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Mashup Score: 5Home – Hallmarks of Cancer - 2 hour(s) ago
Hallmarks of Cancer
Source: www.cell-symposia.comCategories: General Medicine News, Onc News and JournalsTweet
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Mashup Score: 108
Diepstraten et al. demonstrate that p53 enforces apoptosis induced by BH3-mimetic drugs. To boost BH3-mimetic-induced apoptosis in TP53-mutant blood cancers, STING agonists were employed to induce pro-apoptotic BH3-only protein expression in a p53-independent manner. Therefore, BH3-mimetics alongside STING agonists represents a promising new combination therapy for aggressive TP53-mutant blood cancers.
Source: www.cell.comCategories: General Medicine News, Onc News and JournalsTweet
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Mashup Score: 106
The increasing number of approved treatment combinations for metastatic renal cell carcinoma highlights the need for actionable biomarkers to guide treatment selection. In this issue of Cancer Cell, Saliby et al. validate the distinct clinico-genomic profiles of expression-based molecular clusters identified in the IMmotion151 trial in the JAVELIN Renal 101 dataset.
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Mashup Score: 154
Cancer-associated fibroblasts (CAFs) exhibit spatial and functional diversity. Here, Niu et al. unveil SETD2’s function in lipid metabolism and CAF heterogeneity in pancreatic ductal adenocarcinoma. SETD2 deficiency boosts oxidative phosphorylation activity, prompting lipid-laden CAF formation through BMP2 signaling, offering promising therapeutic avenues in personalized cancer treatment.
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Mashup Score: 209
Tumor-associated macrophages (TAMs) are well known to fuel tumor evolution. Blériot et al. advocate for integrating the time dimension when conceptualizing macrophage diversity in pre-malignancy and cancer and propose the term “PreTAMs” to emphasize their early roles in orchestrating inflammatory responses that often precede, and not just result from, tumor onset.
Source: www.cell.comCategories: General Medicine News, Onc News and JournalsTweet
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Mashup Score: 202
Tumor-associated macrophages (TAMs) are well known to fuel tumor evolution. Blériot et al. advocate for integrating the time dimension when conceptualizing macrophage diversity in pre-malignancy and cancer and propose the term “PreTAMs” to emphasize their early roles in orchestrating inflammatory responses that often precede, and not just result from, tumor onset.
Source: www.cell.comCategories: General Medicine News, Onc News and JournalsTweet
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Mashup Score: 202
Tumor-associated macrophages (TAMs) are well known to fuel tumor evolution. Blériot et al. advocate for integrating the time dimension when conceptualizing macrophage diversity in pre-malignancy and cancer and propose the term “PreTAMs” to emphasize their early roles in orchestrating inflammatory responses that often precede, and not just result from, tumor onset.
Source: www.cell.comCategories: General Medicine News, Onc News and JournalsTweet
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Mashup Score: 154
Cancer-associated fibroblasts (CAFs) exhibit spatial and functional diversity. Here, Niu et al. unveil SETD2’s function in lipid metabolism and CAF heterogeneity in pancreatic ductal adenocarcinoma. SETD2 deficiency boosts oxidative phosphorylation activity, prompting lipid-laden CAF formation through BMP2 signaling, offering promising therapeutic avenues in personalized cancer treatment.
Source: www.cell.comCategories: General Medicine News, Onc News and JournalsTweet
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Mashup Score: 192Identification of hypoxic macrophages in glioblastoma with therapeutic potential for vasculature normalization - 13 day(s) ago
Pronounced necrosis in glioblastomas is accompanied by abundant destabilized microvessels. Wang et al. show that the niche cues from the peri-necrotic regions polarize macrophages toward a hypoxic state, which in turn augments vascular hyperpermeability. Targeting adrenomedullin produced by hypoxic macrophages normalizes tumor neovasculature and improves anti-tumor drug delivery and efficacy.
Source: www.cell.comCategories: General Medicine News, Onc News and JournalsTweet
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Mashup Score: 268The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia - 16 day(s) ago
Liu et al. identify a novel feedforward loop between tumor cells and macrophages that promotes muscle wasting. Specifically, tumor-derived CCL2 activates macrophages to facilitate non-autonomous activation of TWEAK in tumor cells via CCL5/p65 signaling, leading to cachexia. Macrophage depletion and TWEAK inhibition represent promising therapeutic targets for pancreatic cancer cachexia.
Source: www.cell.comCategories: General Medicine News, Onc News and JournalsTweet
As we commemorate the 50th anniversary of Cell Press, we invite you to join us in celebrating our unwavering commitment to serving the #cancerresearch community at a special anniversary meeting in Guangzhou, China @CellSymposia #CSHallmarks24 https://t.co/hfPQL3FjCN https://t.co/tcqWhDfenB