| Note | |
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| Entity | Astrocytic gliomas |
| Disease | Astrocytic gliomas are the most common primary brain tumours; they include WHO grade IV tumours, such as glioblastomas with its variants and WHO grade III tumours (anaplastic forms of astrocytoma, oligodendroglioma and oligoastrocytoma). |
| Prognosis | Poor for glioblastoma, relatively better for who grade III tumours. |
| Cytogenetics | Anaplastic astrocytomas carry gain of chromosome 7 or 7q and deletions on chromosomes 6, 9p, 11p, 19q and 22q. Glioblastomas demonstrate deletions of chromosome 10 and allelic losses on 19q and 13q. |
| Oncogenesis | Homozigous deletion of CDKN2A, CDKN2B and (9p), negative regulators of cell cycle or amplification of the cyclin-dependent kinase CDK4 are frequent in astrocytoma gr. III and glioblastoma. Glioblastoma and a subset of anaplastic astrocytoma with no abnormality of CDK4 and CDKN2A carries mutation in the retinoblastoma gene (Rb1); p53-pathway is frequently altered and PTEN is mutated in 30-40% of glioblastoma and in astrocytoma with poor prognosis. Astrocytic gliomas generally stain positive for S-100 proteins; S100-A13 is up-regulated in high-grade gliomas and correlated with microvessel density and tumour grading. |
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| Entity | Endometriosis |
| Disease | Endometriosis is characterized by the presence and proliferation of functional endometrial glands and stroma outside the uterine cavity. It is a multifactorial genetic disorders. Increasing evidence points to the role of angiogenesis in the disease pathogenesis and many angiogenic factors and cytokines such as VEGF-A, FGF1, endoglin and interleukin-1 alpha are up-regulated in endometriotic lesions. S100A13 is over-expressed in endometriotic specimens, particularly in microvascular endothelia. |
| Prognosis | It is a chronic and recurrent disease associated with infertility. |
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| Entity | Lung cancer |
| Disease | Lung cancer is the most preventable of all the major forms of cancer since at least 75% of all cases worldwide are due to tobacco smoking. It can be classified into two main groups: small cell lung cancer and non-small cell lung cancer. The latter group is a heterogeneous aggregate of at least 3 distinct histologies including epidermoid or squamous carcinoma, adenocarcinoma and large cell carcinoma with the potential for cure with surgical resection when localized. Small cell lung carcinoma has a greater tendency to be disseminated by the time of diagnosis but is much more responsive to chemotherapy and radiation compared to non-small cell lung cancer. |
| Prognosis | Poor; small cell carcinoma has the most aggressive clinical course with median survival of only 2-4 months without treatment. |
| Cytogenetics | Loss of heterozigosity in chromosome regions 3p (fragile histidine triad, FHIT, locus), 12p, 13q (Rb1 locus) and 17p (p53 locus). |
| Oncogenesis | Inactivation of p16 by promoter hypermethylation is more frequent in squamous cell carcinoma compared with adenocarcinoma and is almost never found in small-cell lung cancer; K-ras mutations are documented only in non- small cell lung tumours particularly adenocarcinoma. Overexpression of myc family members and inactivation of p53, pRb and FHIT are found in all histologic types of lung cancer. S100P and S100A2 may be predictors of distant metastasis and poor survival in non-small cell lung tumours since they are overexpressed in tumours that metastatized during the course of the disease; S100A13 expression correlates with a more invasive phenotype in vitro. |
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| Endoglin (cd105) and S100A13 as markers of active angiogenesis in endometriosis. |
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