for four tissues was categorized to Strong (brown), Moderate (grey) or Weak/Negative (blue) staining. Samples are ranked by the pathology ID numbers in tumor (left) and normal (right) groups. Bottom: quantification of immunohistochemical data. The number and percentage of tumor (Tu) and normal (No) patient in strong, moderate and weak/negative category was quantified. P-values were calculated by comparing numeric scores in tumor vs normal sample by independent t test. The samples 57964, 58602, 22146, 5931, 26514 represent tumor samples X6, X7, X11, X28 and X34 from the original discovery cohort of 44 HNSCC tumors. B, Representative immunohistochemical results. The representative slides of positive or moderate staining are shown for tumors and compared to normal tissue. Bar, 100 um equivalent. Tumor (T) and normal (N) tissues on each sample are labeled. ID 22146 represented X11 samples, which were used both in array and in immunohistochemical analysis, where protein and RNA expression strongly correlate.

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PDF file - 54K, Effect of gamma-secretase inhibitor on the NOTCH1 pathway genes and cell growth in HNSCC cells with NOTCH1 wildtype status. UPCI-SCC090 cells were growing on the media supplemented with 0.2 uM gamma-secretase inhibitor XXI (GSI-XXI) for up to 72 hours. The effect of GSI-XXI on the NOTCH1 targets HES1 and HEY1 is shown on the left for UPSI-SCC090 cell line.

PDF file - 68K, Growth effects of HEY1 siRNA inhibition in HNSCC cells with wildtype NOTCH1 status. HEY1 was downregulated in UPCI-SCC090 and SCC61 by siRNA as described in methods. The effect of siHEY1 on the expression of HEY1 is shown on the left. The effect of HEY1 downregulation on cell proliferation for these two cell lines is shown on the right. Note, there is over 90% transfection efficiency of HEY1 downregulation for each cell line, however the strong growth inhibition effect was shown only for NOTCH1 wildtype 090 cell line.

PDF file - 108K, Validation of JAG1, JAG2, NOTCH1 and PSEN1 overexpression in TCGA HNSCC cohort. A, Overexpression of JAG1, JAG2 and NOTCH1 in tumors in comparison to that in normal tissues in the TCGA HNSCC cohort. B, Overexpression of JAG1 and PSEN1 in the tumors with increased copy number gains in comparison to that in the normal tissues as well as to that in the tumors without copy number gains in the TCGA HNSCC cohort. N, normal mucosa; T, HNSCC tumors; -, without JAG1 or PSEN1 copy number gain; +, with JAG1 or PSEN1 copy number gain. Dots, relative expression levels in different tissue samples. Boxes represent the interquartile range (25th-75th percentile) and horizontal lines inside the boxes indicate median. Whiskers indicate the minimum and maximum values. P value was calculated by using t test.

PDF file - 88K, Supplementary Table I. Baseline characteristics of the HNSCC patients for microarray analysis. Supplementary Table II. Short Tandem Repeat Profile of the 2 HNSCC Cell Lines. Supplementary Table III. NOTCH Signaling Pathway Genes assigned in KEGG pathway database and shown on expression microarrays. Supplementary Table IV. Summary of the mRNA levels of NOTCH signaling pathway genes in the cohort of 44 HNSCC tumors and 25 normal mucosas measured by Affymetrix expression array.

Head and neck squamous cell carcinoma (HNSCC) encompasses a spectrum of heterogeneous diseases originating in the oral cavity, pharynx, and larynx. Within the United States, head and neck cancer (HNC) accounts for 66,470 new cases, or 3% of all malignancies, annually. 1 The incidence of HNC is rising, largely driven by increases in oropharyngeal cancer. 2 - 4 Recent molecular and clinical advancements, particularly with regard to molecular and tumor biology, reflect the heterogeneity of the subsites contained within the head and neck. Despite this, existing guidelines for post-treatment surveillance remain broad without much consideration given to different anatomic subsites and etiologic factors (such as human papillomavirus [HPV] status or tobacco exposure). 5 Surveillance incorporating the physical examination, imaging, and emerging molecular biomarkers is an essential part of care for patients treated for HNC and allows for the detection of locoregional recurrence, distant metastases, and second primary malignancies aiming for better functional and survival outcomes. Additionally, it allows for evaluation and management of post-treatment complications.

