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Background: There are still certain gaps in the research that need to be filled despite the fact that numerous studies have looked into the transformation of odontogenic cysts into neoplastic lesions. To identify pertinent research that had been published and to synthesise the available data and provide an overview of the current body of knowledge, this review also sought to do so. Materials and Methods: Adopting the Preferred Reporting Items of Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a search strategy was implemented across several online databases to search for relevant articles as per the defined selection criterion. Results: After the search strategy was complete, 31 studies were chosen. Men tended to have more cancer than women. Swelling and discomfort were the primary pathology-related complaints. Although two cases were not detailed, radiologically, well-defined and poorly defined borders were reported in 18 and 11 participants, respectively. Squamous cell carcinoma with good differentiation (n = 12) was the most common cancer kind. More than 74% of patients were still living 6 months to 10 years following follow-up, four (12.90%) experienced recurrences and/or metastases and two (6.45%) experienced a disease-related mortality between 2 months and a year. Conclusion: Prompt surgical follow-ups and cautious excision of odontogenic cysts are essential to avoiding neoplastic change and recurrence. Future research is required to look at possible reasons why odontogenic cysts can convert neoplastically.

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The hyperplasia-carcinoma sequence is a stepwise tumourigenic programme towards endometrial cancer in which normal endometrial epithelium becomes neoplastic through non-atypical endometrial hyperplasia (NAEH) and atypical endometrial hyperplasia (AEH), under the influence of unopposed oestrogen. NAEH and AEH are known to exhibit polyclonal and monoclonal cell growth, respectively; yet, aside from focal PTEN protein loss, the genetic and epigenetic alterations that occur during the cellular transition remain largely unknown. We sought to explore the potential molecular mechanisms that promote the NAEH-AEH transition and identify molecular markers that could help to differentiate between these two states. We conducted target-panel sequencing on the coding exons of 596 genes, including 96 endometrial cancer driver genes, and DNA methylome microarrays for 48 NAEH and 44 AEH lesions that were separately collected via macro- or micro-dissection from the endometrial tissues of 30 cases. Sequencing analyses revealed acquisition of the PTEN mutation and the clonal expansion of tumour cells in AEH samples. Further, across the transition, alterations to the DNA methylome were characterised by hypermethylation of promoter/enhancer regions and CpG islands, as well as hypo- and hyper-methylation of DNA-binding regions for transcription factors relevant to endometrial cell differentiation and/or tumourigenesis, including FOXA2, SOX17, and HAND2. The identified DNA methylation signature distinguishing NAEH and AEH lesions was reproducible in a validation cohort with modest discriminative capability. These findings not only support the concept that the transition from NAEH to AEH is an essential step within neoplastic cell transformation of endometrial epithelium but also provide deep insight into the molecular mechanism of the tumourigenic programme. © 2024 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

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Background: Odontogenic cysts have the potential to transform into neoplasms. However, the characteristics of those which transformed to neoplastic tissues have not been well described and the exact causes of that phenomenon are not yet clear. Objectives: This study aims to describe characteristics of odontogenic cysts that transformed into neoplasms and to look for their potential etiologies. Data Sources: English-written studies indexed in PubMed, Science Direct, and Proquest were assessed using keywords verified by Medical Subject Headings: 'Odontogenic Cyst' and 'Neoplastic Cell Transformation'. Study Eligibility Criteria: Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA) guidelines were used as guidance. Participants: Following steps in PRISMA guidelines, 19 articles were fully reviewed (three case series and 16 case reports) with 27 subjects of 16 males (59%) and 11 females (41%) from 15 to 86 years old. Results: Cystic origins were eight dentigerous cysts, four odontogenic keratocysts, two residual cysts, one radicular cyst, one calcifying odontogenic cyst, one follicular cyst, one glandular odontogenic cyst, and nine unspecified odontogenic cysts that transformed to ameloblastoma (3 cases) and carcinoma (24 cases). Limitations: Neoplastic transformations of odontogenic cysts arose from epithelial remnants of inadequate odontogenic cyst removal and chronic inflammation due to infection. However, the exact causes of their transformations remain unclear. Conclusions: Therefore, careful removal of odontogenic cysts and regular postoperative follow-ups are key to prevent recurrence and neoplastic transformation. Future studies are needed to investigate potential causes of neoplastic transformation of odontogenic cysts.

