Squamous Tumors Research Articles

Perianal squamous cell carcinoma in a Quarter Horse colt

Squamous cell carcinoma (SCC) is a squamous epithelial neoplasm. They are solitary tumors with indolent expansion, are locally invasive, and can be seen in any part of the body. The most commonly affected sites are the head, orbital region, and genitalia of horses. Solar irradiation is one of the main causes, especially in depigmented and hairless areas. SCC is the neoplasm most frequently described in equine species. Several treatments have been described in horses, usually associated with surgical excision with different adjuvant therapies, hoping for a better prognosis and a decrease in cancer-related morbidity. Since the recurrence rates are high, especially in regions that do not have an adequate safety margin after tumor removal, multimodality treatment is essential. The aim of this report was to describe a case of perianal SCC in a Quarter Horse colt clinically treated with the immunomodulatory drug imiquimod. A three-year-old, grey-haired, male Quarter Horse was examined for diagnosis and treatment of an ulcerative lesion in the perianal region. According to the owner's report, the lesion appeared approximately 16 months ago. Based on the medical history and clinical examination, SCC was suspected. To confirm the clinical diagnosis, a biopsy was performed. Histological examination showed infiltrative neoplastic proliferation from the epidermis, consisting of malignant keratinocytes associated with hyperkeratosis, neutrophilic infiltrate, and foci of ulceration. The underlying dermis exhibited an intense chronic inflammatory infiltrate. The findings were compatible with SCC. Due to the location and extension of the lesion, we decided to use immunomodulatory therapy with imiquimod. After 16 weeks of imiquimod application, the lesion completely regressed. The horse was clinically followed for two years, and no recurrence was identified.

BLADDER CANCER: DIFFERENTIATION OF TYPES, AGE, SEX DISTRIBUTION AND ASSOCIATED VARIANTS WITH GRADATION

Background: Urinary bladder cancer (UBC) is the ninth most common cancer in the world, and the third most common cancer among men in West Asian countries, including Arab countries. Despite the increasing prevalence of UBC in developing countries, many places, including Yemen, do not have representative studies showing the true impact of these tumors on the population.
 Aims: To describe the different types of bladder cancers, and their distributions with age, and sex and to correlated different types with gradation, invasion muscles; and schistosomiasis in the last ten years in a single Yemini institute.
 Materials and methods: An observational descriptive study was performed on UBC patients who were subsequently diagnosed selectively by histopathological study in the Department of Pathology at the National Center for Public Health Laboratories (NCPHL) Sana'a, Yemen, over a period of about 10 years from January 1, 2012 to October 31, 2021. The study variables were cancer histological type, sex, grades and age. Types, grading and histological diagnoses were formed in line with the World Health Organization classification of bladder cancer.
 Results: Most of the cases were in the age group 60-69 years (32%), followed by 70 years (22.3%), and 50-59 years (20%). The most common UBCs were urothelial neoplasms (UNs) (71.5%), followed by squamous neoplasms (SNs) (24.4%) while other types were less frequent. There was a cytologically high grade with a significance rate (64.2%) with UNs. There was a significance rate of: schistosomiasis (43.8%) with SNs as OR=19.5 (p < 0.001), and invasion of muscle fibers (66.4%) with SNs as OR=3.3, UNs (37.1%) as OR=11.2 (p < 0.001). Also there was a significance rate of GII grade (46.1%) with SNs as OR=64.1 (p<0.001) and GNs (33.3%) as OR=3.8 (p =0.02). 
 Conclusion: The present study verification data congruence with those in the international literature and reports of neighboring countries, with some minor differences. This study documents a high incidence of urothelial neoplasms, with a male predominance and a peak incidence in the sixth decade of life. Imminent studies are needed to identify risk factors that increase cystitis in more detail and to study genetic susceptibility to inflammation and inflammatory markers before cancer is diagnosed.
 
