1 Basal Cell Carcinoma Description

Basal cell carcinoma (BCC), also known as basal cell epithelioma, was first reported by Kropecher in 1903 as a skin malignant tumor derived from the epidermis or its appendages, the most common skin malignancy. It often occurs in the skin exposed area, especially the face and neck, and relatively less in the trunk. Studies have found that factors such as ultraviolet radiation, human papillomavirus infection, P53 and PTCH gene mutations are closely related to its pathogenesis. Compared with other malignant tumors, BCC is different because of its slow growth, minimal metastasis, multiple histological types, and differentiation in multiple directions. Although the risk of basal cell carcinoma death is small, if left untreated, it can penetrate deep into the skin and into the subcutaneous tissues and bones, causing serious damage.

BCC is the most common type of tissue in skin malignancies (about 60%). The incidence of BCC has obvious regional, ethnic, and skin color differences. Light-colored people, especially white skin, blue eyes and blond hair, are prone to skin cancer. Caucasians are more than 45 times as non-white, but rare in blacks. The incidence of men is higher than that of women, and older people are more likely than young people.

1.1 Basal Cell Carcinoma Etiology

1.1.1 Ultraviolet Radiation

Ultraviolet radiation is the main predisposing factor for BCC and has been accepted by many scholars. However, the relationship between UV exposure, exposure time, exposure and the risk of developing BCC is not fully understood. The main obstacle is that it is difficult for the elderly to have a reliable indicator to evaluate UV exposure. In a study of 2 785 patients with facial BCC, Marc et al found that the sunburn. These studies suggest that adolescence may be important for thelocal accumulation of local UV radiation was not sufficient to predict the frequency and histological features of facial BCC; the structural features of different parts of the face may be the auxiliary of BCC factor. The study found that BCC is more common in children with freckles and frequent severe sunburn, but has no connection with adult onset of adult BCC, and partly explains why increasing cumulative sun exposure after adulthood does not have a significant impact on BCC.

1.1.2 Non-UV factor

Patients with a family history of skin cancer may increase the risk of developing BCC (OR 2.2). Other non-UV environmental factors include ionizing radiation, high-energy diets, especially fat, low vitamin intake, and various hazardous chemicals and dust. Well, Exposure to arsenic preparations may induce multiple BCC. Patients receiving immunosuppressive therapy have an increased risk of developing BCC, and studies have shown that transplant recipients have a 10-fold higher incidence of BCC than the normal population. Non-sunlight exposure generally does not increase the risk of developing a disease, unless the oral psoralen and UVA irradiation for psoriasis can slightly increase the risk of BCC. However, in recent years, the use of sunbeds has increased dramatically for fashion and beauty purposes, especially among young women. There is evidence that the light used in the solarium emits ultraviolet radiation that can damage the skin and increase the risk of skin cancer. In addition, some hereditary diseases are also associated with the risk of developing BCC, including albinism, xeroderma pigmentosum, and Bazex syndrome (patients with respiratory or digestive tract tumors, in the ears, nose, cheeks, hands, feet, and Eczema or psoriasis-like lesions in the knee) and Green's syndrome (basal cell nevus syndrome). A domestic study has shown that human papillomavirus may be associated with BCC, predominantly HPV16, in the vulva.

1.2 Pathogenesis

Although the research on the pathogenesis of BCC has made a lot of progress, the exact mechanism needs to be further explored. Similar to other malignant tumors, the occurrence of BCC is also the result of a combination of genetic and environmental aspects. At present, genes closely related to the pathogenesis of BCC include PTCH, P53, bcl-2, bax, Fas/FasL, c-fos proto-oncogene, P16; in addition, abnormal caspase-3 expression, dysfunction of Hedgehog signaling pathway, cell adhesion Abnormal expression of molecular CD44, E-cadherin, vascular endothelial growth factor (VEGF), and cell proliferating nuclear antigen (PCNA) is also closely related to the occurrence and development of BCC.

1.3 Clinical Features

1.3.1 Clinical manifestations and distribution characteristics

BCC exhibits distinct subtypes and occurs in different anatomical locations. About 80% occur in the head and neck, and the rest mainly occurs in the trunk and lower limbs. It is rare to happen on the back of the hand. Early manifestations are usually small, translucent, pearly, localized bulging lesions with telangiectasia visible around the periphery. Typical manifestations are erosive ulcers, with an ulcer in the center and a hard, curled periphery. Although BCC grows slowly, if neglected, the tumor will infiltrate into the deep and cause severe damage, especially for the tumor around the eyes, nose and ears. It can even invade the periorbital tissue and bone.

