The absence of high-risk HPV combined with specific p53 and p16INK4a expression patterns points to the HPV-independent pathway as the causative agent for vulvar squamous cell carcinoma and its precursor simplex VIN in a young patient.

Simplex vulvar intraepithelial neoplasia (VIN) is an important precursor of vulvar invasive squamous cell carcinoma and characteristically occurs in postmenopausal women. In this report, the absence of high-risk human papillomavirus (HPV) combined with specific p53 and p16INK4a expression patterns points to the HPV-independent pathway as the causative agent for vulvar squamous cell carcinoma in a 28-year-old woman. Its precursor simplex VIN was initially interpreted as eczema.

Lymphangiogenesis in human gynaecological cancers.

The metastatic spread of tumor cells is responsible for the majority of cancer deaths, and with few exceptions, all cancers can metastasize. Clinical findings have for a long time suggested that by providing a pathway for tumor cell dissemination, tumor-associated lymphatics act as key components of metastatic spread. This is believed to occur principally via pre-existing and possibly also newly formed lymphatics (lymphangiogenesis).

Expression of vascular endothelial growth factor (VEGF)-C and VEGF-D, and their receptor VEGFR-3, during different stages of cervical carcinogenesis.

Cervical carcinogenesis has well-defined stages of disease progression including three grades of pre-invasive lesions--cervical intraepithelial neoplasia grades 1-3 (CIN 1-3)--and invasive cervical cancer. However, the biological properties of CIN lesions prone to develop invasive disease are not well defined. Recent observations suggest that early invasive disease spreads to regional lymph nodes in several tumour types and that growth factors (VEGF-C and VEGF-D) involved in new lymphatic vessel formation may play a crucial role in this process.

Combination of microdissection and microarray analysis to identify gene expression changes between differentially located tumour cells in breast cancer.

Comparison of gene expression changes between cancer cells at the periphery and in the centre of breast cancers was performed using a combination of microdissection and microarray analysis. Cancer cells from the two areas were pooled separately from five patients with ductal carcinoma in situ and separately from five patients with frankly invasive cancer. Limited total RNA, 100-200 ng, from this microdissected tissue required use of the Atlas SMART trade mark Probe Amplification Kit to synthesize and amplify cDNA and make (33)P-labelled probes.

Lymphatic dissemination of tumour cells and the formation of micrometastases.

Most human cancers show evidence of metastatic spread to regional lymph nodes, and the extent of lymph-node involvement is directly related to dinical outcome. Increased expression of vascular endothelial growth factor C in primary tumours is associated with increased dissemination of tumour cells to regional lymph nodes in various human carcinomas. Arguments favouring the activation of pre-existing lymphatic endothelium and the de novo formation of lymphatic capillaries (lymphangiogenesis) are discussed.