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:

"Apoptosis is a form of cell death that occurs as part of normal development. Once considered irreversible, apoptosis might not mark the end for all cells—including cancer cells. Growing evidence suggests that cancer cells can be rescued from the brink of death through a process called anastasis, which could explain how tumors resist anticancer therapies. From the Greek for “resurrection,” anastasis can occur through a variety of mechanisms, such as by arresting the activity of caspases, enzymes in charge of dismantling the cell during apoptosis by activating DNA repair mechanisms and by allowing cell fragments to fuse and continue living even after apoptosis has begun. Further studies are needed to explore how cancer cells cheat death through anastasis and how to adjust anticancer therapies accordingly..."

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

The lethal poison Ricin (best known as a weapon of bioterrorism), Diphtheria toxin (the causative agent of a highly contagious bacterial disease), and the widely used antibiotic tetracycline have one thing in common: They specifically target the cell's translational apparatus and disrupt protein synthesis.
In this course, we will explore the mechanisms of action of toxins and antibiotics, their roles in everyday medicine, and the emergence and spread of drug resistance. We will also discuss the identification of new drug targets and how we can manipulate the protein synthesis machinery to provide powerful tools for protein engineering and potential new treatments for patients with devastating diseases, such as cystic fibrosis and muscular dystrophy.
This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching.

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-associated fibroblasts (CAFs) are part of the “soil” in which tumors grow. These cells have diverse origins and can interact with tumor cells in various ways, making it difficult to determine whether they’re friends or foes in cancer treatment. Detecting biomarkers can help address this challenge by allowing researchers to identify different CAF subsets. Several CAF biomarkers are associated with cancer promotion, such as FAP, vimentin, galectin 1, and osteopontin. For example, FAP increases cancer cell invasiveness and leads to immunotherapy resistance. Other CAF biomarkers are associated with cancer inhibition, like meflin, which is linked to a good prognosis in pancreatic and lung cancers. However, some biomarkers can either encourage or suppress cancer depending on the context..."

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:

"Resistance to therapy is a major hurdle in current cancer treatments. A major part of the problem is heterogeneity. Tumors, by their nature, have multiple cell lineages with varying characteristics. Among these are cancer stem cells (CSCs). CSCs can regenerate a tumor even after treatment kills many of its other cells. And they can go dormant, transport drugs outside the cell membrane, avoid apoptosis, and express resistance-conferring non-coding RNAs, all of which boost tumors’ resistance to treatment. A new review describes common CSC surface markers, deregulated signaling pathways, and resistance mechanisms as well as the status of research into CSC therapies. Current therapies targeting CSCs do not address tumor heterogeneity or the complexity of the tumor microenvironment..."

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

In this problem-based learning module, students will work together collaboratively to establish questions and develop these questions into claims after being presented with the problem “How are today’s living standards contributing to the drug resistance disease crisis and what needs to be done to begin to reverse the effects of the contributing factors?”  The students will then work collaboratively to continue researching and will use the research to create a collaborative electronic public service announcement to go along with an individually written letter which will be sent to either a state representative, the FDA, lead community personnel, etc. Both products, the PSA and the letter will include their well defined claim, supported with evidence and backed up with reasoning.Prior to beginning module, please note: Module can be completed in isolation, or can be completed in conjunction with modules "Antibiotic Resistance and Antibiotic Policy" (science) and/or Advancing Change through Public Awareness (social studies) as part of a full interdisciplinary unit between 8th grade social studies, language arts and science.  This would allow for students to have a wider array of questions to guide their claims and the students could build the PSA in social studies and write the letter in Language Arts.

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:

"Prostate cancer remains the second leading cause of cancer death in men, although the mechanisms of its progression are still debated. Extracellular vesicles are critical mediators of communication between prostate cancer cells and their surrounding cells and can influence malignancy. For example, prostasomes released from prostate cancer cells contain factors that promote cell survival and tumor progression, while large oncosomes support target cell reprogramming by delivering molecules related to cell growth, proliferation, and movement or RNA processing. Smaller exosomes can also induce reprogramming by shuttling a wide variety of proteins and nucleic acids. The numbers, cargoes, and structures of exosomes can change depending on prostate health or the cancer stage, which makes these vesicles and their contents good biomarkers, especially since they can be sampled non-invasively from body fluids. Exosomes’ ability to deliver materials to target cells can also be exploited to achieve targeted therapies..."