1.3.2 Clinical Typing

BCC is clinically divided into four types: superficial, nodular (or cystic), pigmented, and hard spotted. The superficial type occurs on the trunk, usually in a flat, clear-cut erythema, which grows very slowly. Nodular type is common in the face, often manifested as a single shiny red nodule, and the peripheral telangiectasia is obvious. One of the most important types is the scleroderma-like type, which is more aggressive than other subtypes and has unclear borders, often resulting in incomplete resection under the naked eye; clinical diagnosis is difficult; it can grow to a large extent, destroying serious. This type accounts for approximately 5% of BCC.

1.3.3 BCC Transfer

Typical BCC is painless and progresses slowly. One of the important features is that it can cause tissue damage in local expansion and rarely shifts. The interpretation of this phenomenon needs further study. The transfer rate of BCC is approximately 0.002 8 % -0.55%. Metastasis often occurs in large, locally invasive, and recurrent lesions after treatment. The time from onset to metastasis is about 7 - 34 years, with an average of 9 years, and its 5-year survival rate is 10%.

The implantation of BCC is clinically rare. Some studies have reported 3 cases of skin BCC implantation, with serious clinical consequences and high mortality. The main reasons for the analysis may be: surgical implantation, radiation stimulation and bad living habits.

1.3.4 Differential diagnosis of BCC

It mainly includes squamous cell carcinoma, malignant melanoma (pigmented BCC), melanin (pigmented BCC), Bowen's disease (superficial BCC), psoriasis (superficial), eczema (superficial), Sebaceous gland hyperplasia, infectious soft palate and other skin appendage tumors.

2 Basal cell carcinoma induces other cancers

Basal cell carcinoma can lead to other cancers. Patients with a history of BCC have an increased risk of recurrent BCC. A meta-analysis report in 2000 indicated that the 3-year cumulative risk ranged from 33% to 77%. The 3-year cumulative risk of recurrent squamous cell carcinoma of BCC is 6%. In response to the risk of recurrent malignant melanoma in patients with BCC, a US study showed a hazard ratio (RR) of 2.2, a Danish study showed a standardized incidence rate of 2.64, and a Swedish study showed that BCC The risk of developing malignant melanoma is 6 times higher in men and 4 times in women, presumably related to UV radiation. The relationship between BCC and other malignant tumors such as lung, thyroid, oral cavity, breast, cervix, and non-Hodgkin's lymphoma is still unclear. Scholars report different, but it is generally believed to be related to exposure to carcinogens, smoking, and arsenic. Studies by Kahn et al have shown that male cancer patients with a history of BCC have a higher cancer mortality rate than male cancer patients without a history of BCC, with a relative risk of 1.23 (CI 95 % 1.15-1.32). Although the increase in mortality is small, the number of patients with BCC worldwide will be large and the impact will remain enormous.

…. To be continued in Part Two

 

Reference

[1] Umair A, S harif K. Horri fying basal cell carcinoma forearm lesion leading to shoulder disarticulation [J]. Plast Reconst r Surg, 2006, 117(1): 6 -9.

[2] Holmes SA, Malinovszky K, Robert s DL .Changing t rends in non-melanoma skin cancer in South Wales , 1988 -1998 [ J ] .Br

J Dermatol, 2000, 143: 1224 -1229.

[3] Marks R, S taples M, Giles G. Trends in non-melanocytic skin cancer t reat ed in Aust ralia: the second national survey [J]. Int J Cancer, 1993, 53: 585 -590.

Christenson, Leslie J, Borrowman, et a l.Incidence of basal cell and squamous cell carcinomas in a population younger than 40years [J]. JAMA, 2005, 294:681-690 .

[4] Mathes R. Health issues of ultraviolet tanning appliances used f or cosmetic purposes [J] . Health Physics , 2003, 84(1): 119 -127 .

[5] Marc H, Frank Z, Birger K. Frequency of f acial basal cell carcinoma does not correlate w ith site-speci fic UV exposure [ J ] . Arch Dermatol , 2002 , 138 : 1494-1497 .

[6] Corona R, Dogliott i E , D' Errico M , et al .Risk factors f or Basal cell carcinoma in a Mediterranean population [ J ] . Arch Dermatol , 2002 , 137 : 1162 -1168 .