Servix Squamous Intraepithelial Lesion (SIL) Squamous Intraepithelial Lesion (SIL) is the abnormal growth of squamous cells on the

surface of the cervix. The cervix is the lower part of the uterus. Both the uterus and the cervix are located in the pelvis and are close to the upper part of the vagina and the ovaries. In fact, the cervix connects the uterus and the vagina. The vagina leads to the outside of the body. The surface of the cervix is made up of two different types of cells, squamous epithelial cells (the lining cells of the outer part of the cervix, or ectocervix) and columnar epithelial cells (the lining cells of the inner part of the cervix, or endocervix). Early detection and treatment of precancerous cells can prevent them from becoming cancerous. Otherwise, the abnormal cells can become cancer and spread to other parts of the body. If you have an abnormal Pap smear or have already been diagnosed with CIN, the Colposcopy Clinic provides treatment. Pap tests can detect precancerous and cancerous conditions by collecting cells from the surface of the cervix. Sometimes these cells appear abnormal, or atypical, when looked at under a microscope, but they are not completely cancerous. These are called premalignant or precancerous cells, which means they might turn into cancer if not found and treated early enough. These precancerous lesions are commonly called cervical intraepithelial neoplasia (CIN). These lesions have also been called squamous intraepithelial lesions (SIL) and there are two types: Low-grade SIL - In this type of SIL, the changes are thought to be just starting. The changes can be in the size, shape, or number of cells that are on the surface of the cervix. In these low-grade lesions, the cells have only a few abnormal characteristics, but are still somewhat similar to the normal cells. Other common names for this low-grade SIL are mild dysplasia or cervical intraepithelial neoplasia type I (CIN 1). High-grade SIL - In this type of SIL, the cells look very abnormal under the microscope. However, these cells are still only on the surface of the cervix. They are not invading the deepest parts of the cervix yet. These lesions are also called moderate or severe dysplasia, CIN II or III or carcinoma in situ (CIS). The next step, in many cases, is a colposcopy (an exam with an instrument that visually magnifies the cervix) and removal of any areas likely to be precancerous or cancerous. Sometimes, the physician and patient may decide to repeat the Pap test later and proceed

to colposcopy only if the second test shows more abnormal cells that might need removal. Other treatments for this type of cervical cancer are:

cone biopsy of the cervix, which is removal of a cone-shaped piece of the cervix with a surgical knife, laser, or wire loop hysterectomy, which is removal of the uterus.

Please note: Carcinoma in Situ is a term used for the early stage of cancer in which the tumor is confined to the organ where it first developed. The disease has not invaded other parts of the organ or spread to distant parts of the body. Most in situ carcinomas are highly curable. SIL can also be considered a carcinoma in Situ. BREAST Many women diagnosed with a precancerous breast lesion known as ductal carcinoma in situ (DCIS) are highly anxious about their prognosis, even though they face a low risk of a recurrence or of developing invasive breast cancer, a new study finds The study noted that 28 percent of the participants "believed that they had a moderate or greater chance of DCIS spreading to other places in their bodies, despite the fact that metastatic breast cancer actually occurs following a diagnosis of DCIS less than 1 percent of the time." DCIS involves abnormal cells in the lining of the breast duct that have not spread outside the duct, according to the National Cancer Institute. In 2006, DCIS accounted for more than 20 percent of all diagnoses linked to breast cancer in the United States -- about 62,000 cases, the study reported

SKIN The most common "precancerous" skin lesion is an "actinic keratosis", which is a sundamaged area of skin that usually appears as a red and scaly patch of skin. Because it is caused by sunlight, the most common location for actinic keratoses is the face, ears, scalp, arms, upper back, and upper chest. These lesions are labeled as being "precancerous" because without treatment, a small percentage of these lesions develop into squamous cell carcinoma, which can be a very invasive skin cancer. It is important to note that not all squamous cell carcinomas develop from actinic keratoses. Although the time of progression from actinic keratosis to squamous cell carcinoma is variable, it is advisable to treat all actinic keratoses. The most common treatment for actinic keratoses is cryotherapy, which is "freezing" the lesions with liquid nitrogen. This is a very quick and effective therapy with minimal pain and scarring. For a person with numerous lesions, treatment with specific creams can chemically treat these lesions. The two most common creams used to treat actinic keratoses are 5-fluorouracil and imiquimod. Both

