Onset Of Basal Cell Carcinoma Research Articles

Dysembryogenetic Pathogenesis of Basal Cell Carcinoma: The Evidence to Date.

The Basal Cell Carcinoma (BCC) is a sort of unique tumour due to its combined peculiar histological features and clinical behaviour, such as the constant binary involvement of the epithelium and the stroma, the virtual absence of metastases and the predilection of specific anatomical sites for both onset and spread. A potential correlation between the onset of BCC and a dysembryogenetic process has long been hypothesised. A selective investigation of PubMed-indexed publications supporting this theory retrieved 64 selected articles published between 1901 and 2024. From our analysis of the literature review, five main research domains on the dysembryogenetic pathogenesis of BCC were identified: (1) The correlation between the topographic distribution of BCC and the macroscopic embryology, (2) the correlation between BCC and the microscopic embryology, (3) the genetic BCC, (4) the correlation between BCC and the hair follicle and (5) the correlation between BCC and the molecular embryology with a specific focus on the Hedgehog signalling pathway. A large amount of data from microscopic and molecular research consistently supports the hypothesis of a dysembryogenetic pathogenesis of BCC. Such evidence is promoting advances in the clinical management of this disease, with innovative targeted molecular therapies on an immune modulating basis being developed.

Exploring the Changing Diagnostic Criteria of Gorlin-Goltz Syndrome: A Case Report

Gorlin-Goltz syndrome, also known as Gorlin syndrome, basal cell nevus syndrome, and nevoid basal cell carcinoma syndrome, is an autosomal dominant genetic disorder. Its hallmark is an early onset of basal cell carcinoma. Additionally, the syndrome is characterized by a spectrum of distinct clinical attributes encompassing oral, skeletal, ophthalmic, neurological, and developmental aberrations. This condition arises due to anomalies in the Hedgehog signaling pathway, leading to constant pathway activity and uncontrolled growth of tumor cells. Early identification of the disorder through available diagnostic methods and clinical and radiological findings is crucial for accurate diagnosis, which subsequently leads to the formulation of an effective treatment regimen. The purpose of this case report is to discuss the role of a dentist in early detection based on various author-prescribed criteria and the need for a multidisciplinary approach to the treatment of patients with this syndrome.

Wnt Signaling Pathways: From Inflammation to Non-Melanoma Skin Cancers.

Canonical and non-canonical Wnt signaling pathways are involved in cell differentiation and homeostasis, but also in tumorigenesis. In fact, an exaggerated activation of Wnt signaling may promote tumor growth and invasion. We summarize the most intriguing evidence about the role of Wnt signaling in cutaneous carcinogenesis, in particular in the pathogenesis of non-melanoma skin cancer (NMSC). Wnt signaling is involved in several ways in the development of skin tumors: it may modulate the inflammatory tumor microenvironment, synergize with Sonic Hedgehog pathway in the onset of basal cell carcinoma, and contribute to the progression from precancerous to malignant lesions and promote the epithelial-mesenchymal transition in squamous cell carcinoma. Targeting Wnt pathways may represent an additional efficient approach in the management of patients with NMSC.

Subsequent Cancers in Patients Affected with Moderate or Severe Chronic Graft-versus-Host Disease

Subsequent cancer (SC) is a significant cause of morbidity and mortality in long-term survivors after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Chronic graft-versus-host disease (cGVHD) and treatment-related immunosuppression have been recognized as risk factors for SC. This study sought to investigate the incidence and risk factors for SC in patients with established cGVHD, assessed separately for onset of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC)-categorized into nonmelanoma skin cancer (NMSC)-and all cancers other than NMSC. Two hundred and four patients were enrolled in the prospective cross-sectional cGVHD Natural History Study and underwent comprehensive clinical evaluation. Patients were followed-up with an annual survey. The cumulative incidences of NMSC and cancers other than NMSC with competing risks were estimated separately, and transplantation- and cGVHD-related factors were assessed for association with outcomes using Gray's test and multivariable Cox models. The time period for all analyses began at 2 years postevaluation to restrict analyses to patients presumed to not have had SC present at evaluation. Nineteen patients were diagnosed with NMSC and 19 were diagnosed with cancers other than NMSC, with 10-year cumulative incidences of 15.5% (95% confidence interval, 9.0% to 27.6%) and 13.8% (95% CI, 8.2% to 20.8%), respectively. Age at transplantation (hazard ratio [HR], 1.94; 95% CI, 1.23 to 3.06) and higher C-reactive protein level at evaluation (HR, 9.49; 95% CI, 1.26 to 71.58) were jointly associated with NMSC, and gastrointestinal cGVHD at evaluation (HR, 0.26; 95% CI, 0.09 to 0.78) was associated with reduced risk of NMSC. T cell depletion at transplantation (HR, 3.09; 95% CI, 1.17 to 8.20), lymphoma as an indication for transplantation (HR, 3.96; 95% CI, 1.56 to 10.05), and oral cGVHD severity at evaluation (HR, 4.36; 95% CI, 1.52 to 12.46) were jointly associated with cancers other than NMSC. This study estimates the incidence of SC in a population of allo-HSCT recipients with severe cGVHD and identifies correlations with the subsequent development of SC. These factors seem to differ between NMSC and cancers other than NMSC. Further longitudinal investigations accounting for dynamic and cumulative processes are needed to improve our understanding and management of SC.

