Gotowe bibliografie tematyczne / Basal cell carcinoma

Gotowa bibliografia na temat „Basal cell carcinoma”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 27 lipca 2024

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Artykuły w czasopismach na temat "Basal cell carcinoma"

Aoki, Natsuko, Hiroyuki Morisaka, Kimiko Nakajima i Shigetoshi Sano. "Adenoid-cystic Basal Cell Carcinoma". Nishi Nihon Hifuka 78, nr 2 (2016): 99–100. http://dx.doi.org/10.2336/nishinihonhifu.78.99.

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Bennani, Mounia, Rhizlane Chaoui, Sara Elloudi, Zakia Douhi, Hanane BayBay i Fatima Zahra Mernissi. "Axillary basal cell carcinoma: New case report". Journal of Clinical Research and Reports 3, nr 4 (13.03.2020): 01–03. http://dx.doi.org/10.31579/2690-1919/058.

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Basal cell carcinoma (BCC) is the most common skin cancer, but significant differences exist in its incidence in the various anatomical locations. Unusual sites include the axillae, breasts, perianal area, genitalia, palms, and soles the axilla is one of the most sun-protected body sites and represents a rare location at which BCC develops, up to 2014, 70 cases of axillary BCC were reported in 69 patients (4) then in 2017, 6 new cases were reported in a Japanese study out of a total of 333 CBC, probably the real incidence is underestimated because no systematic study of axillary BCC has generally been conducted.

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Kiladze, N., T. Shulaia, A. Bulinska i L. Abrahamovych. "Dermatoscopic Criteria of Non-Pigmented Basal Cell Carcinoma". Lviv clinical bulletin 3, nr 7 (12.09.2014): 32–34. http://dx.doi.org/10.25040/lkv2014.03.032.

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Gheewala Dinesh Prasad, Frenali. "A Rare Site of Basal Cell Carcinoma - Axilla!" International Journal of Science and Research (IJSR) 12, nr 2 (5.02.2023): 1349–50. http://dx.doi.org/10.21275/sr23217224739.

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Kuijpers, Danielle I., Monique R. Thissen i Martino H. Neumann. "Basal Cell Carcinoma". American Journal of Clinical Dermatology 3, nr 4 (2002): 247–59. http://dx.doi.org/10.2165/00128071-200203040-00003.

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Alexander Paterson, Luke. "Basal cell carcinoma". InnovAiT: Education and inspiration for general practice 14, nr 4 (15.02.2021): 250–57. http://dx.doi.org/10.1177/1755738021990416.

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Basal cell carcinomas are the most common of all skin cancers, but are often overlooked, perhaps in the wake of increased public awareness of the dangers posed by malignant melanoma. The incidence has been increasing rapidly, adding to the workload of an already stretched primary and secondary care service. A better understanding of how these slow-growing lesions present and behave may help GPs to feel more comfortable managing patients in primary care.

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Arenberger, Petr, i Jiří Ettler. "Basal cell carcinoma". Onkologie 10, nr 2 (1.05.2016): 62–65. http://dx.doi.org/10.36290/xon.2016.015.

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Mustofa, Ali, Tri Rosalia Nur Sholikah, Tapi Singgar Niari i Yuli Wahyu Rahmawati. "Basal Cell Carcinoma". MAGNA MEDICA Berkala Ilmiah Kedokteran dan Kesehatan 9, nr 1 (1.02.2022): 62. http://dx.doi.org/10.26714/magnamed.9.1.2022.62-68.

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Background: Basal Cell Carcinoma (BCC) is a malignant neoplasm of non-keratinized cells in the basal layer of the epidermis, which is locally invasive, aggressive, destructive, and rarely metastasizes. BCC more commonly occurs in the elderly. Exposure to ultraviolet (UV) rays is the main risk factor for BCC, so predilection is areas of the body that are exposed to UV rays, especially the face, ears, and neck.Case presentation: The following is a case report of a 65-year-old female patient who works as a farmer. The patient was diagnosed with basal cell carcinoma (BCC) with complaints of black nodules on the face, itching, and bleeding easily. With Dermatological status obtained. The lesion ad regio Fascialis Dextra shows a solitary hyperpigmented nodule, nummular in size, well-circumscribed, and unilateral.Conclusion:Basal cell carcinoma is a malignant skin tumor originating from non-keratinizing cells in the basal layer of the epidermis.

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AFTAB, MUHAMMAD FARRUKH, IRFAN AHMAD i ABDUL MANAN. "BASAL CELL CARCINOMA". Professional Medical Journal 14, nr 02 (6.09.2007): 204–11. http://dx.doi.org/10.29309/tpmj/2007.14.02.4876.