creams cause treated areas to become very red and inflamed during treatment but this subsides after the treatment period. Lesions are usually treated with the cream for approximately one to three months. It is advisable to monitor an actinic keratosis which does not resolve with therapy as this may indicate is has progressed to become cancerous. The other commonly treated precancerous lesion is the "dysplastic nevus", also known as an atypical mole. These lesions are usually brown or black moles which are biopsied due to having suspicious features of melanoma, such as irregular borders or asymmetry or having multiple colors. While not cancerous, these lesions are also clearly different from harmless, benign moles. These atypical moles have the potential to develop into melanoma, which is why it is advisable to have any changing or growing mole checked as it may be atypical and changing into a cancerous lesion. Importantly, not all atypical moles are equal; some moles are more "atypical" than others. This means that, under the microscope, some moles are closer to being normal in appearance while others are closer to melanoma. If you are diagnosed with an atypical mole, discuss the diagnosis and treatment options with your dermatologist. Treatment for atypical moles usually entails excision of the lesion with a small margin of normal skin, to insure complete removal. However, since each mole has its own features, always talk with your dermatologist regarding the proper treatment for an individual mole. I hope this sheds some light on the term "precancerous". Of course, the best treatment is to prevent cancerous growths from developing so always remember to check with a dermatologist for new and changing growth and moles on the skin. OVARY Although all cell types in the human ovary (including epithelial, stromal, and germ cells) may undergo tumor transformation, 80% to 90% of malignant ovarian tumors are originated from the single layer of epithelial cells covering the ovaries [2]. In addition to the surface epithelium of ovary, there are epithelial inclusion cysts that are simply cysts lined by a single layer of epithelium and located in the human ovarian cortex [3], which can be found in fetal and newborn ovaries [4] but more frequently in the ovaries of aged women [3,5]. Most importantly, the epithelial inclusion cysts have a greater propensity to tumor development than the surface epithelium of the ovary [5]. This may be due to the preferential location of the epithelial inclusion cysts that are exposed to tumor-promoting factors in the microenvironment of ovarian cortex [6]. In the past decade, epidemiological data suggested that chronic inflammation is associated with ovarian tumor development. Studies showed that factors relating to inflammation of the ovarian surface epithelium (OSE; such as asbestos and talc exposure, endometriosis, and pelvis inflammatory diseases) are associated with an increased risk for ovarian cancer [79]. Nevertheless, tubal ligation and hysterectomy were shown to be the protective factors against ovarian cancer because these procedures reduce the exposure of the OSE to inflammatory agents [7,10]. Latest statistics also showed that the use of aspirin or other nonsteroidal anti-inflammatory drugs reduces the risk of ovarian cancer Colon and rectum

Fourty-six cases of polyps and polypoid lesions of the colon and rectum were operated at the First Department of Surgery, Gifu University School of Medicine during the last 16 years. Polyps were classified into five groups according to their degree of atypicality and the relationship between polyps and cancer was investigated. The adenomatous polyps were prone to become malignant and it appears that the larger the polyp size, the greater the incidence of severe atypia and the greater the polyps' malignant potentiality. The malignant polyps developed more frequently in the distal colon and rectum than in other parts. Focal and invasive cancers limited to the submucosal layer were found exclusively in the sigmoid colon and rectum Soft tissue Changes in the texture, composition or appearance of the skin inside the mouth can indicate the formation of a precancerous lesion. There are two main kinds of lesions that patients should watch for: leukoplakias, or white lesions, and erythroplakias, or red lesions. Most leukoplasias are not precancerous, and are instead caused by some type of irritation in the mouth; Erythroplakias are much rarer, but are much more frequently precancerous. If you observe either a white or a red lesion in the soft tissue in your mouth that does not go away in 1-2 weeks, speak with your dentist or oral and maxillofacial surgeon Tiroid Kanker tiroid adalah suatu keganasan pada tiroid yang memiliki 4 tipe ; papiler, folikuler, anaplastik atau meduler. Kanker jarang menyebabkan pembesaran kelenjar, lebih sering menyebabkan pertumbuhan kecil (nodul) di dalam kelenjar. Sebagian besar nodul tiroid bersifat jinak dan biasanya kanker tiroid bisa disembuhkan. Kanker tiroid seringkali membatasi kemampuan menyerap yodium dan membatasi kemampuan menghasilkan hormon tiroid; tetapi kadang kanker menghasilkan cukup banyak hormon tiroid sehingga terjadi hipertiroidisme. Nodul tiroid cenderung bersifat ganas jika: - hanya ditemukan satu - skening tiroid menunjukkan bahwa nodul tidak berfungsi - nodulnya padat dan isinya bukan cairan (kistik) - nodulnya keras - pertumbuhannya cepat BRCA1 BRCA2 CDisease characteristics. Mutations in BRCA1 or BRCA2 predispose to breast cancer and ovarian cancer as well as prostate cancer (BRCA1) and other cancers (BRCA2). The