Cosmetic Tattooing and Early Onset Basal Cell Carcinoma: A Population-based Case-Control Study from New Hampshire.

Cosmetic tattoos use dyes with carcinogenic potential. Skin cancers arising in tattoos have been reported. We investigated whether risk of early onset basal cell carcinoma was related to the site and colors of cosmetic tattoos as part of a population-based case-control study of cases (ages 25-50 years), identified from a state-wide surveillance system, and age- and gender-matched controls, selected from driver's license records, randomly assigned an anatomic site of the cases. One hundred fifty-six cases (17%) with early onset basal cell carcinoma and 213 controls (26%) reported cosmetic tattoos. Among those with tattoos, the adjusted odds ratio of basal cell carcinoma at the tattoo site compared to another site was 1.8 (95% confidence interval = 1.0, 3.2). We observed the strongest associations for yellow and green tattoo colors. Our preliminary findings support the possibility of an enhanced risk of early onset basal cell carcinomas at the site of cosmetic tattoos.

Nonmelanoma Skin Cancers: Embryologically Relevant Sites and UV Exposure.

Background:Traditionally, nonmelanoma skin cancers (NMSCs) are considered mainly UV-related malignancies. Nevertheless, a strong correlation between the embryologically relevant sites (ERS) of the head and neck and the preferential sites of onset of basal cell carcinomas (BCCs) has long been supposed and demonstrated. The aim of this research was the investigation of the potential correlation between the ERS of the head and neck and the sites of tumor onset in all of the NMSCs.Methods:The distribution of 1165 NMSC was correlated with the ERS of the head and neck using the universally accepted anatomical diagrams featuring the congenital head and neck clefts and an original anatomical diagram showing the most credited sites of the embryonic fusion planes of the auricle.Results:In our sample, both BCC and SSC display an increased likelihood of onset in the ERS of the head and neck. A proportion of 93.10% BCCs was distributed within ERS, while 6.90% derived from non-embryologically relevant sites (P < 0.001). A proportion of 69.70% SCCs was distributed within ERS, while 30.30% derived from non-embryologically relevant sites (P < 0.001). The probability of tumors within ERS was significantly higher for BCC versus SCC (P < 0.001), with BCCs having a 5-fold increase in the probability of occurring in ERS compared to SCCs (P < 0.001).Conclusions:The ERS might host areas of cellular instability yielding to the development of an NMSC. The environmental UV exposure plays a relatively main role versus dysontogenic factors in the pathogenesis of SCC.

Basal cell carcinoma genetic susceptibility increases the rate of skin ageing: a Mendelian randomization study.

Onset of basal cell carcinoma (BCC) is connected to skin ageing, but it is unclear whether higher BCC genetic susceptibility drives skin ageing. To investigate whether loci increasing genetic susceptibility to BCC also drive multiple features of skin ageing, independently of confounding factors, using Mendelian randomization. A Mendelian randomization study was conducted in older adults from the Leiden Longevity Study (N=604). A total of 25 BCC loci, selected based on a published genome-wide association study on BCC (P-value<5×10-8 ), were used as genetic instruments for the calculation of a standardized (mean=0, SD=1) weighted BCC genetic risk score. Based on facial photographs, we determined perceived age, and skin wrinkling and pigmented spot grading. A higher BCC genetic risk score was associated with a higher perceived age (adjusted for chronological age and sex) of 0.88years (95% CI: 0.44, 1.31; P-value=7.1e-5 ), greater wrinkling by 0.14 grades (95% CI: 0.05, 0.23; P-value=2.3e-3 ), and greater pigmented spots by 0.17 grades (95% CI: 0.08, 0.25; P-value=1.1e-4 ). These findings were weakened but still present after exclusion of gene variants in MC1R and IRF4 which have potential pleiotropic effects. Mechanisms influenced by genetic loci increasing susceptibility to BCC also drive skin ageing suggesting shared biology and shared targets for interventions.

