Neoadjuvant therapy with conventional chemotherapies have visibly improved the prognosis of locally advanced pancreatic cancer (PCa). However, molecular targeted therapies that have provided durable responses in other tumor entities, have not yet found access into neoadjuvant therapy of PCa. In fact, due to the presence of the tumor burden serving as an antigen source for T cell priming, neoadjuvant chemotherapy may unleash a more potent antitumoral immune response than adjuvant or palliative chemotherapy.
Once metastatic disease has occurred, there is no cure for breast cancer. Consequently, identifying factors that promote and support breast cancer metastasis is critical for understanding how to pharmacologically target this process. Hormonally up-regulated neu-associated kinase (HUNK) is a serine/threonine protein kinase related to the sucrose non-fermenting-1 (Snf-1)/5' adenosine monophosphate-activated protein kinase (AMPK) family of kinases. HUNK has been found to play a role in breast cancer metastasis. However, conflicting reports indicate HUNK is a metastasis promoting factor as well as an inhibiting factor. Our group recently provided evidence that supports the conclusion that HUNK is a metastasis promoting factor by showing that HUNK regulates breast cancer metastasis through phosphorylation of EGFR. Here, we summarize our findings and discuss their implications toward pharmacological targeting of HUNK in breast cancer.
Cancer Research has benefitted from substantial expenditures by federal and nonprofit organizations. The resulting success in patient care has been uneven. Two lessons from the 20th century history of science suggest infrastructural changes that can boost success. We need to better organize big science, explicitly aiming for expedient clinical translation. In parallel, resource allocation should enable investigator-initiated exploration on the basis of productivity per research dollars spent.
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：