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Introduction:- Basal cell carcinoma is the most common skinmalignancy, accounting for about 80% of all skin cancers and may be lethal. Its recognition and management shouldbe familiar to all the general surgeons. Objective:- To describe the prevalence, mode of presentation and varioussurgical options of reconstruction in the management of basal cell carcinoma (BCC) with a local perspective. Setting:-Nishtar Hospital, Multan. Duration:- One year (October 2002 to September 2003). Sample size:- 60 patients. Studydesign:- Descriptive study. Results:- Out of sixty cases, 50 (83%) were male and 10 (17%) were female. Majority ofthe patients presented to us above the age of 45 years and the incidence of BCC increases with the age. The male tofemale ratio was 5:1. Out of 60 cases 26 (20 male, 6 female) 43.3% were farmer, 16 (all male) 26.6% was constructionworkers, 10 (8 male, 2 female) 16.6% were unemployed and 8 (all female) 13.3% were household. No patient presentedbefore 5 years after the development of the lesion. 34 (30 male, 4 female) 56.6% for the last 6-10 years, 20 (16 male,4 female) 33.3% for the last 11-15 years, 2 (all male) 3.3% for 16-20 years and 4 (2 male, 2 female) 6.6% had lesionsfor > 20 years. All the lesions encountered in present study occurred on exposed head and neck region as is evidentfrom the table-III. Most of the patients had the nodular pigmented type of BCC and majority of them were male. Noneof them have Gorlin’s syndrome (Table-IV). Common variant on histopathology was found to be solid type withadenocystic type being the commonest lesion. After the excision of the lesion the skin defect most of the time wasclosed by the mean of split skin graft. Direct closure was done in quarter of the patients. A number of postoperativecomplications were observed after various reconstructive procedures. Wound was found to be commonest complication;with majority of cases getting only minor wound infection. Conclusion:- Delay in presentation has an overall negativeeffect on the outcome. A simple excision, excision biopsy with adequate margin clearance gives surgeon more freedomfor reconstruction.

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Rubin, Adam I., Elbert H. Chen i Désirée Ratner. "Basal-Cell Carcinoma". New England Journal of Medicine 353, nr 21 (24.11.2005): 2262–69. http://dx.doi.org/10.1056/nejmra044151.

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Rozprawy doktorskie na temat "Basal cell carcinoma"

Pirzado, Muhammad Suleman. "Investigating cell senescence in basal cell carcinoma". Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8633.

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The Aim of the project was to investigate cell senescence in basal cell carcinoma (BCC). Although the concept of oncogene-induced senescence (OIS) was originally confined to cultured cells, it is now well established that this mechanism has an important role in tumour biology. OIS represents a physiological response that restricts the progression of benign tumours into their malignant counterparts e.g. nevi to melanoma or adenoma to adenocarcinoma. Full malignancy is associated with the loss of important tumour suppressor genes including RETINOBLASTOMA and/or TP53. BCC of the skin is the most common skin tumour and is associated with mutational inactivation of the PTCH1 tumour suppressor gene (and less frequently oncogenic activation of SMOOTHENED). Although BCC does not appear to stem from precursor lesions - though mouse models of BCC display areas of basaloid hyperproliferation - and it is relatively stable at the genomic level, we sought to determine if these unique tumours display any characteristics of OIS. Human BCCs were positive for Senescence-associated β-galactosidase (SA-β-gal) activity (pH 6.0) and expressed known markers of senescence including DCR2, DEC1 (SHARP2) as well as the cell cycle inhibitors p15INK4b and p16INK4a. Interestingly, SA-β-gal activity was observed in stromal cells surrounding the tumour islands and this may account for why BCCs are difficult to culture in vitro as senescent cells are known to express increased levels of growth factors, cytokines and ECM proteins. To determine if OIS is associated with Hedgehog signalling in BCC, I employed a novel in vitro model of BCC created through PTCH1 suppression in human immortalised NEB1 keratinocytes. NEB1-shPTCH1 cells are viable and proliferative (albeit more slowly than control NEB1-shCON cells) and do not display SA-β-gal activity but they express higher levels of several senescent markers including DCR2 and p21WAF1. I also investigated senescence in a Mouse model of BCC in which one allele of Ptch1 is mutated and which on x-ray irradiation results in BCC formation. The expression of known markers of senescence including DCR2, DEC1 (SHARP2) as well as the cell cycle inhibitors p15INK4b, p16INK4a and p53 were all with the exception of p21WAF1 detected in these tumours. Together these data suggest that senescence is a characteristic of BCC and may explain why these tumours rarely metastasise.

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Verhaegh, Marcus Emile Johannes Maria. "Growth characteristics of basal cell carcinoma". Maastricht : Maastricht : UPM, Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=8543.