Sam68 is required for the growth and survival of nonmelanoma skin cancer.

Although targeting DNA repair signaling pathways has emerged as a promising therapeutic for skin cancer, the relevance of DNA damage responses (DDR) in the development and survival of nonmelanoma skin cancer (NMSC), the most common type of skin cancer, remains obscure. Here, we report that Src‐associated substrate during mitosis of 68 kDa (Sam68), an early signaling molecule in DDR, is elevated in skin tumor tissues derived from NMSC patients and skin lesions from Gli2‐transgenic mice. Downregulation of Sam68 impacts the growth and survival of human tumor keratinocytes and genetic ablation of Sam68 delays the onset of basal cell carcinomas (BCC) in Gli2‐transgenic mice. Moreover, Sam68 plays a critical role in DNA damage‐induced DNA repair and nuclear factor kappa B (NF‐κB) signaling pathways in keratinocytes, hence conferring keratinocyte sensitivity to DNA damaging agents. Together, our data reveal a novel function of Sam68 in regulating DDR in keratinocytes that is crucial for the growth and survival of NMSC.

Abstract 3556: Sam68 is required for the growth and survival of non-melanoma skin cancer

Abstract Skin cancer is the most commonly diagnosed malignancy in the United States, and the incidence of skin cancer has increased dramatically over the last few decades. Non-melanoma skin cancer (NMSC), which includes squamous cell carcinomas (SCC) and basal cell carcinomas (BCC), is the most common type of skin cancer with substantial associated morbidity and mortality. Whereas targeting DNA repair signaling pathways has emerged as a promising therapeutic for skin cancer, the relevance of DNA damage responses (DDR) in the development and survival of non-melanoma skin cancer (NMSC) remains obscure. Here we report that Src-associated substrate during mitosis of 68 kDa (Sam68), an early signaling molecule in DDR, is elevated in skin tumor tissues derived from NMSC patients and skin lesions from Gli2-transgenic mice. Downregulation of Sam68 impacts the growth and survival of human tumor keratinocytes and genetic ablation of Sam68 delays the onset of basal cell carcinomas (BCC) in Gli2-transgenic mice. Moreover, Sam68 plays a critical role in DNA damage-induced DNA repair and nuclear factor kappa B (NF-κB) signaling pathways in keratinocytes, hence conferring keratinocyte sensitivity to DNA damaging agents. Together our data reveal a novel function of Sam68 in regulating DDR in keratinocytes that is crucial for the growth and survival of NMSC. Citation Format: Kai Fu, Fengyi Wan. Sam68 is required for the growth and survival of non-melanoma skin cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3556.

Correlation Between the Sites of Onset of Basal Cell Carcinoma and the Embryonic Fusion Planes in the Auricle.

Objectives:This study aims at the identification of the distribution of basal cell carcinomas (BCCs) in the auricle in correlation with the currently most credited sites of the embryonic fusion planes of the auricle.Methods:An overall number of 69 patients with 72 BCCs of the auricle were enrolled in the study over a period of 14 years, from June 2003 to October 2017. All the cases underwent medical preoperative digital photography and the specific location of each BCC was coded on an original full-size anatomical diagram of the auricle derived from the reports by Streeter, Wood-Jones, Park, Porter, and Minoux showing the currently most credited sites of the embryonic fusion planes arbitrarily featured as two 5-mm-wide ribbon-like areas: (1) the hyoid-mandibular fusion plane (HM-FP) running from the upper margin of the tragus toward the concha and then deflecting toward the lower margin of the tragus and (2) the free ear fold-hyoid fusion plane (FEFH-FP) running from the cranial-most portion of the helix to the mid-portion of the ascending helix. The latter fusion planes were comprehensively termed embryological fusion planes (EFP) while all of the remaining surface of the auricle was comprehensively termed non-fusion area (NFA). The surfaces of all of the latter areas were calculated using the ImageJ software.Results:According to our data, the greatest number of BCCs was observed within the currently most credited sites of the embryonic fusion planes of the auricle. The latter sites displayed a 12-fold increased tumor incidence in comparison with the remaining surface of the ear.Conclusions:A correspondence between the sites of onset of BCCs and the sites of merging and/or fusion of embryonal processes was demonstrated in the auricle. Therefore, the latter sites might be considered as high-risk areas for the development of a BCC. Such an evidence provides further support to the hypothesis of an embryological pathogenesis of BCC.

