Carla Oliveira

Um grande consórcio liderado pela Universidade de Tübingen, o Radboud University Medical Center de Nijmegen e a Universidade de Leicester, e no qual o Ipatimup/i3S participa, foi financiado com 15 milhões de euros para desenvolver o programa de investigação SOLVE-RD. O consórcio usará este financiamento para melhorar o diagnóstico de doenças raras.

A collaboration between researchers from Ipatimup/i3S, INEB/i3S and Universidade de Aveiro  led to the development of a novel photoimmunoconjugate of porphyrin conjugated to trastuzumab that specifically and efficiently eliminates HER2+ gastric cancer cells following photodynamic therapy in vitro and in vivo (when compared to trastuzumab alone).

This study suggests that, in the setting of human disease, repetitive cycles of Trast:Porph photoimmunotherapy may improve treatment of HER2+ gastric cancer patients.

Authors and Affiliations:

Uma colaboração entre investigadores do Ipatimup/i3S, INEB/i3S e Universidade de Aveiro permitiu desenvolver um novo fotoimunoconjugado de Porfirina e Trastuzumab que elimina específica e eficazmente células de cancro gástrico que expressam a proteína HER2. Este resultado foi obtido após tratamentos in vitro e in vivo e comparado com tratamento apenas com trastuzumab. Este estudo sugere que na doença humana, ciclos repetidos de tratamento com este tipo de fotoimunoterapia podem melhorar o tratamento de doentes com cancros gástricos HER2 positivos.

Citing Michael Le Page in «New Scientist»:

«In many diseases, including cancer, DNA mutations create a stop codon in the wrong place. A single mutation can truncate a protein that should be 100 amino acids long to one that is just 15 long, rendering it completely useless. These are known as nonsense mutations, and they cause about 10 per cent of all genetic diseases.

It’s possible to make artificial tRNAs that recognise a premature stop codon, and instead of terminating the protein-making process, add the amino acid required to make a useful protein.

Citing Michael Le Page in «New Scientist»:

«In many diseases, including cancer, DNA mutations create a stop codon in the wrong place. A single mutation can truncate a protein that should be 100 amino acids long to one that is just 15 long, rendering it completely useless. These are known as nonsense mutations, and they cause about 10 per cent of all genetic diseases.

It’s possible to make artificial tRNAs that recognise a premature stop codon, and instead of terminating the protein-making process, add the amino acid required to make a useful protein.

Authors and Affiliations:

Oliveira P^1,2, Carvalho J^1,2, Rocha S^1,2, Azevedo M², Reis I², Camilo V², Sousa B^1,2, Valente S^1,2, Paredes J^1,2,3, Almeida R^1,2,3, Huntsman D⁴, Oliveira C^1,2,3.

Autores e Afiliações:

Oliveira P^1,2, Carvalho J^1,2, Rocha S^1,2, Azevedo M², Reis I², Camilo V², Sousa B^1,2, Valente S^1,2, Paredes J^1,2,3, Almeida R^1,2,3, Huntsman D⁴, Oliveira C^1,2,3.

Authors and Affiliations:

Autores e Afiliações:

Authors and Affiliations:

Carla Oliveira*, Hugo Pinheiro*, Joana Figueiredo, Raquel Seruca, Fátima Carneiro

Ipatimup-Institute of Molecular Pathology and Immunology & Instituto Instituto de Investigação e Inovação em Saúde,

(C Oliveira PhD, H Pinheiro PhD, J Figueiredo PhD, R Seruca MD, Prof F Carneiro MD), and

Department of Pathology and Oncology, Faculty of Medicine (C Oliveira, R Seruca, F Carneiro),

University of Porto, Porto, Portugal; and Centro Hospitalar S João, Porto, Portugal (F Carneiro)