Publications by authors named "Maria Del Mar Abad Hernandez"

Article Synopsis
  • Luminal A breast cancer has a good outlook, but around 10% of patients may have tumors come back after 10 years, especially within the first 5 years after diagnosis.
  • A study was done to see how a specific protein called NCAPH affects the growth of luminal A breast cancer, looking for gene patterns that could indicate a higher risk of bad outcomes.
  • The findings showed that high levels of NCAPH are linked to more aggressive tumors and poorer responses to chemotherapy, leading to a new gene score (GSLA10) that can help predict which patients might have worse outcomes.
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Despite their generally favorable prognosis, luminal A tumors paradoxically pose the highest ten-year recurrence risk among breast cancers. From those that relapse, a quarter of them do it within five years after diagnosis. Identifying such patients is crucial, as long-term relapsers could benefit from extended hormone therapy, whereas early relapsers may require aggressive treatment.

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SNAI2 overexpression appears to be associated with poor prognosis in breast cancer, yet it remains unclear in which breast cancer subtypes this occurs. Here we show that excess SNAI2 is associated with a poor prognosis of luminal B HER2/ERBB2 breast cancers in which SNAI2 expression in the stroma but not the epithelium correlates with tumor proliferation. To determine how stromal SNAI2 might influence HER2 tumor behavior, -deficient mice were crossed with a mouse line carrying the protooncogene to generate HER2/ERBB2 breast cancer.

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Despite the frequency of infections with herpesviridae family, only eight subtypes affect humans (Herpex Simplex Virus types 1 and 2, Varicella Zoster Virus, Epstein-Barr Virus, Citomegalovirus and Human Herpes Virus types 6, 7 and 8). Amongst enteroviruses infections, the most important are Poliovirus, Coxackievirus and Echovirus. Symptoms can vary from mild to severe and early diagnosis is of upmost importance.

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Background: An essential question in cancer is why individuals with the same disease have different clinical outcomes. Progress toward a more personalized medicine in cancer patients requires taking into account the underlying heterogeneity at different molecular levels.

Results: Here, we present a model in which there are complex interactions at different cellular and systemic levels that account for the heterogeneity of susceptibility to and evolution of ERBB2-positive breast cancers.

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