Instituto de Medicina Molecular
Faculdade de Medicina de Lisboa
Edifício Egas Moniz, P2-B60
Av. Prof. Egas Moniz
Phone: + 351 21 799 9476
Internal phone extension: 47273
|Susana Constantino Rosa Santos||PIemail@example.com|
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|Joana Simões||Researcher IEFPemail@example.com|
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If you are interested in doing your postdoctoral work in the laboratory please contact firstname.lastname@example.org.
Angiogenesis is the formation of new blood vessels from pre-existing ones and is an essential process during development. Nonetheless, it also occurs in adulthood, during wound healing and restoration of blood flow to injured tissues.
Angiogenesis is orchestrated by a variety of pro and anti-angiogenic signals. Their imbalance, promoting either excessive or insufficient angiogenesis, can lead to disease. In cancer, diabetic eye disease and rheumatoid arthritis, excessive angiogenesis feeds diseased tissue and destroys normal tissue. Conversely, insufficient angiogenesis underlies conditions such as coronary heart disease, stroke and delayed wound healing, where inadequate blood-vessel growth leads to poor circulation and tissue death.
The overall goal of the Angiogenesis Unit is to study the molecular and cellular mechanisms that regulate the angiogenic process.
Radiotherapy is a widely used local treatment for malignant tumors. However, clinical and experimental observations indicate that ionizing radiation might promote a metastatic behavior of cancer cells and that the irradiated host microenvironment might exert tumor-promoting effects. Therefore, a careful analysis of the putative tumor-promoting and pro-metastatic effect of IR is imperative, as radiotherapy is an essential part of cancer treatment.
Recently, we demonstrated in vitro and in vivo, using zebrafish and mice, that low doses of ionizing radiation promote tumor growth and metastasis by enhancing angiogenesis. Our work focused, in an innovative way, in the vasculature that surrounds the tumor and receives relatively low doses of ionizing radiation. We are now interested in investigating the molecular mechanisms by which low doses of ionizing radiation induce angiogenesis and to validate our findings in an human model.
Simultaneously, we are investigating if low doses of ionizing radiation enhance neovascularization in ischemic disease patients by inducing angiogenesis or vasculogenesis.
A collaborative clinical research project: The differential effect of the wild-type or mutated Transthyretin in the hepatic microenvironment and vasculature response.
In Portugal we have a serious metabolic liver disease called Familial Amyloidotic Polyneuropathy (FAP), which is an autosomal dominant disease caused by an abnormal protein, the Transthyretin (TTR) V30M.
Since the liver is the main site of production of TTR, normal or mutated, liver transplantation is the only successful treatment for the disease.
However, it has been a surprise that patients with FAP have the highest incidence of hepatic artery thrombosis, which is statistically significant when compared to other patients. This complication has devastating effects on the survival of the graft and survival of the patient, as well as important morbidity. So, it is crucial the study of the cause for this complication in FAP patients after transplantation.
We have no knowledge of the effects of either the wild-type or mutated TTR in the endothelial cell biology. So, we are now investigating the effect of the wild-type or mutated TTR in the hepatic microenvironment and in the differential response of the hepatic vasculature.
Instituto de Medicina Molecular / Angiogenesis Unit IMM UAG
European Association for Cancer Research EACR
The European School of Haematology ESH
American Association for Cancer Research (AACR)AACR
Associação Viver a Ciência VAC