 Peer Review History: 
 Received: 1 November 2021; Revised: 17 December; Accepted: 31 December, Available online: 15 January 2022
 Academic Editor: Dr. Nuray Arı, Ankara University, Turkiye, ari@ankara.edu.tr
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 Received file: Reviewer's Comments:
 Average Peer review marks at initial stage: 6.0/10
 Average Peer review marks at publication stage: 7.0/10
 Reviewers:
 Dr. Bilge Ahsen KARA, Ankara Gazi Mustafa Kemal Hospital, Turkey, ahsndkyc@gmail.com
 Dr. Eyassu Mathewos, School of public health, college of health sciences and medicine, Wolaita Soddo university- P.O. Box 158, Wolaita Soddo, Ethiopia. 
 Md. Monirul Islam, Department of Pharmacy, Faculty of Health Sciences, Northern University Bangladesh, Dhaka, Bangladesh. monirul.islam@nub.ac.bd
 Dr. Rawaa Souhil Al-Kayali, Aleppo University, Syria, rawah67@hotmail.com
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Impression Cytology's Reliability as an Effective Method for Ophthalmic Neoplasm Detection.

Background:The current investigation was intended to evaluate the precision of impression cytology and tissue histology in the detection of ocular surface neoplasia.Materials and Methods:We examined the histories of patients detected with ocular surface neoplasia at the Department of Ophthalmology, Kalinga Institute of Medical Sciences, Bhubaneswar. All the patients had their impressions cytology and tissue samples taken. The outcomes of both strategies were compared.Results:There were a total of 55 patients (33 males and 22 females) aged 12–99 years (average age, 51 years). Twenty patients had injuries to the right eye and 35 had injuries to the left eye. Conjunctival–corneal intraepithelial neoplasia (38.2%), squamous cell carcinoma (34.5%), squamous epithelium (10.9%), squamous papilloma (7.3%), conjunctival nevi (7.3%), Along with the most common histological research, malignant melanoma (1.8%). Compared with the histological results, impression cytology showed positive and negative assessment accuracies of 97.4% and 52.9%, respectively. In squamous neoplasms, squamous cell carcinoma exhibited a strong link with histology. The occurrence of dysplastic cells raised suspicion of malignancy.Conclusion:Because of its increased accuracy in detecting lesions, along with tissue histology, impression cytology exhibits enormous potential in identifying ocular surface neoplasia. However, impression cytology has an undesirable prognostic accuracy, indicating that it is a useful screening tool but cannot be considered as a “gold standard.”

TAp73α is Upregulated in the Most Common Human Cancers

The transcription factor p73 is a member of the p53 tumor suppressor gene family and one of the key regulators of apoptosis. TP73 gene encodes two protein isoforms classes with diverse functions, TAp73 and DNp73, and TAp73 expression in tumor tissues is altered. Unlike the TP53 gene, TP73 is not mutated in cancers. Here, we sought to explore the expression of p73 isoforms across eight major cancer types using the publicly available data deposited at the GDC data portal and the TSVdb database. Our results showed that TAp73α is overexpressed in breast invasive carcinoma, stomach adenocarcinoma, lung squamous cell carcinoma, colon adenocarcinoma, and esophageal carcinoma tumors, whereas the expression of DNp73 isoforms is downregulated in breast invasive carcinoma (DNp73α,β,γ), Prostate Adenocarcinoma (DNp73β), Lung Adenocarcinoma (DNp73α), Lung Squamous Cell Carcinoma (DNp73α) tumors. In summary, this study revealed that TAp73α has higher expression than the DNp73 isoforms in several cancer types.

Current Research Progress of the Role of LncRNA LEF1-AS1 in a Variety of Tumors.

Long non-coding RNAs (lncRNA), as key regulators of cell proliferation and death, are involved in the regulation of various processes in the nucleus and cytoplasm, involving biological developmental processes in the fields of immunology, neurobiology, cancer, and stress. There is great scientific interest in exploring the relationship between lncRNA and tumors. Many researches revealed that lymph enhancer-binding factor 1-antisense RNA 1 (LEF1-AS1), a recently discovered lncRNA, is downregulated in myeloid malignancy, acting mainly as a tumor suppressor, while it is highly expressed and carcinogenic in glioblastoma (GBM), lung cancer, hepatocellular carcinoma (HCC), osteosarcoma, colorectal cancer (CRC), oral squamous cell carcinoma (OSCC), prostatic carcinoma, retinoblastoma, and other malignant tumors. Furthermore, abnormal LEF1-AS1 expression was associated with tumorigenesis, development, survival, and prognosis via the regulation of target genes and signaling pathways. This review summarizes the existing data on the expression, functions, underlying mechanism, relevant signaling pathways, and clinical significance of LEF1-AS1 in cancer. It is concluded that LEF1-AS1 can serve as a novel biomarker for the diagnosis and prognosis of various tumors, thus deserves further attention in the future.