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OBJECTIVES: Lung cancer models in large animals are lacking. Oncopigs are transgenic pigs that carry both KRASG12D and TP53R167H Cre-inducible mutations. This study aimed to develop and histologically characterize a swine model of lung cancer that could serve for preclinical studies evaluating locoregional therapies. MATERIALS AND METHODS: In two Oncopigs, an adenoviral vector encoding the Cre-recombinase gene (AdCre) was injected endovascularly through the pulmonary arteries or inferior vena cava. In two other Oncopigs, a lung biopsy was performed and incubated with AdCre, before reinjecting the mixture into the lungs percutaneously. Animals were clinically and biologically (complete blood count, liver enzymes and lipasemia) monitored. Obtained tumors were characterized on computed tomography (CT) and on pathology and immunohistochemistry (IHC). RESULTS: Neoplastic lung nodules developed following 1 (1/10, 10%) endovascular inoculation, and 2 (2/6, 33%) percutaneous inoculations. All lung tumors were visible at the 1-week CT, and appeared as well-circumscribed solid nodules, with a median longest diameter of 14 mm (range: 5-27 mm). Only one complication occurred: an extravasation of the mixture into the thoracic wall during a percutaneous injection that resulted in a thoracic wall tumor. Pigs remained clinically healthy during the entire follow-up (14-21 days). On histology, tumors consisted of inflammatory undifferentiated neoplasms composed of atypical spindle and epithelioid cells and/or a fibrovascular stroma and abundant mixed leukocytic infiltrate. On IHC, atypical cells diffusely displayed expression of vimentin and some showed expression of CK WSS and CK 8/18. The tumor microenvironment contained abundant IBA1 + macrophages and giant cells, CD3 + T cells, and CD31 + blood vessels. CONCLUSION: Tumors induced in the lungs of Oncopigs are fast growing poorly differentiated neoplasms associated with a marked inflammatory reaction that can be easily and safely induced at site specific locations. This large animal model might be suitable for interventional and surgical therapies of lung cancer.

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Squamous cell carcinoma (SCC) arising from an epidermal inclusion cyst (EIC) is uncommon. We present a case of a 70-year-old man with a scalp nodule with persistent discharge that was resected based on the clinical impression of an EIC. Histopathologic exam showed an infundibular EIC with an epidermal type of squamous epithelium; however, some of the cyst lining and lumen was replaced by squamous proliferation with malignant features. There are 56 cases of SCC arising in EICs reported in the English literature. Though suspected EICs are commonly benign, a thorough pathologic evaluation is required to rule out malignancy.

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Background: Recurrence in pleomorphic adenoma (PA) has been debated as a risk factor for malignant transformation (MT). In this study, we investigated whether recurrence is a risk factor for MT, by longitudinally analyzing cases with recurrent PA (RPA), and carcinomas from PA (CXPA) or RPA (CXRPA). Methods: The study population included 24 CXPA, 24 RPA, 6 CXRPA, and 386 PA cases (study period 2010−2018). Time and event data were collected from the medical documents to identify the time−event sequences. Results: The time interval to MT in CXRPA was significant longer than that of benign recurrence (median 342.0 vs. 109.5 months). In CXRPA, the recurrence intervals were not shorter than those in RPA according to recurrence frequency. Crudely, the MT rate was 5.9% among primary cases and 20.0% among recurrent cases. However, the time-adjusted MT rates increased up to 11.4% (incubation time > 60 months) and 20.0% (>120 months) in primary cases, which were not different from recurrent cases. Conclusion: In these longitudinal analyses, we did not find any clinical evidence that recurrence facilitates MT in the background of PA. Instead, a long incubation time seems to be a key factor for MT of underlying RPA.