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Richmond-Sinclair, Naomi Monique. "The epidemiology of basal cell carcinoma". Thesis, Queensland University of Technology, 2010. https://eprints.qut.edu.au/68152/1/Naomi_Richmond-Sinclair_Thesis.pdf.

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Basal cell carcinoma (BCC) is a skin cancer of particular importance to the Australian community. Its rate of occurrence is highest in Queensland, where 1% to 2% of people are newly affected annually. This is an order of magnitude higher than corresponding incidence estimates in European and North American populations. Individuals with a sun-sensitive complexion are particularly susceptible because sun exposure is the single most important causative agent, as shown by the anatomic distribution of BCC which is in general consistent with the levels of sun exposure across body sites. A distinguishing feature of BCC is the occurrence of multiple primary tumours within individuals, synchronously or over time, and their diagnosis and treatment costs contribute substantially to the major public health burden caused by BCC. A primary knowledge gap about BCC pathogenesis however was an understanding of the true frequency of multiple BCC occurrences and their body distribution, and why a proportion of people do develop more than one BCC in their life. This research project sought to address this gap under an overarching research aim to better understand the detailed epidemiology of BCC with the ultimate goal of reducing the burden of this skin cancer through prevention. The particular aim was to document prospectively the rate of BCC occurrence and its associations with constitutional and environmental (solar) factors, all the while paying special attention to persons affected by more than one BCC. The study built on previous findings and recent developments in the field but set out to confirm and extend these and propose more adequate theories about the complex epidemiology of this cancer. Addressing these goals required a new approach to researching basal cell carcinoma, due to the need to account for the phenomenon of multiple incident BCCs per person. This was enabled by a 20 year community-based study of skin cancer in Australians that provided the methodological foundation for this thesis. Study participants were originally randomly selected in 1986 from the electoral register of all adult residents of the subtropical township of Nambour in Queensland, Australia. On various occasions during the study, participants were fully examined by dermatologists who documented cumulative photodamage as well as skin cancers. Participants completed standard questionnaires about skin cancer-related factors, and consented to have any diagnosed skin cancers notified to the investigators by regional pathology laboratories in Queensland. These methods allowed 100% ascertainment of histologically confirmed BCCs in this study population. 1339 participants had complete follow-up to the end of 2007. Statistical analyses in this thesis were carried out using SAS and SUDAAN statistical software packages. Modelling methods, including multivariate logistic regressions, allowed for repeated measures in terms of multiple BCCs per person. This innovative approach gave new findings on two levels, presented in five chapters as scientific papers: 1. Incidence of basal cell carcinoma multiplicity and detailed anatomic distribution: longitudinal study of an Australian population The incidence of people affected multiple times by BCC was 705 per 100,000 person years compared to an incidence rate of people singly affected of 935 per 100,000 person years. Among multiply and singly affected persons alike, site-specific BCC incidence rates were far highest on facial subsites, followed by upper limbs, trunk, and then lower limbs 2. Melanocytic nevi and basal cell carcinoma: is there an association? BCC risk was significantly increased in those with forearm nevi (Odds Ratios (OR) 1.43, 95% Confidence Intervals (CI) 1.09-1.89) compared to people without forearm nevi, especially among those who spent their time mainly outdoors (OR 1.6, 95%CI 1.1-2.3) compared to those who spent their time mainly indoors. Nevi on the back were not associated with BCC. 3. Clinical signs of photodamage are associated with basal cell carcinoma multiplicity and site: a 16-year longitudinal study Over a 16-year follow-up period, 58% of people affected by BCC developed more than one BCC. Among these people 60% developed BCCs across different anatomic sites. Participants with high numbers of solar keratoses, compared to people without solar keratoses, were most likely to experience the highest BCC counts overall (OR 3.3, 95%CI 1.4-13.5). Occurrences of BCC on the trunk (OR 3.3, 95%CI 1.4-7.6) and on the limbs (OR 3.7, 95%CI 2.0-7.0) were strongly associated with high numbers of solar keratoses on these sites. 4. Occurrence and determinants of basal cell carcinoma by histological subtype in an Australian community Among 1202 BCCs, 77% had a single growth pattern and 23% were of mixed histological composition. Among all BCCs the nodular followed by the superficial growth patterns were commonest. Risk of nodular and superficial BCCs on the head was raised if 5 or more solar keratoses were present on the face (OR 1.8, 95%CI 1.2-2.7 and OR 4.5, 95%CI 2.1-9.7 respectively) and similarly on the trunk in the presence of multiple solar keratoses on the trunk (OR 4.2, 95%CI 1.5-11.9 and OR 2.2, 95%CI 1.1-4.4 respectively). 5. Basal cell carcinoma and measures of cumulative sun exposure: an Australian longitudinal community-based study Dermal elastosis was more likely to be seen adjacent to head and neck BCCs than trunk BCCs (p=0.01). Severity of dermal elastosis increased on each site with increasing clinical signs of cutaneous sun damage on that site. BCCs that occurred without perilesional elastosis per se, were always found in an anatomic region with signs of photodamage. This thesis thus has identified the magnitude of the burden of multiple BCCs. It does not support the view that people affected by more than one BCC represent a distinct group of people who are prone to BCCs on certain body sites. The results also demonstrate that BCCs regardless of site, histology or order of occurrence are strongly associated with cumulative sun exposure causing photodamage to the skin, and hence challenge the view that BCCs occurring on body sites with typically low opportunities for sun exposure or of the superficial growth pattern are different in their association with the sun from those on typically sun-exposed sites, or nodular BCCs, respectively. Through dissemination in the scientific and medical literature, and to the community at large, these findings can ultimately assist in the primary and secondary prevention of BCC, perhaps especially in high-risk populations.

