This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Breast cancer is the most common cancer among women, and metastatic breast cancer remains highly lethal. During metastasis, cancer cells migrate from the breast to areas called pre-metastatic niches, which are favorable for cancer growth. These niches are created with the help of small extracellular vesicles (sEVs) released by breast cancer cells. Via their protein and RNA cargoes, sEVs encourage inflammation in the niches and suppress immunity, allowing arriving cancer cells to escape immune detection. By promoting new blood vessel formation and leakage of existing blood vessels, sEVs ensure a supply of nutrients for cancer growth in the niches. They can also transform certain cell types in the niches into cancer-supporting cells called cancer-associated fibroblasts. The expression patterns of proteins called integrins in sEVs help determine exactly where metastatic cancer cells will settle, such as in the lungs, liver, or brain..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This health education program explains why smoking is addictive and unhealthy for smokers and people around them. This resource is a MedlinePlus Interactive Health Tutorial from the National Library of Medicine, designed and developed by the Patient Education Institute.

Episode 1, part 1: Interview with Sir Michael Marmot, Professor of Epidemiology and Public Health at University College London about the current state of Global Health, with special focus on Health Equity. The first episode consists of two parts.
-------
The Swedish Global Health Podcast - A Podcast about Global Health and Sustainable Development is aimed at anyone interested in knowing more about this exciting topic! It is co-produced by the Swedish Society of Medicine's Committee for Global Health and the Swedish Society of Medicine's student and junior doctor section.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer with a poor prognosis and limited treatment options. M2-like tumor-associated macrophages (TAMs) are known to promote TNBC aggressiveness, but the mechanisms are unclear. To learn more, a recent study investigated the roles of TAMs in regulating epithelial–mesenchymal transition (EMT) and cancer stem cell (CSC) properties in TNBC, both of which contribute to malignant progression. The results revealed that human TNBC tissues exhibited severe infiltration of TAMs (marked by CD163) and that TAMs were associated with an unfavorable prognosis. In addition, culture media from TAM-like macrophages promoted EMT and CSC-like properties in two TNBC cell lines. Specifically, TAM-secreted CCL2 protein activated AKT signaling to increase β-catenin expression and nuclear localization, and knockdown experiments confirmed the importance of β-catenin in the TAM-induced changes..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Proteins in the tumor necrosis factor (TNF) family are known to regulate the immune system in cancers, and trials targeting these proteins are currently being conducted. However, the TNF family profile in glioma, the most common cancer originating in the adult central nervous system, is unclear. A recent study analyzed the TNF family profile and clinical characteristics of 1749 glioma cases using data from four public datasets. The expression levels of most TNF family members were positively correlated in the gliomas and were linked to patients’ overall survival. A TNF family signature was identified based on the expression levels in 702 of the cases and validated in the other cases, and a prognostic model was developed to predict 1-, 3-, and 5-year survival for individual patients with glioma. The TNF family-based signature was related to clinical, molecular and genetic characteristics of the patients..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cancer and autoimmune disease are two sides of the same coin Autoimmune diseases, such as diabetes, arthritis, and inflammatory bowel disease, are caused by overactivation of the immune response while cancer cells downregulate the immune response in order to promote their own growth One attractive therapeutic target, lymphotoxin β receptor (LTβR) on the cell surface, is central to both processes but its detailed signaling mechanisms have remained unclear, making it difficult to target the pathway Now, researchers have identified a way to alter the strength of LTβR-mediated signaling Using drugs to lower the cholesterol levels in the plasma membrane they showed that the lipid content of the cell membrane affects LTβR-dependent signaling and LTβR internalization Depleting membrane cholesterol caused increased LTβR signaling through the well-known canonical NF-κB signaling pathway suggesting that cholesterol depletion could be used to augment LTβR-based therapies for cancer and choles.."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Phosphatidylserine (PS) is a lipid found in the cell membrane. When exposed on the outside of a cell during stress or during cell death, PS can trigger immune suppression. PS also engages PS receptors on immune cells, resulting in clearance of the cell and production of immune suppressive factors. One way tumors evade the host immune system is by engaging PS signaling. Therefore, inhibiting PS signaling suppression is a promising option for treating cancer. A recent review highlights the contributions of the TIM and TAM family of receptors to PS signaling and immune suppression in tumors. and some of the immunotherapy strategies targeting these receptors that are being investigated in preclinical and clinical trials. Due to the complexity of PS-induced immune suppression, there are still many unknowns. such as the detailed mechanisms and signaling pathways that are involved. or the consequences of interrupting these signaling pathways..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Students are introduced to the unit challenge discovering a new way to assess a person's risk of breast cancer. Solving this challenge requires knowledge of refraction and the properties of light. After being introduced to the challenge question, students generate ideas related to solving the challenge, and then read a short online article on optical biosensors that guides their research towards solving the problem.