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Sea stars or starfish (class Asteroidea) and holothurians or sea cucumbers (class Holothuroidea), belonging to the phylum Echinodermata (echinoderms), are characterized by different sets of glycosidic metabolites: the steroid type in starfish and the triterpene type in holothurians. However, herein we report the isolation of eight new triterpene glycosides, pacificusosides D−K (1−3, 5−9) along with the known cucumarioside D (4), from the alcoholic extract of the Far Eastern starfish Solaster pacificus. The isolated new compounds are closely related to the metabolites of sea cucumbers, and their structures of 1−3 and 5−9 were determined by extensive NMR and ESIMS techniques. Compounds 2, 5, and 8 have a new type of tetrasaccharide chain with a terminal non-methylated monosaccharide unit. Compounds 3, 6, and 9 contain another new type of tetrasaccharide chain, having 6-O-SO3-Glc as one of the sugar units. The cytotoxic activity of 1−9 against non-cancerous mouse epidermal cells JB6 Cl41 and human melanoma cell lines SK-MEL-2, SK-MEL-28, and RPMI-7951 was determined by MTS assay. Compounds 1, 3, 4, 6, and 9 showed potent cytotoxicity against these cell lines, but the cancer selectivity (SI > 9) was observed only against the SK-MEL-2 cell line. Compounds 1, 3, 4, 6, and 9 at the non-toxic concentration of 0.1 µM significantly inhibited neoplastic cell transformation of JB6 Cl41 cells induced by chemical carcinogens (EGF, TPA) or ionizing radiation (X-rays and UVB). Moreover, compounds 1 and 4 at the non-toxic concentration of 0.1 µM possessed the highest inhibiting activity on colony formation among the investigated compounds and decreased the colonies number of SK-MEL-2 cells by 64% and 70%, respectively. Thus, triterpene glycosides 1 and 4 can be considered as prospective cancer-preventive and anticancer-compound leaders.

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The aim of this study was to identify the risk factors associated with developing oral squamous cell carcinoma (OSCC) from surgically excised oral leukoplakia (OL) in patients with previous oral cavity cancer. Clinicopathological data of 84 patients who were treated for OL between July 2002 and July 2020 and who had previously received treatment for OSCC were reviewed retrospectively. The follow-up time ranged from 0.69 to 17.99 years (mean 6.78 ± 4.25 years). The overall cumulative malignant transformation rate was 25% and the annual transformation rate was 5.73%. Kaplan-Meier survival analysis and the log-rank test showed that Candida infection (P = 0.010) was a risk factor associated with malignant transformation. In the multivariate Cox regression analysis, tongue and floor of the mouth as the location of the leukoplakia (P = 0.039), multifocal lesions of OL (P = 0.047), and Candida infection (P = 0.018) were the three independent prognostic factors related to the development of OSCC from the treated OL. A cautious approach to OL of the tongue with Candida infection or multifocal disease in this group of patients would be appropriate.

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Cryptotanshinone is known for its inhibitory activity against tumorigenesis in various human cancer cells. However, exact mechanisms underlying the anticancer effects of cryptotanshinone are not fully elucidated. Here, we propose a plausible molecular mechanism, wherein cryptotanshinone represses rapamycin-sensitive mTORC1/S6K1 mediated cancer cell growth and cell transformation. We investigated the various effects of cryptotanshinone on the mTORC1/S6K1 axis, which is associated with the regulation of cell growth in response to nutritional and growth factor signals. We found that cryptotanshinone specifically inhibited the mTORC1-mediated phosphorylation of S6K1, which consequently suppressed the clonogenicity of SK-Hep1 cells and the neoplastic transformation of JB6 Cl41 cells induced by insulin-like growth factor-1. Finally, we observed that cryptotanshinone prevented S6K1 from binding to the Raptor/mTOR complex, rather than regulating mTOR and its upstream pathway. Overall, our findings provide a novel mechanism underlying anti-cancer effects cryptotanshinone targeting mTORC1 signaling, contributing to the development of anticancer agents involving metabolic cancer treatment.

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Sporadic colorectal cancer (CRC) is a leading cause of worldwide cancer mortality. It arises from a complex milieu of host and environmental factors, including genetic and epigenetic changes in colon epithelial cells that undergo mutation, selection, clonal expansion, and transformation. The gut microbiota has recently gained increasing recognition as an additional important factor contributing to CRC. Several gut bacteria are known to initiate CRC in animal models and have been associated with human CRC. In this Review, we discuss the factors that contribute to CRC and the role of the gut microbiota, focusing on a recently described mechanism for cancer initiation, the so-called microbiota-induced bystander effect (MIBE). In this cancer mechanism, microbiota-driven parainflammation is believed to act as a source of endogenous mutation, epigenetic change and induced pluripotency, leading to the cancerous transformation of colon epithelial cells. This theory links the gut microbiota to key risk factors and common histologic features of sporadic CRC. MIBE is analogous to the well-characterized radiation-induced bystander effect. Both phenomena drive DNA damage, chromosomal instability, stress response signaling, altered gene expression, epigenetic modification and cellular proliferation in bystander cells. Myeloid-derived cells are important effectors in both phenomena. A better understanding of the interactions between the gut microbiota and mucosal immune effector cells that generate bystander effects can potentially identify triggers for parainflammation, and gain new insights into CRC prevention.