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 ligand protein PD-L1 on tumor cells can bind to the receptor protein PD-1 on T cells. This binding negatively regulates T cells to suppress immunity, facilitating large-scale tumor growth. Antibody drugs have been designed to block cell-surface PD-L1/PD-1 binding, but they’re not very effective, possibly because tumor cells can secrete extracellular vesicles (EVs) that express PD-L1. The PD-L1 on EVs can also induce immunosuppression, leading to drug resistance. EV PD-L1 plays tumor-promoting roles in many cancers, such as breast cancer, prostate cancer, and melanoma, and unlike cell-surface PD-L1, which isn’t expressed stably enough to be reliable, EV PD-L1 may be a useful biomarker. Because of its location, EV PD-L1 may also be a good treatment target. For example, drugs preventing EV release have been shown to activate antitumor responses in melanoma cells and to reduce prostate tumor growth and increase anti-PD-L1 efficacy against colon cancer in mice..."

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:

"One of the hallmarks of cancer is the reprogramming of the body’s metabolism to support tumor growth. That includes the breakdown of glucose into lactate, a process that normally occurs only under low-oxygen conditions. High levels of lactate are known to boost tumor invasion and suppress attacks by the immune system, and a new study suggests that lactate might also make cancer cells increasingly resistant to chemotherapy drugs. Experiments showed that exposure to the chemotherapy drug etoposide reprogrammed non-small lung cancer cells to generate increasing amounts of lactate. The resulting buildup of lactic acid was identified as the key process conferring drug resistance through the upregulation of multidrug resistance-associated protein 1 (MRP1). MRP1 expression inhibits the toxic effects of chemotherapy drugs like etoposide by increasing their expulsion from cancer cells. Removing lactate with sodium bicarbonate was sufficient to overcome resistance to etoposide..."

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

This presentation provides an introduction to antimalarial drug resistance. First we will focus on how drug resistance is observed and measured. Thereafter we will describe the historical emergence and spread of drug resistance. Third we will focus on molecular aspects of drug resistance, the so-called molecular markers and finally we will describe how we can use our knowledge regarding these molecular markers in the surveillance of drug resistance and eventually help in guide us in the decision-making when developing new drug policies.

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 colorectal cancer, resistance to the chemotherapy drug 5-fluorouracil (5-FU) is a major barrier to treatment success, but the mechanism isn’t clear. To learn more, a recent study investigated 5-FU resistance in two colon cancer cell lines. Cell culture medium derived from 5-FU-resistant cells reduced 5-FU sensitivity when applied to other cells, indicating that the resistant cells secreted a resistance-inducing substance. The resistance development was accompanied by changes in the number and shape of Cajal bodies, nuclear structures that regulate RNA processing and increased phosphorylation of an important Cajal body component called coilin. Additional studies revealed that the protein UHMK1 as a kinase was responsible for resistance induction. Specifically, UHMK1 altered Cajal body assembly/disassembly and phosphorylated coilin. In turn, these effects markedly altered RNA splicing in the nucleus to affect cellular characteristics and survival and to promote protumor signaling..."

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:

"Non-small cell lung cancer (NSCLC) is the most common form of lung cancer, and it tends to have a poor prognosis. For NSCLC with EGFR gene mutation, the tyrosine kinase inhibitor osimertinib can be an effective targeted therapy. However, patients usually develop resistance to osimertinib over time, often due to additional changes in the EGFR gene. For example, tumors can develop mutations in exons 18 and 20 of EGFR that reduce osimertinib's ability to bind to its target. In addition, the EGFR gene can become amplified, leading to extra copies in the genome. This leads to abnormally high amounts of the EGFR protein, overwhelming osimertinib and triggering signaling pathways that promote cancer progression. Over time, tumor cells with resistance-promoting mutations can replace the original drug-sensitive cells that are killed off by osimertinib. Combination therapies or next-generation tyrosine kinase inhibitors might help address these limitations of osimertinib..."