The epidemic spreading of basal cell carcinoma: incidence trend, demographic features, characteristics and risk factors in a retrospective study of 8557 lesions in Bologna. A 25-year analysis in a Dermatology referral center.

The aim of this study was to retrospectively analyze all the cases of BCC histologically diagnosed in the Cutaneous Tumor Center of Dermatology of Bologna University, in a period between 1990 and 2014. All the consecutive histopathologically diagnosed BCCs at the Dermatology of the Bologna University from 1990 to 2014 were retrospectively reviewed. We evaluated the absolute number of basal cell carcinoma (BCCs), the demographic features of patients and the characteristics of BCCs with statistically significant correlations. During the investigated 25 years, 8557 BCCs were collected in 7297 patients. We observed that the incidence of this cancer, after stabilizing around a plateau of 400 cases/year in 2005, progressively increased onwards reaching a maximum of cases (821) in 2014 (+105.25%), with an 8.32% mean increase per year in those last 9 years. Moreover, we found a significant correlation (P<0.01%) between gender and the onset of BCC, between the anatomic location and the occurrence of the tumor, between the onset of recurrent or new BCCs and sun exposure. The present study collects the largest series in the Italian literature focused on demographic features and characteristics of BCC, highlights its higher increasing incidence in Bologna and the need to improve preventive strategies to stem the epidemic diagnosis of BCC.

Distinct Histologic Subtypes and Risk Factors for Early Onset Basal Cell Carcinoma: A Population-Based Case Control Study from New Hampshire

Distinct Histologic Subtypes and Risk Factors for Early Onset Basal Cell Carcinoma: A Population-Based Case Control Study from New Hampshire

History of allergy and atopic dermatitis in relation to squamous cell and Basal cell carcinoma of the skin.

Little is known about whether history of allergies and atopy is related to the occurrence of keratinocyte cancers. Thus, we evaluated the association between history of allergies and atopy and the incidence of squamous cell carcinoma (SCC) and early onset basal cell carcinoma (BCC). As part of a population-based case-control study, interviews were conducted with 1,050 residents of New Hampshire (375 early onset BCC cases and 251 controls, 254 SCC cases and 432 controls). ORs of SCC and early onset BCC and history of allergy and atopic dermatitis were computed using logistic regression, while controlling for potential confounding factors. An overall inverse association was observed between a history of allergy and early onset BCC [OR, 0.61; 95% confidence interval (CI), 0.38-0.97] but not SCC (OR, 1.18; 95% CI, 0.78-1.79). Among women, we found reduced ORs of both early onset BCC and of SCC in relation to allergy history (early onset BCC OR, 0.53; 95% CI, 0.31-0.92 and SCC OR, 0.59; 95% CI, 0.29-1.19). Among men, we observed no clear association with early onset BCC (OR, 0.87; 95% CI, 0.39-1.99) and an increased risk of SCC (OR, 1.58; 95% CI, 0.93-2.69). Our findings suggest that allergies and atopy may influence risk of early onset BCC and SCC, and that effects may be gender specific. A deeper understanding of the immune mechanisms underlying allergies and atopy may provide new routes of preventing keratinocyte cancers.

Early Onset Basal Cell Carcinoma: Surgical Approach

Summary Basal cell carcinoma (BCC) is the most frequent non-melanoma skin cancer. Only 5-15% of BCC cases can be found in patients aged 20-40 years (so-called early onset). The early onset BCC is characterized by active and aggressive tumour growth, clinically presenting in most of the cases as a morpheaform, locally infiltrating or recurrent BCC. Despite the advances in the study of the pathogenesis of this tumour, surgery remains the most used, most effective and most suitable treatment modality. We describe a case of a 39-year-old woman who developed an early onset BCC of the nasolabial fold. After the subsequent surgical excision an excellent cosmetic result was achieved.