Higher metastasis and death rates in cutaneous squamous cell carcinomas with lymphovascular invasion

Lymphovascular invasion (LVI) is an aggressive histologic finding but is excluded from current staging systems due to its lack of demonstrated independent prognostic significance. To evaluate the impact of LVI on cutaneous squamous cell carcinoma tumor outcomes. In total, 10,707 cutaneous squamous cell carcinoma tumors from a 20-year, retrospective, multicenter cohort were stratified by the presence (LVI+) or absence (LVI-) of LVI. Outcomes (local recurrence, in-transit metastasis, nodal metastasis, disease-specific death) were compared based on low (Brigham and Women's Hospital [BWH] stage T1/T2a) and high (BWH T2b/T3) tumor stages. Of the 10,707 tumors, 78 had LVI. The analysis of low-stage BWH tumors showed the LVI+ group had a significantly higher 5-year cumulative incidence of local recurrence (LVI+: 12.3%; LVI-: 1.1%; P<.01), metastasis (LVI+: 4.2%; LVI-: 0.4%; P<.01), and disease-specific death (LVI+: 16.2%; LVI-: 0.4%; P<.01). The analysis of BWH high-stage tumors showed the LVI+ group maintained a higher 5-year cumulative incidence of metastasis (LVI+: 28.5%; LVI-: 16.8%; P=.06) and disease-specific death (LVI+: 25.3%; LVI-: 13.9%; P=.03), however, there was no difference in local recurrence (LVI+: 16.3%; LVI-: 15.8%; P=.11). Retrospective study design. LVI+cutaneous squamous cell carcinomas have higher rates of metastasis and death at 5years. Future staging systems should consider incorporating LVI.

Incorporation of vaginal brachytherapy to external beam radiotherapy in adjuvant therapy for high-risk early-stage cervical cancer: A comparative study

PURPOSETo examine trends, characteristics, and outcomes related to addition of vaginal brachytherapy (VBT) to external beam radiotherapy (EBRT) for adjuvant radiotherapy in high-risk early-stage cervical cancer. METHODS AND MATERIALSThis comparative study is a retrospective observational analysis of the National Cancer Institutes’ Surveillance, Epidemiology, and End Results Program. Surgically treated women with stage T1-2 cervical cancer who had high-risk factors (nodal metastasis and/or parametrial invasion) and received adjuvant radiotherapy from 2000 to 2018 were examined. Propensity score inverse probability of treatment weighting was used to assess the survival estimates for addition of VBT use. RESULTSAmong 2470 women with high-risk factors receiving EBRT, 760 (30.8%) had additional VBT. During the study period, there was an increasing trend of VBT use from 27.4% to 36.1% (p< 0.001). In a multivariable analysis, year of diagnosis and high-risk tumor factors: parametrial involvement, large tumor size, and use of chemotherapy remained independent characteristics associated with VBT use (all, p< 0.05). In propensity score-weighted models, VBT use with EBRT and EBRT alone had comparable overall survival (5-year rates 73.8% vs. 77.4%, hazard ratio [HR] 1.07, 95% confidence interval [CI] 0.92–1.25). Nonsignificant association was also observed in squamous or nonsquamous tumors, young or old age, low or high nodal ratio, chemotherapy use, and simple or radical hysterectomy (all, p> 0.05). Lastly, the addition of VBT was not associated with cervical cancer-specific survival (subdistribution-HR 1.15, 95% CI 0.94–1.41). CONCLUSIONSUtilization of VBT with EBRT for adjuvant radiotherapy in high-risk early-stage cervical cancer is increasing in the United States. Addition of VBT was associated with neither overall survival nor cancer-specific survival.