risk of developing cancer that is associated with a BRCA1 or BRCA2 cancer-predisposing mutation is not known and appears to be variable even within families of similar ethnic background with the same mutation. Estimates of breast cancer and ovarian cancer risks have been derived from families with multiple affected individuals as well as from families with few affected individuals and from population-based studies. Prognosis for breast cancer survival depends upon the stage at which breast cancer is diagnosed. Prognosis for individuals with BRCA1 or BRCA2 cancer-predisposing mutations may not be different from that for controls. ancer-predisposing mutations in the BRCA1 and BRCA2 genes are inherited in an autosomal dominant manner. Each offspring of an individual with a BRCA1 or BRCA2 cancer-predisposing mutation has a 50% chance of inheriting the mutation. Molecular genetic testing of asymptomatic family members at risk of inheriting either a BRCA1 or BRCA2 cancer-predisposing mutation is possible once the family-specific mutation has been identified. Prenatal testing is possible for pregnancies at increased risk; however, requests for prenatal diagnosis of adult-onset diseases are uncommon and require careful genetic counseling. Pathology

Breast cancer pathology. To summarize, BRCA1-related tumors show an excess of medullary histopathology, are of higher histologic grade, and are more likely than sporadic tumors to be estrogen receptornegative and progesterone receptor-negative. At the molecular level, a higher frequency of TP53 mutations and less HER2/c-erbB-2/neu overexpression are observed than in sporadic tumors. These features include both favorable and adverse prognostic factors. Emerging data suggest that BRCA1-related breast cancers are more likely than sporadic tumors to be derived from the basal epithelial layer of cells of the mammary gland, cells thought to represent the breast stem cells and to give rise to cancers with the same high-grade features seen in BRCA1related cancers [Foulkes et al 2003, Foulkes et al 2004, Lacroix & Leclercq 2005, Lakhani et al 2005]. Information regarding BRCA2-related tumors is more limited, but they do not seem to have a characteristic histopathology, and are at least as likely to be hormone receptor-positive as control tumors. Ovarian cancer pathology. An excess of serous adenocarcinomas has been observed in women with BRCA1 and BRCA2 cancer-predisposing mutations compared to controls. Over 90% of tumors in women with BRCA1 cancer-predisposing mutations are serous, compared to approximately 50% in women without a BRCA1 cancer-predisposing mutation [Rubin et al 1996, Aida et al 1998, Berchuck et al 1998, Lu et al 1999]. Serous adenocarcinomas are generally of higher grade and are more frequently bilateral than mucinous cancers. Preliminary support

for distinct molecular pathways of carcinogenesis comes from the finding of differential expression of genes in BRCA1, BRCA2 and sporadic ovarian cancer using DNA microarray technology [Jazaeri et al 2002]. This approach may ultimately lead to the identification of unique histopathologic subtypes. Genotype-Phenotype Correlations Cancer risks may differ by gene and also by mutation position. It has been suggested that families with mutations in the ovarian cancer cluster region (OCCR) of exon 11 of the BRCA2 gene have a higher ratio of ovarian to breast cancer than families with mutations elsewhere in the BRCA2 gene. Recently, 440 families with a BRCA2 mutation were investigated for the presence of cancer of the ovary, male breast, pancreas, prostate, colon, and stomach, and melanoma in first- and second-degree relatives of mutation-positive individuals. Families with ovarian cancer were more likely to harbor mutations in the OCCR than elsewhere in the gene. Differences in ethnic groups were documented as well. Families of Polish ancestry had a lower frequency of pancreatic cancer than families of other ethnic origins, suggesting that both position of mutation and ethnic background contribute to the phenotypic variation observed in families with BRCA2 mutations [Lubinski et al 2004].