Contact urticaria from beer

and acral regions, with acrochordon-like lesions on the neck (Fig. 1c). Suspecting naevoid BCC syndrome (NBCCS), we performed a complete molecular analysis of the Patched 1 gene (PTCH1), sequencing both strands of all exons and flanking intronic fragments, and visualizing the sequences by capillary electrophoresis (Fig. 2). A frameshift mutation c.2315_2318delAGAC in exon 15 of the PTCH1 gene was found. This mutation shifts the framework from codon 772, which causes a stop codon at position 1004 (p.R772RfsX232), resulting in loss of protein function. Genetic studies of both parents and the patient’s sister were negative, suggesting that this is a sporadic mutation. In 1996, two reports described germline mutations in the PTCH gene in patients with NBCCS. Since then, around 300 different mutations have been reported, the majority being frameshift or nonsense mutations. Many of the reported cases are sporadic, emphasizing the high frequency of spontaneous mutations in the PTCH1 gene. NBCCS or Gorlin syndrome is an autosomal dominant condition characterized by the early onset of multiple basal cell carcinomas (BCC), usually between the first and second decades of life, mandibular odontogenic cysts, palmar or plantar pits, skeletal abnormalities, ectopic calcifications, facial dysmorphia, and a predisposition to other malignancies such as medulloblastomas, meningiomas, ovarian tumours, cardiac fibromas and fibrosarcomas. A germline mutation in the PTCH1 gene, located on chromosome 9q22-31, is responsible for NBCCS. No description exists of a consistent correlation between genotype and phenotype in patients with NBCCS; there is great variability in the clinical presentation, even within members of the same family with the same genetic mutation. Environmental exposure and other modifier genes may contribute to this variability. Therefore, different mutations of PTCH1 do not seem to offer prognostic information about age at onset of BCC, or the number of carcinomas that will develop. In conclusion, we present a previously undescribed spontaneous mutation in exon 15 of the PTCH1 gene in a girl with striking skin symptoms of multiple BCCs since birth. Future research will confirm or exclude the relationship between genotype and phenotype in patients with NBCCS.

Features of basal cell carcinomas in basal cell nevus syndrome

Basal cell nevus syndrome (BCNS) is an autosomal dominant genodermatosis that is characterized by early onset basal cell carcinomas (BCCs) that define the disease and often lead to diagnosis of the underlying syndrome. The objective of this study was to investigate the anatomic location, subtypes, and impact of BCCs on a group of 61 individuals affected with BCNS attending a research colloquium. Fifty individuals had at least one prior BCC with 22 participants having over 100 lesions. The median age of syndrome diagnosis was 11 years and median age of first BCC was 16 years. Males had more lesions on the upper back, upper extremities, and M-zone of the face, while females had more lesions on the scalp, back, and lower extremities. Pigmented BCCs were concentrated on the neck, upper trunk, and extremities. Subjects with >100 lesions showed wider anatomic distribution. The number of BCCs did not correlate with any of the other major features of the syndrome. Eighty percent of affected individuals reported great concern related to BCCs, citing the limitations and morbidity of available treatments. Vigilant surveillance, which was found to be inconsistent for participants in this study, is warranted. Future work should include development of a consensus guideline on skin examinations and strategies to optimize therapy of BCCs in this syndrome.

Basal Cell Nevus Syndrome Showing Several Histologic Types of Basal Cell Carcinoma

Basal cell nevus syndrome (BCNS), or Gorlin Syndrome, is an autosomal dominant disorder, characterized by multiple developmental abnormalities and associated with germline mutations in the PTCH gene. Patients show multiple and early onset basal cell carcinomas (BCCs) in skin, odontogeniccysts in the jaw, pits on palms and soles, medulloblastoma, hypertelorism, and calcification of the falx cerebri. Clinical features of BCCs in these patients are indistinguishable from ordinary BCCs. However, some patients show variable histologic findings in subtypes of BCCs, and only one case associated with several histologic types of BCCs in the syndrome has been reported in Korea. We present a case of BCNS characterized by multiple BCCs, odontogenic keratocysts, multiple palmar pits, and calcified falx cerebri. Histopathologic findings of BCCs showed several patterns, which were nodular, superficial, and pigmented types.