Regulation of 5-Hydroxymethylcytosine by TET2 Contributes to Squamous Cell Carcinoma Tumorigenesis

DNA methylation is a key regulatory event controlling a variety of physiological processes and can have dramatic effects on gene transcription. Methylated cytosine (5-methylcytosine) can be oxidized by the TET family of enzymes to 5-hydroxymethylcytosine (5-hmC), a key intermediate in the demethylation cycle, and 5-hmC levels are reduced in malignancies such as acute myeloid leukemia and melanoma. We constructed a tissue microarray of human cutaneous squamous cell carcinoma tumors and found a global reduction in 5-hmC levels compared with that in the adjacent skin. Using a murine K14-CreER system, we have found that loss of Tet2 promotes carcinogen-induced squamous cell carcinoma and cooperates with loss of Tp53 to drive spontaneous squamous cell carcinoma tumors in epithelial tissues. Analysis of changes in 5-hmC and gene expression after loss of Tet2 in the epidermis revealed focal alterations in 5-hmC levels and an increase in hair follicle transient amplifying cell genes along with a reduction in epidermal differentiation genes. These results show a role for TET2 in epidermal lineage specification, consistent with reported roles for TET enzymes in controlling lineage commitment in hematopoietic stem cells and embryonic stem cells and establishing TET2 as a bone fide tumor suppressor in squamous cell carcinoma.

Self-assembling protein nanocarrier for selective delivery of cytotoxic polypeptides to CXCR4+ head and neck squamous cell carcinoma tumors

Loco-regional recurrences and distant metastases represent the main cause of head and neck squamous cell carcinoma (HNSCC) mortality. The overexpression of chemokine receptor 4 (CXCR4) in HNSCC primary tumors associates with higher risk of developing loco-regional recurrences and distant metastases, thus making CXCR4 an ideal entry pathway for targeted drug delivery. In this context, our group has generated the self-assembling protein nanocarrier T22-GFP-H6, displaying multiple T22 peptidic ligands that specifically target CXCR4. This study aimed to validate T22-GFP-H6 as a suitable nanocarrier to selectively deliver cytotoxic agents to CXCR4+ tumors in a HNSCC model. Here we demonstrate that T22-GFP-H6 selectively internalizes in CXCR4+ HNSCC cells, achieving a high accumulation in CXCR4+ tumors in vivo, while showing negligible nanocarrier distribution in non-tumor bearing organs. Moreover, this T22-empowered nanocarrier can incorporate bacterial toxin domains to generate therapeutic nanotoxins that induce cell death in CXCR4-overexpressing tumors in the absence of histological alterations in normal organs. Altogether, these results show the potential use of this T22-empowered nanocarrier platform to incorporate polypeptidic domains of choice to selectively eliminate CXCR4+ cells in HNSCC. Remarkably, to our knowledge, this is the first study testing targeted protein-only nanoparticles in this cancer type, which may represent a novel treatment approach for HNSCC patients.

Genomic Signatures in HPV-Associated Tumors

Papillomaviruses dysregulate the G1/S cell cycle transition in order to promote DNA synthesis in S phase, which is a requirement for viral replication. The human papillomaviruses (HPV) E6 and E7 oncoproteins mediate degradation of the cell cycle regulators p53 and Rb, which are two of the most universally disrupted tumor-suppressor genes in all of cancer. The G1/S checkpoint is activated in normal cells to allow sufficient time for DNA repair in G1 before proceeding to replicate DNA and risk propagating unrepaired errors. The TP53 pathway suppresses a variety of such errors, including translocation, copy number alterations, and aneuploidy, which are thus found in HPV-associated tumors similarly to HPV-negative tumors with other mechanisms of TP53 disruption. However, E6 and E7 maintain a variety of other virus–host interactions that directly disrupt a growing list of other DNA repair and chromatin remodeling factors, implying HPV-specific repair deficiencies. In addition, HPV-associated squamous cell carcinomas tumors clinically respond differently to DNA damaging agents compared to their HPV negative counterparts. The focus of this review is to integrate three categories of observations: (1) pre-clinical understanding as to the effect of HPV on DNA repair, (2) genomic signatures of DNA repair in HPV-associated tumor genomes, and (3) clinical responses of HPV-associated tumors to DNA damaging agents. The goals are to try to explain why HPV-associated tumors respond so well to DNA damaging agents, identify missing pieces, and suggest clinical strategies could be used to further improve treatment of these cancers.