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Gore, S. "Neuronal differentiation markers in basal cell carcinoma". Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445574/.

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Basal cell carcinoma (BCC) is the most common skin cancer in humans. The demonstration of genetic and protein alterations has, so far, had limited correlation with either biological behaviour or histological classification of these tumours. It was observed that Glil-overexpressing keratinocytes express elevated levels of genes known to be associated with neuronal development, including p-tubulin III, GAP-43, Arc and neurofilament. It was proposed that these genes may similarly be overexpressed in BCCs and that different levels of expression may be present in different BCC subtypes Immunohistochemistry of BCCs demonstrated that neuronal differentiation marker proteins are expressed in BCCs, but that this expression is significantly reduced in tumours that behave aggressively. Elevated neuronal differentiation marker gene expression was shown in BCCs. Again, expression was more prominent in tumour types that behave indolently. Results were obtained for tumour samples processed by laser capture microdissection, needle microdissection and homogenised tissue. Expression of neuronal differentiation marker genes in Gli-overexpressing keratinocytes was examined by semi-quantitiative PCR. Neuronal differentiation marker expression was associated with GUI and GH2 over-expression in some cases {P-tubulin III and Arc). GUI and GH2 also promoted the expression of each other in a positive-feedback loop. Expression of these markers was examined in archival tumours for which the clinical outcome was known in terms of recurrence. In completely excised tumours P-tubulin III was significantly reduced in tumours that went on to subsequently recur. Other markers were not expressed in significantly different amounts. In summary, I have shown that expression of markers associated with neuronal development is a feature of Basal Cell carcinoma, and that the expression of these markers correlates strongly with the tumour histological subtype but only weakly with tumour recurrence. More work will be required to discover further alterations in BCC molecular biology that impact significantly on tumour behaviour.

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Gao, Wendi. "Investigation of immune privilege in basal cell carcinoma". University of British Columbia, 2017. http://hdl.handle.net/2429/63553.

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Basal cell carcinoma (BCC) is the most common type of skin cancer which arises in the skin’s basal cells that line the deepest layer of the epidermis. Previous studies have identified some immune privilege (IP) related genes and products expressed in some malignancies. IP is also believed to exist in BCC tumors during BCC development. However, quantitative analyses and functional studies to clearly demonstrate IP in BCC tumors are required. My goal was to examine BCC tumor cells to identify novel functional mechanisms of IP. My hypothesis was that BCC tumors have functional IP capabilities. With in vitro experiments, I found that cultured BCC cells appeared to suppress histo-incompatible peripheral blood mononuclear cell (PBMC) T cells’ activation, as well as IFN-γ secretion. In contrast, non-tumor skin cells from the same subject elicited significant T cell activation. I screened for expression of candidate IP-related genes in BCC tumors relative to normal skin from healthy people by quantitative RT-PCR. I found significant upregulation of CD200, and a downregulation of its receptor CD200R. There were also several other genes related to IP expressed differently in BCC tumors compared to healthy control tissues. We also demonstrated the upregulation of CD200 and downregulation of CD200R at the protein level by flow cytometry. In summary, these experiments give further evidence in support of BCC IP and predict a potential role of CD200 in BCC IP.
Medicine, Faculty of
Experimental Medicine, Division of
Medicine, Department of
Graduate

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Koreeda, Satoshi. "Basal cell carcinoma cells resemble follicular matrix cells rather than follicular bulge cells". Kyoto University, 2004. http://hdl.handle.net/2433/147556.

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de, Zwaan Sally Elizabeth. "The Genetics of Basal Cell Carcinoma of the Skin". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3878.