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Halomonas halocynthiae KMM 1376T is a Gram-negative bacterium that has been isolated from gill tissue of the ascidian Halocynthia aurantium. Mild acid hydrolysis of the lipopolysaccharide of H. halocynthiae KMM 1376T afforded an O-polysaccharide, which was studied by sugar analysis and NMR spectroscopy. The following structure of the O-polysaccharide presented as sulfated α-D-mannan was established: →2)-α-D-Manp3,6S-(1→3)-α-D-Manp2Ac(∼71%)6S-(1→3)-α-D-Manp-(1→. Study of biological activity has shown that sulfated α-D-mannan can specifically reduce the cell viability and colony formation of the human breast adenocarcinoma MDA-MB-231 cells in a concentration-dependent manner. In addition, polysaccharide inhibits epidermal growth factor induced neoplastic cell transformation in mouse epidermal JB6 Cl41 cells.

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Inflammatory bowel diseases (IBDs) increase the risk for colorectal cancer (CRC). In IBD, the evolution of potential tumor clones occurs long before neoplastic lesions become evident and these clones can be undetectable by endoscopy and histology at early stages. The spectrum of genomic alterations in IBD-associated colorectal carcinogenesis is distinct from the changes observed in the sporadic adenoma-carcinoma sequence. Predominant alterations include aneuploidies and mutations of TP53, which both occur early in IBD-related tumorigenesis. In some IBD patients, genomic alterations can already be detected in colonic mucosa without any histologic signs of dysplasia. Genomic analysis of multiregional samples from colectomy specimens of IBD patients revealed distinct tumor evolutionary patterns. This suggests an increased genomic instability in the chronically inflamed bowel that enables the emergence of multiple, phylogenetically unrelated neoplastic lesions within the colorectum of a single IBD patient. This article summarizes the genomic alterations underlying IBD-associated colorectal tumorigenesis and the evolutionary patterns from inflamed, not yet dysplastic epithelium to CRC. Furthermore, it is discussed how this knowledge can eventually be exploited for early detection of malignant progression of IBD and thus help to improve the clinical management and surveillance schedule of IBD patients.

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ABSTRACT Tumor development is a multistep process whereby local mechanisms enable somatic mutations during preneoplastic stages. Once a tumor develops, it becomes a complex organ composed of multiple cell types. Interactions between malignant and non-transformed cells and tissues create a tumor microenvironment (TME) comprising epithelial cancer cells, cancer stem cells, non-tumorous cells, stromal cells, immune-inflammatory cells, blood and lymphatic vascular network, and extracellular matrix. We review reports and present a hypothesis that postulates the involvement of growth hormone (GH) in field cancerization. We discuss GH contribution to TME, promoting epithelial-to-mesenchymal transition, accumulation of unrepaired DNA damage, tumor vascularity, and resistance to therapy. Arch Endocrinol Metab. 2019;63(6):568-75

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OBJECTIVE: To identify the prognostic biomarker candidates for stratification and long-term surveillance of oral leukoplakia progressing to cancer via a systematic literature review. MATERIALS AND METHODS: Systematic searches with no date restrictions were conducted on March 29, 2018, targeting the databases PubMed (Ovid), EMBASE (Ovid), EBM (Ovid), and Web of Science (ISI). Bias was assessed using the Quality in Prognosis Studies tool. Biomarkers were stratified based on hallmarks of cancer. RESULTS: Inclusion criteria were met by 25 of 3,415 studies. A range of biomarkers were evaluated experimentally for risk stratification, prognosis, and surveillance of oral leukoplakia in tissue, blood, and saliva. However, the studies were highly heterogeneous and require further validation. Biomarkers reported in these studies included inflammatory or oxidative markers, growth factors, ion channels, genetic and cellular regulatory factors, and epigenetic biomarkers. Studies tended to include small sample sizes, under-reported or variably reported histopathological data, did not address potential confounding, reported limited/variable follow-up data, or lacked a control group. Inclusion of subsets from chemoprevention trials may have introduced bias regarding reported malignant transformation rates and accuracy of prognostic biomarkers. CONCLUSIONS: This review identified insufficient longitudinal evidence to support validated prognostic biomarkers for oral leukoplakia. Further studies are needed to identify molecular targets with the potential to mitigate risk of malignant transformation.