Inhibition of USP28 overcomes Cisplatin-resistance of squamous tumors by suppression of the Fanconi anemia pathway

Squamous cell carcinomas (SCC) frequently have an exceptionally high mutational burden. As consequence, they rapidly develop resistance to platinum-based chemotherapy and overall survival is limited. Novel therapeutic strategies are therefore urgently required. SCC express ∆Np63, which regulates the Fanconi Anemia (FA) DNA-damage response in cancer cells, thereby contributing to chemotherapy-resistance. Here we report that the deubiquitylase USP28 is recruited to sites of DNA damage in cisplatin-treated cells. ATR phosphorylates USP28 and increases its enzymatic activity. This phosphorylation event is required to positively regulate the DNA damage repair in SCC by stabilizing ∆Np63. Knock-down or inhibition of USP28 by a specific inhibitor weakens the ability of SCC to cope with DNA damage during platin-based chemotherapy. Hence, our study presents a novel mechanism by which ∆Np63 expressing SCC can be targeted to overcome chemotherapy resistance. Limited treatment options and low response rates to chemotherapy are particularly common in patients with squamous cancer. The SCC specific transcription factor ∆Np63 enhances the expression of Fanconi Anemia genes, thereby contributing to recombinational DNA repair and Cisplatin resistance. Targeting the USP28-∆Np63 axis in SCC tones down this DNA damage response pathways, thereby sensitizing SCC cells to cisplatin treatment.

USP28: Oncogene or Tumor Suppressor? A Unifying Paradigm for Squamous Cell Carcinoma.

Squamous cell carcinomas are therapeutically challenging tumor entities. Low response rates to radiotherapy and chemotherapy are commonly observed in squamous patients and, accordingly, the mortality rate is relatively high compared to other tumor entities. Recently, targeting USP28 has been emerged as a potential alternative to improve the therapeutic response and clinical outcomes of squamous patients. USP28 is a catalytically active deubiquitinase that governs a plethora of biological processes, including cellular proliferation, DNA damage repair, apoptosis and oncogenesis. In squamous cell carcinoma, USP28 is strongly expressed and stabilizes the essential squamous transcription factor ΔNp63, together with important oncogenic factors, such as NOTCH1, c-MYC and c-JUN. It is presumed that USP28 is an oncoprotein; however, recent data suggest that the deubiquitinase also has an antineoplastic effect regulating important tumor suppressor proteins, such as p53 and CHK2. In this review, we discuss: (1) The emerging role of USP28 in cancer. (2) The complexity and mutational landscape of squamous tumors. (3) The genetic alterations and cellular pathways that determine the function of USP28 in squamous cancer. (4) The development and current state of novel USP28 inhibitors.

MA14.07 EGFR-Mutant NSCLC With de novo or Acquired Squamous Histology: Molecular Features and Clinical Outcomes

Activating EGFR mutations occur predominantly in lung cancers with adenocarcinoma histology but can rarely be found in squamous tumors. Histologic “transformation” from adenocarcinoma to squamous is also seen at acquired resistance to EGFR TKIs. While squamous transformation may potentially be a driver of resistance, the biological characteristics of and treatment recommendations for squamous histology in the setting of EGFR-mutant NSCLC remain incompletely understood.

Cutaneous tricholemmal carcinoma: a 15-year single center experience.