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BCC is the commonest cancer in European-derived populations and Australia has the highest recorded incidence in the world, creating enormous individual and societal cost in management of this disease. The incidence of this cancer has been increasing internationally, with evidence of a 1 to 2% rise in incidence in Australia per year over the last two decades. The main four epidemiological risk factors for the development of BCC are ultraviolet radiation (UVR) exposure, increasing age, male sex, and inability to tan. The pattern and timing of UVR exposure is important to BCC risk, with childhood and intermittent UVR exposure both associated with an increased risk. The complex of inherited characteristics making up an individual’s ‘sun sensitivity’ is also important in determining BCC risk. Very little is known about population genetic susceptibility to BCC outside of the rare genodermatosis Gorlin syndrome. Mutations in the tumour suppressor gene patched (PTCH) are responsible for this BCC predisposition syndrome and the molecular pathway and target genes of this highly conserved pathway are well described. Derangments in this pathway occur in sporadic BCC development, and the PTCH gene is an obvious candidate to contribute to non-syndromic susceptibility to BCC. The melanocortin 1 receptor (MC1R) locus is known to be involved in pigmentary traits and the cutaneous response to UVR, and variants have been associated with skin cancer risk. Many other genes have been considered with respect to population BCC risk and include p53, HPV, GSTs, and HLAs. There is preliminary evidence for specific familial aggregation of BCC, but very little known about the causes. 56 individuals who developed BCC under the age of 40 in the year 2000 were recruited from the Skin and Cancer Foundation of Australia’s database. This represents the youngest 7 – 8% of Australians with BCC from a database that captures approximately 10% of Sydney’s BCCs. 212 of their first degree relatives were also recruited, including 89 parents and 123 siblings of these 56 probands. All subjects were interviewed with respect to their cancer history and all reports of cancer verified with histopathological reports where possible. The oldest unaffected sibling for each proband (where available) was designated as an intra-family control. All cases and control siblings filled out a questionnaire regarding their pigmentary and sun sensitivity factors and underwent a skin examination by a trained examiner. Peripheral blood was collected from these cases and controls for genotyping of PTCH. All the exons of PTCH for which mutations have been documented in Gorlin patients were amplified using PCR. PCR products were screened for mutations using dHPLC, and all detectable variants sequenced. Prevalence of BCC and SCC for the Australian population was estimated from incidence data using a novel statistical approach. Familial aggregation of BCC, SCC and MM occurred within the 56 families studied here. The majority of families with aggregation of skin cancer had a combination of SCC and BCC, however nearly one fifth of families in this study had aggregation of BCC to the exclusion of SCC or MM, suggesting that BCCspecific risk factors are also likely to be at work. Skin cancer risks for first-degree relatives of people with early onset BCC were calculated: sisters and mothers of people with early-onset BCC had a 2-fold increased risk of BCC; brothers had a 5-fold increased risk of BCC; and sisters and fathers of people with early-onset BCC had over four times the prevalence of SCC than that expected. For melanoma, the increased risk was significant for male relatives only, with a 10-fold increased risk for brothers of people with early-onset BCC and 3-fold for fathers. On skin examination of cases and controls, several phenotypic factors were significantly associated with BCC risk. These included increasing risk of BCC with having fair, easyburning skin (ie decreasing skin phototype), and with having signs of cumulative sun damage to the skin in the form of actinic keratoses. Signs reflecting the combination of pigmentary characteristics and sun exposure - in the form of arm freckling and solar lentigines - also gave subjects a significantly increased risk BCC. Constitutive red-green reflectance of the skin was associated with decreased risk of BCC, as measured by spectrophotometery. Other non-significant trends were seen that may become significant in larger studies including associations of BCC with propensity to burn, moderate tanning ability and an inability to tan. No convincing trend for risk of BCC was seen with the pigmentary variables of hair or eye colour, and a non-significant reduced risk of BCC was associated with increasing numbers of seborrhoeic keratoses. Twenty PTCH exons (exons 2, 3, 5 to 18, and 20 to 23) were screened, accounting for 97% of the coding regions with published mutations in PTCH. Nine of these 20 exons were found to harbour single nucleotide polymorphisms (SNPs), seen on dHPLC as variant melting curves and confirmed on direct sequencing. SNPs frequencies were not significantly different to published population frequencies, or to Australian general population frequencies where SNP database population data was unavailable. Assuming a Poisson distribution, and having observed no mutations in a sample of 56, we can be 97.5% confident that if there are any PTCH mutations contributing to early-onset BCC in the Australian population, then their prevalence is less than 5.1%. Overall, this study provides evidence that familial aggregation of BCC is occurring, that first-degree relatives are at increased risk of all three types of skin cancer, and that a combination of environmental and genetic risk factors are likely to be responsible. The PTCH gene is excluded as a major cause of this increased susceptibility to BCC in particular and skin cancer in general. The weaknesses of the study design are explored, the possible clinical relevance of the data is examined, and future directions for research into the genetics of basal cell carcinoma are discussed.

