Sentence examples for development of a tumor from inspiring English sources

The concept of early metastatic dissemination, however, postulates that cancer cell spread might arise early during the development of a tumor.

A mutation that helps make cells immortal is critical to the development of a tumor, but new research at UC Berkeley suggests that becoming immortal is a more complicated process than originally thought.

An important objective in nowadays research remains the development of a tumor marker panel with a sufficient accuracy for risk assessment, early diagnosis, prognosis, and response to therapeutic treatment of cancer.

Sustained angiogenesis, through either local sprouting (angiogenesis) or the recruitment of bone marrow-derived cells (BMDCs) (vasculogenesis), is essential to the development of a tumor.

Over the past year, our panel of over 20 experts has studied the biology of breast cancer development – including known risk factors and other biological events that precede development of a tumor.

Tumor growth and metastasis are both dependent on the development of a tumor vasculature in a process termed angiogenesis.

We herein report the development of a tumor-targeting, pH-responsive, and enzymatically degradable crosslinked fluorescent nanogel (F-nanogel) of boronic acid-conjugated lactose modified-chitosan (chitlac-BOH) and dopamine- and nitric oxide-conjugated partially carbonized hyaluronic acid [NO/DA-FNP HA)] for doxorubicin (DOX) loading.

Moreover, MDSCs produce a substantial amount of IL-10, which allows to form an immunosuppressive in vivo niche, implying the critical role of IL-10 for development of a tumor-permissive TME (Hart et al., 2011).

Pro-inflammatory ATP can be hydrolyzed to immunosuppressive adenosine, which could lead to immune suppression and development of a tumor-promoting microenvironment that reduces the efficacy of anti-tumor immune responses.

Taken together, our data suggest that ERK-dependent induction of INPP4B triggers the development of a tumor-resistance phenotype via Akt signaling and identify INPP4B as a potentially important target molecule for resolving the radioresistance of cancer cells.

However, despite promising preclinical results, targeting mTOR complex 1 (mTORC1) with rapamycin and its analogues failed to show clinical efficacy in PCa (Amato et al, 2008) due to the emergence of survival feedback loops (O'Reilly et al, 2006; Carracedo et al, 2008; Rodrik-Outmezguine et al, 2011) or concomitant development of a tumor-driven lipogenic phenotype (Menendez & Lupu, 2007).