Through four lessons and three hands-on activities, students learn the concepts of refraction and interference in order to solve an engineering challenge: "In 2013, actress Angelina Jolie underwent a double mastectomy, not because she had been diagnosed with breast cancer, but merely to lower her cancer risk. But what if she never inherited the gene(s) that are linked to breast cancer and endured surgery unnecessarily? Can we create a new method of assessing people's genetic risks of breast cancer that is both efficient and cost-effective?" While pursuing a solution to this challenge, students learn about some high-tech materials and delve into the properties of light, including the equations of refraction (index of refraction, Snell's law). Students ultimately propose a method to detect cancer-causing genes by applying the refraction of light in a porous film in the form of an optical biosensor. Investigating this challenge question through this unit is designed for an honors or AP level physics class, although it could be modified for conceptual physics.

Student teams conduct an experiment that uses gold nanoparticles as sensors of chemical agents to determine which of four sports drinks has the most electrolytes. In this way, students are introduced to gold nanoparticles and their influence on particle or cluster size and fluorescence. They also learn about surface plasmon resonance phenomena and how it applies to gold nanoparticle technologies, which touches on the basics of the electromagnetic radiation spectrum, electrolyte chemistry and nanoscience. Using some basic chemistry and physics principles, students develop a conceptual understanding of how gold nanoparticles function. They also learn of important practical applications in biosensing.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"In cancer cells, even seemingly small gene expression changes can have a devastating impact, but for some molecules, like the enzyme USP22, researchers don’t know how their expression is regulated. High expression of USP22 is associated with poor prognosis in many human cancers. But the gene for USP22 is rarely mutated, suggesting that the expression changes happen at the transcription step. So, researchers set out to find transcription factors, which are transcription-modulating proteins, that regulate USP22. After identifying several that modulate USP22 expression, they focused on two related factors that increased USP22 expression, AP2α, and AP2β. Overexpressing AP2α/β in cultured non-small cell lung cancer (NSCLC) cells increased the expression of USP22 and the protein it targets, Cyclin D1, while also increasing the cancer cell behaviors proliferation, migration, and invasion..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The MAPK/ERK inhibitor vemurafenib is frequently used to treat late-stage melanomas with the BRAF V600E mutation, but acquired resistance is a major challenge, and it’s unclear if this resistance is due to unintended effects on normal stromal cells. To find out, a recent study examined early vemurafenib-induced molecular changes in human dermal fibroblasts (HDFs), a main stromal cell type of melanomas. Sequencing revealed that vemurafenib upregulated proliferation-related genes but downregulated genes related to autophagy and protein degradation in the HDFs, while it exerted the opposite effects in melanoma (MaMel) cells. The expression changes were consistent with the observed paradoxical effects of vemurafenib. Specifically, vemurafenib hyperactivated MAPK/ERK signaling in normal HDFs despite inhibiting it in melanoma cells, which seemed to be facilitated by a permissive chromatin landscape. The paradoxical effects indicate that vemurafenib monotherapy may promote cancer progression in normal cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Gastric cancer is the third leading cause of cancer-related mortality worldwide. Treatment of metastatic gastric cancer typically aims to prolong overall survival and maximize health-related quality of life. For patients who have failed previous gastric cancer treatments, the oral, fixed-dose tablet trifluridine/tipiracil, appears to do just that. Adding tipiracil slows trifluridine metabolism, boosting the anti-cancer effect at a manageable level of drug toxicity by increasing trifluridine bioavailability in the body. Once inside the cancer cell, trifluridine inhibits cell proliferation by interfering with DNA synthesis. The pivotal phase 3 TAGS trial examined trifluridine/tipiracil’s efficacy and tolerability in previously treated patients with metastatic gastric cancer or adenocarcinoma of the gastroesophageal junction..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cancer cells don’t just exist in isolation. Their dynamic interactions with cells and non-cell components in the tumor microenvironment (TME) allow cancer cells to grow and evolve. A new review highlights the complexity of the TME, the implications for cancer therapy, and advances in TME research. Tumor cells control the function of their environment, co-opting complex signaling networks for their own benefit, resulting in multi-drug resistance, metastasis, and cancer progression. To fully understand this phenomenon, we must go beyond 2D systems, using novel technologies such as 3D platforms and lab-on-chip devices to better simulate TME biology and function. Researchers can replicate the behavior of cells in the TME, including tumor epithelial cells, pericytes, cancer-associated fibroblasts, and tumor-associated macrophages. Non-cellular factors, including extracellular matrix components, exosomes, circulating free DNA, and apoptotic bodies, are also more easily studied using 3D systems..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Tumor pathophysiology plays a central role in the growth, invasion, metastasis and treatment of solid tumors. This class applies principles of transport phenomena to develop a systems-level, quantitative understanding of angiogenesis, blood flow and microcirculation, metabolism and microenvironment, transport and binding of small and large molecules, movement of cancer and immune cells, metastatic process, and treatment response. 