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OBJECTIVE: This study aimed to analyze the clinical features of clear cell carcinoma in relation to endometriosis and to determine an appropriate surveillance strategy for the early detection of malignant transformation of endometrioma in asymptomatic patients. METHODS: We retrospectively reviewed the clinicopathologic data of 50 patients with ovarian clear cell carcinoma. Clinicopathologic characteristics, treatment outcomes, and the association between endometriosis and the risk of malignant transformation were analyzed. RESULTS: Ten (20%) patients had been diagnosed with endometrioma before the diagnosis of clear cell carcinoma. The median period from the diagnosis of endometrioma to clear cell carcinoma diagnosis was 50 months (range, 12-213 months). After complete staging surgery, histological confirmation of endometriosis was possible in 35 (70%) patients. Of the 50 patients, 39 (78%) had not undergone any gynecologic surveillance until the onset of symptoms, at which time many of them presented with a rapidly growing pelvic mass (median 10 cm, range 4.6-25 cm). With the exception of 2 patients, all cancer diagnoses were made when the patients were in their late thirties, and median tumor size was found to increase along with age. Asymptomatic patients (n=11) who had regular gynecologic examinations were found to have a relatively smaller tumor size, lesser extent of tumor spread, and lower recurrence rate (P=0.011, 0.283, and 0.064, respectively). The presence of endometriosis was not related to the prognosis. CONCLUSION: Considering the duration of malignant transformation and the timing of cancer diagnosis, active surveillance might be considered from the age of the mid-thirties, with at least a 1-year interval, in patients with asymptomatic endometrioma.

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OBJECTIVE: This study aimed to analyze the clinical features of clear cell carcinoma in relation to endometriosis and to determine an appropriate surveillance strategy for the early detection of malignant transformation of endometrioma in asymptomatic patients. METHODS: We retrospectively reviewed the clinicopathologic data of 50 patients with ovarian clear cell carcinoma. Clinicopathologic characteristics, treatment outcomes, and the association between endometriosis and the risk of malignant transformation were analyzed. RESULTS: Ten (20%) patients had been diagnosed with endometrioma before the diagnosis of clear cell carcinoma. The median period from the diagnosis of endometrioma to clear cell carcinoma diagnosis was 50 months (range, 12–213 months). After complete staging surgery, histological confirmation of endometriosis was possible in 35 (70%) patients. Of the 50 patients, 39 (78%) had not undergone any gynecologic surveillance until the onset of symptoms, at which time many of them presented with a rapidly growing pelvic mass (median 10 cm, range 4.6–25 cm). With the exception of 2 patients, all cancer diagnoses were made when the patients were in their late thirties, and median tumor size was found to increase along with age. Asymptomatic patients (n=11) who had regular gynecologic examinations were found to have a relatively smaller tumor size, lesser extent of tumor spread, and lower recurrence rate (P=0.011, 0.283, and 0.064, respectively). The presence of endometriosis was not related to the prognosis. CONCLUSION: Considering the duration of malignant transformation and the timing of cancer diagnosis, active surveillance might be considered from the age of the mid-thirties, with at least a 1-year interval, in patients with asymptomatic endometrioma.

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Inverted papilloma is a benign epithelial tumor that arises from the sinonasal epithelium and occurs in 0.5–4% of all sinonasal tumors. Although benign, it is associated with malignant transformation in 2–27% of the cases, with the most commonly accompanying malignant tumor being squamous cell carcinoma. The malignant transformation of inverted papilloma into adenocarcinoma is extremely rare, with two cases reported worldwide to date. Here, along with a literature review, we report a recent case of a 53-year-old man with non-intestinal type adenocarcinoma associated with a sinonasal inverted papilloma. This case shows the possibility of a malignant transformation of inverted papilloma into non-intestinal type adenocarcinoma, which may be associated with human papilloma virus and thus requires further investigation.