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de, Zwaan Sally Elizabeth. "The Genetics of Basal Cell Carcinoma of the Skin". University of Sydney, 2008. http://hdl.handle.net/2123/3878.

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Doctor of Philosophy(PhD)
BCC is the commonest cancer in European-derived populations and Australia has the highest recorded incidence in the world, creating enormous individual and societal cost in management of this disease. The incidence of this cancer has been increasing internationally, with evidence of a 1 to 2% rise in incidence in Australia per year over the last two decades. The main four epidemiological risk factors for the development of BCC are ultraviolet radiation (UVR) exposure, increasing age, male sex, and inability to tan. The pattern and timing of UVR exposure is important to BCC risk, with childhood and intermittent UVR exposure both associated with an increased risk. The complex of inherited characteristics making up an individual’s ‘sun sensitivity’ is also important in determining BCC risk. Very little is known about population genetic susceptibility to BCC outside of the rare genodermatosis Gorlin syndrome. Mutations in the tumour suppressor gene patched (PTCH) are responsible for this BCC predisposition syndrome and the molecular pathway and target genes of this highly conserved pathway are well described. Derangments in this pathway occur in sporadic BCC development, and the PTCH gene is an obvious candidate to contribute to non-syndromic susceptibility to BCC. The melanocortin 1 receptor (MC1R) locus is known to be involved in pigmentary traits and the cutaneous response to UVR, and variants have been associated with skin cancer risk. Many other genes have been considered with respect to population BCC risk and include p53, HPV, GSTs, and HLAs. There is preliminary evidence for specific familial aggregation of BCC, but very little known about the causes. 56 individuals who developed BCC under the age of 40 in the year 2000 were recruited from the Skin and Cancer Foundation of Australia’s database. This represents the youngest 7 – 8% of Australians with BCC from a database that captures approximately 10% of Sydney’s BCCs. 212 of their first degree relatives were also recruited, including 89 parents and 123 siblings of these 56 probands. All subjects were interviewed with respect to their cancer history and all reports of cancer verified with histopathological reports where possible. The oldest unaffected sibling for each proband (where available) was designated as an intra-family control. All cases and control siblings filled out a questionnaire regarding their pigmentary and sun sensitivity factors and underwent a skin examination by a trained examiner. Peripheral blood was collected from these cases and controls for genotyping of PTCH. All the exons of PTCH for which mutations have been documented in Gorlin patients were amplified using PCR. PCR products were screened for mutations using dHPLC, and all detectable variants sequenced. Prevalence of BCC and SCC for the Australian population was estimated from incidence data using a novel statistical approach. Familial aggregation of BCC, SCC and MM occurred within the 56 families studied here. The majority of families with aggregation of skin cancer had a combination of SCC and BCC, however nearly one fifth of families in this study had aggregation of BCC to the exclusion of SCC or MM, suggesting that BCCspecific risk factors are also likely to be at work. Skin cancer risks for first-degree relatives of people with early onset BCC were calculated: sisters and mothers of people with early-onset BCC had a 2-fold increased risk of BCC; brothers had a 5-fold increased risk of BCC; and sisters and fathers of people with early-onset BCC had over four times the prevalence of SCC than that expected. For melanoma, the increased risk was significant for male relatives only, with a 10-fold increased risk for brothers of people with early-onset BCC and 3-fold for fathers. On skin examination of cases and controls, several phenotypic factors were significantly associated with BCC risk. These included increasing risk of BCC with having fair, easyburning skin (ie decreasing skin phototype), and with having signs of cumulative sun damage to the skin in the form of actinic keratoses. Signs reflecting the combination of pigmentary characteristics and sun exposure - in the form of arm freckling and solar lentigines - also gave subjects a significantly increased risk BCC. Constitutive red-green reflectance of the skin was associated with decreased risk of BCC, as measured by spectrophotometery. Other non-significant trends were seen that may become significant in larger studies including associations of BCC with propensity to burn, moderate tanning ability and an inability to tan. No convincing trend for risk of BCC was seen with the pigmentary variables of hair or eye colour, and a non-significant reduced risk of BCC was associated with increasing numbers of seborrhoeic keratoses. Twenty PTCH exons (exons 2, 3, 5 to 18, and 20 to 23) were screened, accounting for 97% of the coding regions with published mutations in PTCH. Nine of these 20 exons were found to harbour single nucleotide polymorphisms (SNPs), seen on dHPLC as variant melting curves and confirmed on direct sequencing. SNPs frequencies were not significantly different to published population frequencies, or to Australian general population frequencies where SNP database population data was unavailable. Assuming a Poisson distribution, and having observed no mutations in a sample of 56, we can be 97.5% confident that if there are any PTCH mutations contributing to early-onset BCC in the Australian population, then their prevalence is less than 5.1%. Overall, this study provides evidence that familial aggregation of BCC is occurring, that first-degree relatives are at increased risk of all three types of skin cancer, and that a combination of environmental and genetic risk factors are likely to be responsible. The PTCH gene is excluded as a major cause of this increased susceptibility to BCC in particular and skin cancer in general. The weaknesses of the study design are explored, the possible clinical relevance of the data is examined, and future directions for research into the genetics of basal cell carcinoma are discussed.