Additional Faculty 
Dr. Pat D’Amore
Dr. Dan Duda
Dr. Robert Langer
Prof. Robert Weinberg
Dr. Marsha Moses
Dr. Raghu Kalluri
Dr. Lance Munn

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Lung cancer and breast cancer are the two most common types of cancer worldwide. Despite abundant research, the detailed molecular mechanisms behind their progression have remained elusive. A recent study uncovered a key signaling pathway underlying lung and breast cancer development. Receptor for advanced glycation end products (RAGE) is a ubiquitous transmembrane receptor that is upregulated in inflammatory conditions. One of its ligands, lysophosphatidic acid (LPA), is a biologically active phospholipid involved in atherosclerosis, inflammation, diabetes, and cancer. Although these proteins are known to contribute together to other types of cancer, their role in lung and breast cancer has remained unknown. Using in vitro and in vivo mouse studies to evaluate markers of tumor development and progression, researchers found that signaling through RAGE via LPA increased the proliferation, migration, and invasion of lung and breast cancer cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Esophageal cancer causes over 500,000 deaths worldwide each year One major subtype of the disease, ESCC, is driven by the sustained growth of tumor cells with stem cell characteristics The “stemness” of the tumor cells allows the cells to grow and metastasize, causing treatment resistance Unfortunately, how these cells retain their stemness is unclear In a recent study, researchers sought to determine what regulates tumor cell stemness Using molecular biology techniques, they evaluated the genes and proteins expressed in tissue from ESCC patients The results showed that ESCC tumor cells were stimulated by a pro-inflammatory molecule called LPS LPS induced the expression of genes that are known to regulate stemness Overexpressing the genes led to larger xenograft tumors in mice, suggesting that these genes are responsible for tumor growth The signaling pathway initiated by LPS may be an ideal target for new therapies for ESCC Giving new hope to patients struggling with this difficult disease.."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Breast cancer affects 1 in 8 women worldwide. While early diagnosis and treatment have improved, recurring cancer is difficult to control, resulting in a poor survival rate. A recent study focused on better understanding the role of a hormone signaling component in breast cancer progression. Progesterone receptor membrane component 1 (Pgrmc1) is a non-classical progesterone receptor with diverse roles in metabolism and steroidogenesis. Using a mouse model of breast cancer, researchers examined tumor development and lung metastasis in mice with or without Pgrmc1. They found that while silencing Pgrmc1 did not affect tumor size at 13 weeks, mice lacking Pgrmc1 survived significantly longer than wild-type mice. Mice without Pgrmc1 also exhibited a lower degree of lung metastasis and lower expression of migration and metastasis markers and in breast cancer cell lines, silencing Pgrmc1 reduced the migration rate..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The hormone and receptor pair IGF-1 and IGF-1R and the Hippo-YAP signaling pathway are critical to breast cancer stem cells, but if or how these pathways interact in these cells remained unclear. So, researchers recently examined YAP and IGF-1R in triple negative breast cancer cell lines and xenograft models. YAP knockdown reduced viability and stemness in cell culture and tumorigenicity in vivo, suggesting that YAP contributes to stemness in breast cancer cells. Further tests determined that IGF-1R regulated YAP expression, and in turn, YAP regulated IGF-1 expression but not IGF-1R. Specifically, depleting IGF-1R decreased YAP expression, while addition of IGF-1 upregulated YAP and increased its nuclear localization. YAP overexpression increased IGF-1 expression without impacting IGF-1R expression. In clinical data from basal-like breast cancer patients, higher levels of YAP and IGF-1 are correlated with shorter overall survival..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Breast cancer remains one of the most common cancers among women, indicating that better treatments are needed. The drug THZ1 is effective against triple-negative breast cancer, which frequently features overexpression-inducing mutations in the protein p53. However, THZ1 is ineffective against breast cancer cells with nonmutated (wild-type, WT) p53. To improve treatment options, researchers recently tried to increase the THZ1 sensitivity of WT p53 breast cancer cells. Treating the cells with nutlin-3, a molecule that indirectly prevents p53 degradation, enhanced the killing ability of THZ1, and overexpression experiments confirmed that this sensitization was due to upregulation of functional p53. Further investigation into the mechanism revealed that p53 accumulated in the nuclei and mitochondria of the dying cells after nutlin-3 and THZ1 treatment..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.