Background Clear cell morphology has been described in several cutaneous neoplasms either as a specific feature of some entities either as a morphological variant in the spectrum, and these two entities are frequently considered together in the differential diagnosis. Methods We reviewed our series of cases occurred in our laboratory in order to further quantify the number of cases showing morphological features of tricholemmal differentiation and to investigate other clinical or histological difference. We retrieved 91 cases and, for each of them, all the clinical data regarding age, sex, clinical features, and clinical suspicious were collected, when available. Results The revision of the specimens concluded with a final diagnosis of tricholemmal carcinoma in 15 cases (17%), all the other cases were thus considered as squamous cell carcinoma with clear cell features. No statistically significant correlations were observed with the demografic or clinicopatholagical parameters such as age, sex or dimensions, but morphological revision highlighted a potentially greater vertical growth frequently not matched by a concomitant radial one in tricholemmal carcinoma than in squamous tumors. Conclusions The debate upon the diagnostic distinction of these tumors is still ongoing with authors proposing the tricholemmal carcinoma as a variant of a squamous cell carcinoma rather than a distinct entity. Further studies are needed to confirm our data and to evaluate the reproducibility of this feature.

MA11.06 Multi-Omic Characterization of Lung Tumors Implicates AKT and MYC Signaling in Adenocarcinoma to Squamous Cell Transdifferentiation

Lineage plasticity, the ability to transdifferentiate among distinct phenotypic identities, facilitates therapeutic resistance in multiple cancers. In lung adenocarcinomas (LUADs), this phenomenon includes small cell and squamous cell (LUSC) histologic transdifferentiation in the context of acquired resistance to targeted inhibition of driver mutations. The incidence of transdifferentiation into squamous carcinoma in EGFR mutant tumors, the setting where this histologic shift has been most extensively described, occurs in up to 9% of cases relapsed on osimertinib and has been associated to poor prognosis. The paucity of well annotated pre- and post-transdifferentiation clinical samples has precluded the performance of informative molecular analyses: little is known about the molecular mechanisms leading to this histological transition. We hypothesized that multi-parameter profiling of the components of mixed histology (LUAD/LUSC) tumors, together with pre- and post-transdifferntiation clinical samples, could provide insight into factors licensing lineage plasticity between these histologies and promoting squamous transdifferentiation of LUAD. We performed detailed genomic (whole exome sequencing), epigenomic (bisulfite sequencing), transcriptomic (RNAseq) and proteomic (antibody arrays) characterization. Clinical findings were validated in preclinical models including cell lines and patient-derived xenograft treatments. Our results suggest that LUSC transdifferentiation is primarily driven by transcriptional reprogramming rather than mutational events, and indicate that the resulting squamous tumors retain transcriptomic and methylation profiles of their previous LUAD state. We observed coordinated upregulation of PI3K/AKT, MYC and PRC2 pathway genes in the LUSC component of mixed histology tumors. Concurrent activation of PI3K/AKT and MYC induced squamous features in EGFR-mutant LUAD preclinical models, further augmented under selective pressure of osimertinib. Pharmacologic inhibition of EZH1/2 in combination with osimertinib prevented relapse and squamous transdifferentiation in an EGFR-mutant patient-derived xenograft model, and inhibition of EZH1/2 or PI3K/AKT signaling re-sensitized resistant transdifferentiated LUSC tumors to osimertinib. Our findings provide the first comprehensive molecular characterization of LUSC transdifferentiation, suggesting putative drivers and promising therapeutic targets to constrain or prevent lineage plasticity in this setting.

745 YIELD OF EXTENDED AND TOTAL MEDIASTINAL LYMPHADENECTOMY IN OESOPHAGEAL CANCER

Abstract The extent of lymphadenectomy in oesophageal cancer surgery is currently controversial, although current evidence shows that survival is directly related to the number of lymph nodes removed during surgery. Methods Descriptive study of patients with oesophageal cancer who underwent oesophagectomy with extended and total mediastinal lymphadenectomy using a minimally invasive approach (right prone thoracoscopy, laparoscopy and left cervicotomy) in our hospital for 2 years (2019 and 2020). Extended lymphadenectomy was indicated in patients with adenocarcinoma of the distal oesophagus, while total lymphadenectomy was indicated in patients with squamous tumours and adenocarcinoma of the middle oesophagus. The characteristics of the series studied and the results obtained in the 90 days postoperatively are described. Results 26 patients, mean age 65 ± 7.8 years, were operated. 21 with total mediastinal lymphadenectomy and 5 with extended lymphadenectomy. 80.7% received neoadjuvant treatment (CROSS scheme). The mean number of lymph nodes removed was 33.6 ± 14.3, with a 50% probability of being affected. As much in the lymphadenectomy of the right (106R) as in the left (106 L) recurrent groups, it was more frequently affected in the distal oesophagus adenocarcinomas. Postoperative morbidity was not negligible, with anastomotic leak rate of 7.7% (thoracic location) and 23.1% (cervical location) the majority mild, 23.1% of recurrent injury and 11.5% of chylothorax. Mortality at 90 days was 15.38%. Conclusion Based on our results, extended and total lymphadenectomy increases as much the global number of lymph nodes removed as the lymph nodes cancer-positive. In addition, it supports the performance of wide lymphadenectomies also in adenocarcinomas of the distal oesophagus. We cannot forget the greater radicalism is taxed with significant morbidity. We should remember the limitation of this study is the low number of cases, the extent of lymphadenectomy continues to be a matter of controversy.