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Wallberg, Peter. "A clinical and experimental study of basal cell carcinoma : aspects on epidemiology, genetics and microphysiology /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-3993-4/.

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Wong, Deanna A. "Cytokine profiles in regressing and non-regressing basal cell carcinomas". Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27687.

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Książki na temat "Basal cell carcinoma"

Migden, Michael R., Leon Chen i Sirunya Silapunt, red. Basal Cell Carcinoma. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-26887-9.

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National Cancer Institute (U.S.), red. Skin cancers: Basal cell and squamous cell carcinomas. [Bethesda, Md.?]: National Cancer Institute, 1990.

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Surgery of basal cell carcinoma of the face. Berlin: Springer Verlag, 1988.

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Marchac, Daniel. Surgery of Basal Cell Carcinoma of the Face. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-72811-2.

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Society, American Cancer. Basal and squamous cell skin cancer: What you need to know-- now. Atlanta, Ga: American Cancer Society/Health Promotions, 2012.

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Nonmelanoma skin cancers: Basal and squamous cell carcinomas. Bethesda, Md: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, 1988.

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S, Weber Randal, Miller Michael J. 1955- i Goepfert Helmuth, red. Basal and squamous cell skin cancers of the head and neck. Baltimore: Williams & Wilkins, 1996.

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Shuck, Carolyn. Saving face: My victory over skin cancer. Forest Dale, Vt: Paul S. Eriksson, 2000.

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S, Weber Randal, Miller Michael J. 1955- i Goepfert Helmuth, red. Basal and squamous cell skin cancers of the head and neck. Media, Pa: Williams & Wilkins, 1995.

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Parker, Philip M., i James N. Parker. Basal cell carcinoma: A medical dictionary, bibliography, and annotated research guide to internet references. San Diego, CA: ICON Health Publications, 2004.

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Części książek na temat "Basal cell carcinoma"

Knowlton, Christin A., Michelle Kolton Mackay, Tod W. Speer, Robyn B. Vera, Douglas W. Arthur, David E. Wazer, Rachelle Lanciano i in. "Carcinomas: Basal Cell Carcinoma". W Encyclopedia of Radiation Oncology, 96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_1059.

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Shaikh, Waqas R., i Zeena Y. Nawas. "Epidemiology and Risk Factors of Basal Cell Carcinoma". W Basal Cell Carcinoma, 1–18. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_1.

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Ng, Sweet Ping, Jae Phan, Danna K. Fullen, William H. Morrison i G. Brandon Gunn. "Radiotherapy for Basal Cell Carcinoma". W Basal Cell Carcinoma, 177–88. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_10.

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Kash, Natalie, i Sirunya Silapunt. "Photodynamic Therapy for the Treatment of Basal Cell Carcinoma". W Basal Cell Carcinoma, 189–212. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_11.

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Kash, Natalie, i Sirunya Silapunt. "Laser Therapy for the Treatment of Basal Cell Carcinoma". W Basal Cell Carcinoma, 213–32. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_12.

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Chen, Leon, Sirunya Silapunt i Michael R. Migden. "Hedgehog Signaling Pathway Inhibitors for Basal Cell Carcinoma". W Basal Cell Carcinoma, 233–49. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_13.

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Chen, Leon, Sirunya Silapunt i Michael R. Migden. "Immunotherapy for Basal Cell Carcinoma". W Basal Cell Carcinoma, 251–64. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_14.

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Ramelyte, Egle, Gaetana Restivo i Reinhard Dummer. "Treatment: Future Directions". W Basal Cell Carcinoma, 265–77. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_15.

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Chang, Anne Lynn S. "Pathophysiology of Basal Cell Carcinoma and Its Associated Genetic Syndromes". W Basal Cell Carcinoma, 19–23. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_2.

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Nagarajan, Priyadharsini, Michael T. Tetzlaff i Jonathan L. Curry. "Histopathology of Basal Cell Carcinoma and Its Variants". W Basal Cell Carcinoma, 25–48. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26887-9_3.