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Antecedentes: Los desórdenes potencialmente malignos (DPM) son aquellas situaciones clínicas en la cavidad bucal que presentan un riesgo aumentado de malignización neoplásica, debido a la exposición a factores de riesgo o alteraciones genéticas. Es necesario realizar revisiones de la evidencia de este tipo de desórdenes para desarrollar o actualizar guías de práctica clínica idóneas. Objetivo: Identificar, a través de una revisión integrativa de la literatura, la evidencia reciente sobre DPM de la cavidad bucal y su transformación maligna, con el fin de proporcionar recomendaciones de manejo diagnóstico y terapéutico. Métodos: Se realizó una búsqueda de literatura en las bases de datos PubMed, Elsevier, SciELO y EMBASE, utilizando la combinación de seis descriptores. Resultados: La búsqueda inicial arrojó 1743 títulos y la muestra consistió en 67 artículos después de aplicar los criterios de inclusión y exclusión. Las DPM identificadas fueron liquen plano oral, palatitis nicotínica, hábito de fumar invertido, queilitis actínica, eritroplasia y leucoplasia oral y úlcera traumática crónica. Conclusión: Cada tipo de lesión tiene distinto potencial de malignización, entre los cuales la eritroplasia, el liquen plano oral variante erosivo y la queilitis actínica poseen el mayor riesgo.

Background: Potentially malignant disorders (PMD) are clinical oral cavity conditions that pose an increased risk of neoplastic malignization due to exposure to risk factors or genetic alterations. It is necessary to conduct evidence-based reviews of this type of disorders to develop or update adequate clinical practice guidelines. Purpose: Identify, through an integrative review of literature, recent evidence on PMDs in the oral cavity and their malignant transformation, in order to provide diagnostic and treatment recommendations. Methods: A literature search was carried out in the PubMed, Elsevier, SciELO, and EMBASE, using a combination of six descriptors. Results: The initial search showed 1743 titles and the sample, after applying the inclusion and exclusion criteria, consisted of 67 articles. The PMDs identified were oral lichen planus, nicotinic palatitis, inverted smoking habit, actinic cheilitis, oral erythroplakia and leukoplakia, and chronic traumatic ulcer.

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OBJECTIVE: Caffeic acid phenethyl ester (CAPE), a natural honeybee product exhibits a spectrum of biological activities including antimicrobial, anti-inflammatory, antioxidant and antitumor actions. The purpose of this research was to investigate the anticancer potential of CAPE and its molecular mechanism in human oral cancer cell lines (YD15, HSC-4 and HN22 cells). DESIGN: To determine the apoptotic activity of CAPE and identify its molecular targets, trypan blue exclusion assay, soft agar assay, Western blot analysis, DAPI staining, and live/dead assay were performed. RESULTS: CAPE significantly suppressed transformation of neoplastic cells induced by epidermal growth factor (EGF) and 12-O-tetradecanoylphorbol 13-acetate (TPA) without inhibiting growth. CAPE treatment inhibited cell growth, increased the cleavages of caspase-3 and poly (ADP-ribose) polymerase (PARP), and augmented the number of fragmented nuclei in human oral cancer cell lines. CAPE activated Bax protein causing it to undergo a conformational change, translocate to the mitochondrial outer membrane, and oligomere. CAPE also significantly increased Puma expression and interestingly Puma and Bax were co-localized. CONCLUSION: Overall, these results suggest that CAPE is a potent apoptosis-inducing agent in human oral cancer cell lines. Its action is accompanied by up-regulation of Bax and Puma proteins.

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The true incidence of inverted papilloma (IP) is not yet known. From hospital-based studies, its incidence has been estimated to approximately 0.5/100,000 person years. Earlier hospital case studies have shown that IP can undergo a malignant transformation in 1-53 %. The frequency of its malignant transformation on a population basis is unknown. To our knowledge, no standardised incidence ratio (SIR) has been reported for malignancies among IPs. This study aims to investigate these incidences on a population basis. Using the data from the Swedish Cancer Registry (SCR), we have identified patients with IP and patients with Squamous Cell Carcinoma (SCC) diagnosed between 1960 and 2010 in Sweden. Incidence of IP and incidence of SCC among patients with IP and SIR were analyzed. Eight hundred and fourteen patients with IP were identified. The incidence of IPs reported to the SCR increased from 1960 to 2010. In this cohort, SCC was overrepresented, as compared with the general population. The incidence of IP in the Swedish population seems to have increased.

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