MDM2 polymorphisms and cancer risk in basal cell carcinoma

Sir, Wilkening et al. recently reported in this Journal that there was no association between a single nucleotide polymorphism (SNP) in the MDM2 gene and the risk or age at onset of basal cell carcinoma (BCC).1 Given the functional consequence of the SNP, these results are predictable.2 MDM2 is a proto-oncogene that acquires oncogenicity through increased expression (for review see Iwakuma and Lozano3). Upregulation of MDM2 has been shown to be a significant factor in a range of common cancers, and increased MDM2 expression has been found to be associated with poor outcome in studies of several common cancers, e.g. of the bladder.4 MDM2 interacts directly with p53 and most of the oncogenic effects of MDM2 are due to its ability to negatively regulate the p53 tumour suppressor protein. Increased expression of MDM2 often results from gene amplification, and tumours with MDM2 gene amplification rarely harbour p53 mutations.5 p53 levels and activity are regulated by MDM2 and it is increasingly clear that this is substantially due to the ability of MDM2 to act as a ubiquitin ligase with specificity for, inter alia, p53. MDM2 targets p53 for ubiquitination, leading to export of p53 from the nucleus and/or degradation by proteasomes. The importance of negative regulation of p53 by MDM2 has been beautifully demonstrated in studies of knock-out mice which have shown that MDM2 is an essential gene precisely because it is able to negatively regulate p53.6,7 The interplay between these two critical genes extends further, with p53 acting as a transcriptional regulator of MDM2, and thus an autoregulatory feedback loop connects these molecules.8 The discovery of a SNP (SNP309 T/G) in the MDM2 gene that is associated with increased expression from the G haplotype has been shown to be linked with early onset of cancer in patients with wild-type p53.9 Not surprisingly, given what is known regarding the function of MDM2 in negatively regulating p53, the SNP309 is not informative in patients with mutant p53. The study by Wilkening et al. failed to show any link between SNP309 status and BCC, but the authors did not take into account the p53 status of the patients studied. As the utility of SNP309 genotyping depends upon the status of p53, a re-analysis of the data that takes into account p53 mutational information is clearly warranted. Analysis of SNP309 can prove highly informative, but not in the absence of information regarding p53 status, except perhaps in those cancers where p53 is rarely mutated. This is not, however, the case for BCC where p53 mutation has been reported to occur in approximately 50% of cases.10 Thus the important question that should be asked by studies of this type is not whether SNP309 alone is associated with clinical parameters, but rather whether the SNP is informative in cases that retain wild-type p53.

Basal cell carcinoma in childhood: Case report and literature review

Childhood onset basal cell carcinoma is uncommon. In addition to occurring in children with albinism, Bazex syndrome, basal cell carcinoma nevus syndrome, nevus sebaceus, radiotherapy-treated cancers, solid organ transplants, and xeroderma pigmentosum, childhood onset basal cell carcinoma has also occurred, albeit less commonly, de novo. We describe a boy with idiopathic childhood onset basal cell carcinoma. Previously published children with de novo basal cell carcinoma were collected from computerized medical literature search (PubMed) and citations from earlier reports. To our knowledge, childhood onset idiopathic basal cell carcinoma has been observed in a total of 107 children, including our patient. Tumors were most commonly located on the head (90%). The tumors are most frequently nodular in appearance (52%) and in histology (at least 17%); however, aggressive histologic variants were observed in 20% of tumors. Basal cell carcinoma in children may be associated with prior sun exposure. The most common treatment is excision, with or without using the Mohs technique. However, 15 of 85 children, nearly 20%, developed recurrent tumors during a follow-up period ranging from 4 months to 20 years.

A case of antiphospholipid antibody syndrome that manifested in the course of basal cell carcinoma

A case of antiphospholipid antibody syndrome (APS) is presented, which manifested 5 years after onset of basal cell carcinoma (BCC). There were multiple collateral veins due to portal vein thrombosis. Because immunological abnormalities including anti-cardiolipin beta(2) glycoprotein-I antibody improved after surgical resection of BCC, it is likely that APS had occurred as a paraneoplastic syndrome with BCC. This case suggests that it is necessary to investigate the presence of APS when BCC is complicated by some coagulopathies.