Squamous Odontogenic Tumor of Posterior Maxilla-A Report of a New Unusual Case &amp; Literature Review

Squamous odontogenic tumor is a benign epithelial odontogenic tumor that is very unusual in the maxilla &amp; mandible. Mostly, these are present as single lesions, but rarely they can be multifocal lesions. The nature of maxillary lesions is more aggressive. Because of their benign nature, these lesions are frequently treated with conservative surgical techniques that include curettage and surgical enucleation. We will discuss the instance of a 29-year-old lady who was misdiagnosed and treated conservatively by us. This case was examined in the light of current knowledge of the prevalence, genesis, diagnosis, and treatment of squamous odontogenic tumors, as well as a literature review.

Genomic and Molecular Analyses Identify Molecular Subtypes of Pancreatic Cancer Recurrence

Genomic and Molecular Analyses Identify Molecular Subtypes of Pancreatic Cancer Recurrence

Programmed Death-Ligand 1 Tumor Proportion Score and Overall Survival From First-Line Pembrolizumab in Patients With Nonsquamous Versus Squamous NSCLC

IntroductionFor patients with NSCLC receiving immune checkpoint inhibitors, programmed death-ligand 1 (PD-L1) tumor proportion score (TPS) has been validated as a predictive biomarker for improved overall survival (OS). Nevertheless, its histology-specific predictive value in patients with advanced squamous versus nonsquamous cancers remains unclear. To evaluate the differential value of PD-L1 TPS as a predictive biomarker for OS after first-line pembrolizumab in patients with squamous versus nonsquamous NSCLC. MethodsRetrospective, observational study of patients diagnosed with having advanced NSCLC who were treated between October 2015 and April 2019 at community oncology clinics and academic medical centers in a deidentified electronic health record–derived database. Included patients were diagnosed with having advanced or metastatic NSCLC, received treatment with first-line, single-agent pembrolizumab, and had documentation of PD-L1 testing with a numeric result. Exclusion criteria included alterations in EGFR, ALK, and ROS1. The primary end point was OS from start of first-line pembrolizumab therapy by squamous or nonsquamous histology and PD-1 expression level measured by TPS (low, <50% or high, ≥50%). ResultsThe cohort of 1460 patients with NSCLC who received pembrolizumab as a first-line therapy had a mean age of 72 years. Histology was 28% squamous and 72% nonsquamous. PD-L1 expression was low in 13% and high in 87%. No meaningful differences in age, sex, or smoking history were observed by PD-L1 TPS or histology type. A generalized gamma model adjusting for sex and stage at diagnosis found that for patients with nonsquamous histology, high PD-L1 TPS was significantly associated with improved OS by a median OS difference of 8.4 months (p < 0.001). In contrast, for patients with squamous histology, there was no evidence of association between PD-L1 expression level and OS (p = 0.283). PD-L1–related incremental differences in median OS between the patients with squamous and nonsquamous tumors were significantly different (p = 0.034). ConclusionsAmong patients with NSCLC treated with first-line pembrolizumab, high PD-L1 TPS is associated with OS among patients with nonsquamous NSCLC, but not among patients with squamous NSCLC.

PO-0954 REPORT; REirradiation and PD-1 blockade On Recurrent squamous cell head and neck Tumors

PO-0954 REPORT; REirradiation and PD-1 blockade On Recurrent squamous cell head and neck Tumors