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:

"Combination therapy with BRAF and MEK inhibitors have become the standard of care for patients with metastatic melanoma harboring BRAF mutations. But one persistent problem is the emergence of drug resistance. A new study reports that one way to overcome this obstacle could be the incorporation of reverse transcriptase inhibitors, or RTIs. RTIs target genetic elements called retrotransposons, which are activated by tumor formation and have been frequently used in treating HIV. Combining the RTI SPV122 with BRAF and MEK inhibitors was shown to have a favorable effect against BRAF-mutant melanoma, inhibiting cell growth, inducing cell death through apoptosis, and delaying the emergence of drug resistance. Further experiments revealed the RTI mechanisms giving rise to these effects, including DNA double-strand breaks, mitochondrial membrane depolarization and increased levels of reactive oxygen species..."

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 is now the second leading cause of cancer-related deaths in women. However, because of its resistance to many cancer-fighting drugs, only a few treatment options are available. Emphasizing the need to discover and develop new methods for battling this disease. Signal transducer and activator of transcription 3 (STAT3) is known to contribute to breast cancer progression, proliferation, metastasis, and drug resistance. Making STAT3 a promising target for breast cancer therapy. A recent review reports what is currently known about the role of STAT3 pathways in breast cancer. and gives an update on the drugs currently available for targeting STAT3 pathways. New upstream regulators and downstream targets of STAT3 have been discovered and are potential drug targets, and combination therapy targeting mammalian target of rapamycin (mTOR) and STAT3 is a promising treatment option..."

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:

"Gliomas are the most common brain tumors They’re also the most aggressive, able to resist various forms of chemotherapy Part of that ability comes from cancer stem cells rare cells with the capacity to form new tumors Researchers recently set out to understand how these cells are linked to drug resistance and prognosis among patients with glioma Using data from gene atlases, they developed a so-called risk signature This signature was designed to identify genetic factors tied to an increased risk of resistance to the popular chemotherapy drug temozolomide Tests showed that the risk signature could well predict the prognosis of patients with drug-resistant gliomas with a high risk score indicating shorter survival and malignant traits The risk signature also provides new ways to classify gliomas which could help clinicians deliver targeted treatment sooner With further refinement, the signature could serve as a stand-alone biomarker for the personalized treatment of patients with glioma.."

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.

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:

"Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related deaths worldwide, and its mortality continues to rise. Its aggressiveness, presentation at an advanced stage, and resistance to most treatments have made this cancer very difficult to treat. Therefore, identifying novel PDAC biomarkers for predicting survival and monitoring therapy response is critical. Most studies have searched for gene signature biomarkers for PDAC. But the complexity of this cancer has made finding these types of biomarkers difficult. A recent study analyzed the usefulness of using functional signatures as biomarkers for this disease. Using an analytical method called Functional Analysis of Individual Microarray Expression (FAIME), the researchers converted transcriptional information into molecular functional profiles. They identified a functional signature belonging to the drug metabolism-cytochrome P450 pathway that better predicted prognosis, drug response, and chemotherapeutic efficacy for PDAC..."

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:

"MicroRNAs (miRNAs) are small RNA molecules that can modulate gene expression to affect numerous biological processes. One such molecule, miRNA-93, is dysregulated in various diseases and might be a valuable marker of prognosis. For example, it’s generally upregulated in lung cancer, prostate cancer, glioma, osteosarcoma, and hepatocellular carcinoma, where it promotes cell proliferation, migration, and invasion to drive cancer progression. It can also induce the development of chemotherapy resistance. Furthermore, miRNA-93 contributes to coronary artery blockage, Parkinson’s disease, postmenopausal osteoporosis, and acute kidney injury. However, it’s not always upregulated in disease. In fact, it’s downregulated in gastric, bladder, cervical, and renal cancer, sometimes exerting anti-tumor effects. These differences emphasize the need to truly understand miRNA-93’s role in a specific disease before using miRNA-93 as a prognostic marker or treatment target..."

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