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Streszczenia konferencji na temat "Basal cell carcinoma"

Zeng, Haishan, David I. McLean, Calum E. MacAulay, Branko Palcic i Harvey Lui. "Autofluorescence of basal cell carcinoma". W BiOS '98 International Biomedical Optics Symposium, redaktorzy R. Rox Anderson, Kenneth E. Bartels, Lawrence S. Bass, C. Gaelyn Garrett, Kenton W. Gregory, Harvey Lui, Reza S. Malek i in. SPIE, 1998. http://dx.doi.org/10.1117/12.312300.

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Puspaningtyas, Adelia Hanung, Lydia Kurniasari, Renni Yuniati, Buwono Puruhito i Puji Sriyani. "Late Diagnosis Merkel Cell Carcinoma with History of Basal Cell Carcinoma". W The 2nd International Conference on Tropical Medicine and Infectious Disease. SCITEPRESS - Science and Technology Publications, 2019. http://dx.doi.org/10.5220/0009989203710374.

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Piotrzkowska, Hanna, Jerzy Litniewski, Andrzej Nowicki i Elzbieta Szymanska. "Basal Cell Carcinoma lesions characterization with ultrasound". W 2012 IEEE International Ultrasonics Symposium. IEEE, 2012. http://dx.doi.org/10.1109/ultsym.2012.0596.

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von Fournier, A., A. Scherzad, S. Hackenberg i R. Hagen. "Metastastatic basal cell carcinoma – A case report". W Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1711008.

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Larraona-Puy, M., A. Ghita, A. Zoladek, W. Perkins, S. Varma, I. H. Leach, A. A. Koloydenko i in. "Towards Automated Diagnosis of Basal Cell Carcinoma". W XXII INTERNATIONAL CONFERENCE ON RAMAN SPECTROSCOPY. AIP, 2010. http://dx.doi.org/10.1063/1.3482560.

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Cicchi, R., P. Carli, D. Massi, S. Sestini, D. Stambouli i F. S. Pavone. "Multiphoton imaging of basal cell carcinoma (BCC)". W Biomedical Optics 2006, redaktorzy Jose-Angel Conchello, Carol J. Cogswell i Tony Wilson. SPIE, 2006. http://dx.doi.org/10.1117/12.644224.

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Cicchi, R., S. Sestini, V. De Giorgi, D. Stambouli, P. Carli, D. Massi i F. S. Pavone. "Time-resolved multiphoton imaging of basal cell carcinoma". W Biomedical Optics (BiOS) 2007, redaktorzy Ammasi Periasamy i Peter T. C. So. SPIE, 2007. http://dx.doi.org/10.1117/12.700216.

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Coelho, Vitória Helena Maciel, Wagner Correr, Cristina Kurachi, Vanderlei Salvador Bagnato i Cacilda da Silva Souza. "Fluorescence Diagnosis in the characterization of basal cell carcinoma". W Latin America Optics and Photonics Conference. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/laop.2012.lt2a.26.

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Gutiérrez, Ricardo, Andrea Rueda i Eduardo Romero. "Learning semantic histopathological representation for basal cell carcinoma classification". W SPIE Medical Imaging, redaktorzy Metin N. Gurcan i Anant Madabhushi. SPIE, 2013. http://dx.doi.org/10.1117/12.2007117.

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Maradong, Radema, Yulia Farida Yahya i Theresia Lumban Toruan. "Characteristic of Basal Cell Carcinoma in Tertiary Health Care". W The 23rd Regional Conference of Dermatology 2018. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0008149500050008.

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Raporty organizacyjne na temat "Basal cell carcinoma"

Drucker, Aaron, Gaelen P. Adam, Valerie Langberg, Abhilash Gazula, Bryant Smith, Farah Moustafa, Martin A. Weinstock i Thomas A. Trikalinos. Treatments for Basal Cell and Squamous Cell Carcinoma of the Skin. Agency for Healthcare Research and Quality, 2017. http://dx.doi.org/10.23970/ahrqepccer199.

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Untaaveesup, Suvijak, Pornteera Srichana, Gynna Techataweewan, Chanamon Pongphaew, Wichapol Dendumrongsup, Ben Ponvilawan, Nichanant Nampipat i Chanin Limwongse. Prevalence of Genetic Alterations in Advanced Basal Cell Carcinoma Patients with Resistant to Hedgehog Pathway Inhibitors: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, grudzień 2023. http://dx.doi.org/10.37766/inplasy2023.12.0106.

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Untaaveesup, Suvijak, Wichapol Dendumrongsup, Pornteera Srichana, Chanamon Pongphaew, Gynna Techataweewan, Kanmanee Viratkapan, Nichanant Nampipat i in. Effectiveness and Side Effects of Hedgehog Pathway Inhibitors for Advanced Basal Cell Carcinoma in the Patients with or without Previous Treatment: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2024. http://dx.doi.org/10.37766/inplasy2024.5.0104.

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