PurposeThe theory-building around the quality of human resources has received extensive attention in recent years. Numerous quantitative studies discuss and test theories related to total quality management and human resource linkages. The study aims to understand interlinkages of quality and human resources using Interpretative Structural Modeling (ISM) methodology and DEMATEL.Design/methodology/approachThis paper uses ISM methodology to examine the interrelationship between the identified variables and the DEMATEL approach to find cause–effect relationships. An integrated approach helps managers for better total quality management (TQM) implementation. This study further extended using Total Interpretative Structural Modeling (TISM).FindingsThe integrated approach of ISM and DEMATEL shows that leadership development, hiring process and training development become most important for TQM implementation. The outcome of ISM shows customer satisfaction and corporate image are depending on other practices, where DEMATEL analysis revealed that eight practices cause and remaining are effective practices.Originality/valueThis research's integrated approach helps the firm identify essential practices, and further interdependency can be developed from cause and effect analysis. The study also provided a novel approach to implementing TQM practices.

Objectives To provide a consensus statement describing best practices and evidence regarding head and neck cancer survivorship. Methods Key topics regarding head and neck cancer survivorship were identified by the multidisciplinary membership of the American Head and Neck Society Survivorship, Supportive Care & Rehabilitation Service. Guidelines were generated by combining expert opinion and a review of the literature and categorized by level of evidence. Results Several areas regarding survivorship including dysphonia, dysphagia, fatigue, chronic pain, intimacy, the ability to return to work, financial toxicity, lymphedema, psycho‐oncology, physical activity, and substance abuse were identified and discussed. Additionally, the group identified and described the role of key clinicians in survivorship including surgical, medical and radiation oncologists; dentists; primary care physicians; psychotherapists; as well as physical, occupational, speech, and respiratory therapists. Conclusion Head and neck cancer survivorship is complex and requires a multidisciplinary approach centered around patients and their caregivers. As survival related to head and neck cancer treatment improves, addressing post‐treatment concerns appropriately is critically important to our patient's quality of life. There continues to be a need to define effective and efficient programs that can coordinate this multidisciplinary effort toward survivorship.

PurposeThe study of supply chain disruption (SCD) and supply chain resilience (SCR) remains to be studied deeply in the field of business management. The purpose of this paper is to showcase a framework of SCR strategies to reduce the adverse effects of SCD using systematic literature review and data visualization.Design/methodology/approachUsing a systematic literature review approach, the paper explores the concepts of supply chain disruption and supply chain resilience. Through rigorous systematic screening, authors studied papers on both the concepts and have proposed a framework for the same. The authors also have used data visualization and network diagram approaches for better understanding of the topic.FindingsThe systematic literature review of both the concepts brings out some exciting results which give a new direction to supply chain field. The outcome of this research also outlines numerous future research direction, which will be useful for the research community.Practical implicationsThe numerous strategies of SCR should be implemented by manufacturing as well as a service organization. The framework reported in this research help academician and practitioners to understand SCR and to easily overcome any level of disruption. Supply chain managers must also formulate strategies accordingly and make plans to continually expand the system.Originality/valueThis research is the first such attempt to showcase a formal systematic framework and co-occurrence networks as well as overlay networks of SCR and SCD.

Lip and oral cavity squamous cell carcinoma (SCC) develop from progressive dysplasia of these mucosal structures. The cancers are often preceded by premalignant lesions, and any nonhealing ulcers of the lip or oral cavity should be biopsied. Some risk factors for these 2 subsites overlap and include tobacco use, alcohol use, and an immunocompromised state. Lip and oral cavity SCC are clinically staged based on physical examination and imaging. The 5-year overall survival for early-stage lip and oral cavity SCC is around 70% to 90% but decreases to about 50% for late-stage disease.