What makes epithelial cells prone to cancer

Carcinomas are divided into two major subtypes: adenocarcinoma , which develops in an organ or gland , and squamous cell carcinoma , which originates in the squamous epithelium. Adenocarcinomas generally occur in mucus membranes and are first seen as a thickened plaque -like white mucosa.

They often spread easily through the soft tissue where they occur. Squamous cell carcinomas occur in many areas of the body. Most carcinomas affect organs or glands capable of secretion, such as the breasts, which produce milk, or the lungs, which secrete mucus, or colon or prostate or bladder. Sarcoma refers to cancer that originates in supportive and connective tissues such as bones, tendons, cartilage , muscle , and fat.

Generally occurring in young adults, the most common sarcoma often develops as a painful mass on the bone. The abnormal lymphocytes start to collect in the lymph nodes or other places such as the bone marrow or spleen. They can then grow into tumours. You can find out about lymphomas. Myeloma is a cancer that starts in plasma cells. Plasma cells are a type of white blood cell made in the bone marrow. They produce antibodies, also called immunoglobulins, to help fight infection.

Plasma cells can become abnormal and multiply out of control. They make a type of antibody that doesn't work properly to fight infection. Cancer can start in the cells of the brain or spinal cord. The brain controls the body by sending electrical messages along nerve fibres. The fibres run out of the brain and join together to make the spinal cord, which also takes messages from the body to the brain.

The brain and spinal cord form the central nervous system. The brain is made up of billions of nerve cells called neurones. It also contains special connective tissue cells called glial cells that support the nerve cells. The most common type of brain tumour develops from glial cells. It is called glioma. Some tumours that start in the brain or spinal cord are non cancerous benign and grow very slowly. First, this will lead to a clearer understanding of the contributions of different genes to the transformation process and provide new populations of breast tumor cells that can be used to test novel molecule-based therapies.

Second, genes suspected to play roles in promoting later stages of tumorigenesis including metastasis can be introduced into these cells and their effects analyzed. It is now possible to test whether other genes known to be involved in breast cancer will yield more differentiated malignancies that more closely resemble either ductal carcinoma in situ or lobular carcinoma.

In this way, it may be possible to link the genotypes of cancer cells with specific clinical and histopathological features of the tumors. On reaching confluence, the fibroblasts were separated from the epithelial cells by differential trypsinization as described Olumi et al. Immunohistochemical staining was carried out by use of the conventional ABC technique and heat-induced epitope retrieval. Retroviral infections were performed serially with drug selection used to purify polyclonal-infected populations after each infection.

Amphotropic LT retrovirus was generated by transient infection of the PT67 producer cell line Clontech. Blots were developed by ECL chemiluminescent detection Amersham. For HMEC soft agar assays, a bottom layer of 0. HMECs were seeded in 0.

Fresh top agar was added after 1. Irradiation with this dose may suppress natural killer cell activity Feuer et al. Tumor size was measured every 3—4 days. The time of initial tumor formation was defined as the time when the tumor had reached a diameter of 3 mm.

Mice were sacrificed when the tumors grew to 1 cm in diameter or after 12 wk of monitoring. Tumor cells were reisolated by mincing the tumor, incubation in collagenase for 4 hr, washing the cells in PBS, and replating the cells in MEGM. Mice were anesthetized with avertin intraperitoneal and the inguinal mammary glands exposed for injection. The incision was closed with surgical staples.

Mice were sacrificed and the mammary glands excised for histological analysis after 10 wk or earlier when tumors were visible. Chromosomes were prepared by use of an improved procedure for chromosome preparation from solid tumors Zimonjic and Popescu and kept at room temperature for 5—6 days prior to hybridization for SKY analysis.

SKY analysis was performed as originally described Schrock et al. Visualization for biotin- and digoxigenin-labeled DNAs of the probe cocktail was carried out with avidin-Cy5 Amersham and antidigoxigenin-Cy5. Spectral information, upon recovery by Fourier transformation, was used to produce a multicolor digital image with red, green, and blue colors assigned to certain ranges of recorded spectrum.

Further analysis and classification were performed in SKY View 1. Detection of the hybridization signal, digital image acquisition, and analysis were carried out as described previously Zimonjic et al We thank the members of the Weinberg laboratory for helpful discussions, M.

Griffin for excellent technical assistance. Harold and Leila Y. Mathers Charitable Foundation. Ludwig Cancer Research Professor. The publication costs of this article were defrayed in part by payment of page charges.

Article and publication are at www. View all Human breast cancer cells generated by oncogenic transformation of primary mammary epithelial cells Brian Elenbaas 1 , Lisa Spirio 1 , Frederick Koerner 2 , Mark D. Fleming 3 , Drazen B. Popescu 4 , William C. Hahn 1 , 5 , and Robert A. Previous Section Next Section. Figure 1. View this table: In this window In a new window. Table 1. Figure 2.

Figure 3. Figure 4. Figure 6. Figure 5. Figure 7. Table 2. Figure 8. Previous Section. Balmain A. Cancer Suppl. Medline Google Scholar. Band V. Barcellos-Hoff M. Cancer Res. Bartek J. Cell Sci. Bos J. Brenner A. Campbell S. Oncogene 17 : — Clark G. Breast Cancer Res. Escot C. Ethier S. Mammary Gland Biol. CrossRef Medline Google Scholar. Facchini L. Feuer G. Fidler I. Cancer Metastasis Rev. Finney R. Science : — Foster S. Oncogene 12 : — Medline Web of Science Google Scholar.

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