Cancer Biology Research’s Post

I'm excited to share our recent article "Cancer therapy with the viral and bacterial pathogens: The past enemies can be considered the present allies" has just been published in the journal of Life Sciences. Despite advancements, cancer remains a leading cause of death. Conventional treatments like chemotherapy and radiotherapy face challenges like poor drug penetration and drug resistance. This review examines bacterial-based therapies and oncolytic viruses (OVs) as promising alternatives. These methods can selectively target and kill cancer cells, offering new hope for effective treatments. The article discusses the latest research, strategies, and the need to optimize these therapies for better outcomes. Thanks to all contributing authors for this valuable review. Link to this article: https://lnkd.in/dJ-Y-9Np #CancerResearch #CancerTherapy #Oncology #BacterialTherapy #OncolyticViruses #MedicalResearch

Pre-initiation in at least some cancer is polyclonal – not just due to one aberrant cell. This has been demonstrated in a study that that pairs long-term temporal tracking in mice with human single-cell multi-omics data to address questions regarding cellular origins and chronology in development and cancer. This was based on a custom CRISPR-based platform called "NSC-seq" for temporal recording and lineage tracking at single-cell resolution. They adapted NSC-seq to single-cell resolution with high gRNA detection and transcriptome quality, introduced of a mutational density metric to track temporal changes and augmented hgRNA mutational information with somatic mitochondrial variants (mtVars) to improve lineage tracking. This goes some way to explaining the inherent diversity in tumors, which has been known since Ken Pienta’s groundbreaking studies in the early 2000s that showed there is as much diversity between tumors in a single patient than between patients. It also implies that cancer vaccine strategies based on neoantigens are likely to be suboptimal both in response levels and durability. https://lnkd.in/dNz8TYiS

📚New Research Alert! Discover how cell type specific PD-L1 expression predicts treatment outcomes in urothelial cancer. 🔬 In this study, CellCarta scientists Mark Kockx and Roos Van Elzen leveraged their expertise in PD-L1 scoring and multiplex IHC to perform assays and analysis demonstrating how immune cell PD-L1 expression was associated with improved responses to treatment compared to tumor cell-dominant PD-L1 expression. Key Findings: ⭐ PD-L1 staining on immune cells is associated with improved responses to checkpoint inhibitors over PD-L1 staining predominantly on tumor cells ⭐ The SP142 assay preferentially detects PD-L1- expressing dendritic cells Read the full article here: https://buff.ly/4azZGAU This research demonstrates why some PD-L1 testing has inconsistent predictive results for immune checkpoint blockade benefits, and shows how multiplex IHC can be applied to identify the specific cell types expressing PD-L1, contributing to an improved understanding of treatment outcomes.

síndrome genética brca e tumores envolvidos Mutations in the **BRCA1** and **BRCA2** genes significantly increase the risk of developing certain cancers, particularly breast and ovarian cancers. These genes are crucial for DNA repair; when mutated, they lead to genomic instability and a higher likelihood of tumor formation. Approximately 5-10% of breast cancers and 20% of ovarian cancers are linked to these mutations, elevating breast cancer risk up to 80% and ovarian cancer risk up to 40% over a lifetime. Additionally, BRCA mutations are associated with prostate cancer and other malignancies, such as pancreatic and colon cancers.

Do you need to get a mammogram? The American Cancer Society provides the following screening guidelines for women at average risk of breast cancer: "These guidelines are for women at average risk for breast cancer. For screening purposes, a woman is considered to be at average risk if she doesn't have a personal history of breast cancer, a strong family history of breast cancer, or a genetic mutation known to increase risk of breast cancer (such as in a BRCA gene), and has not had chest radiation therapy before the age of 30. *Women between 40 and 44 have the option to start screening with a mammogram every year. *Women 45 to 54 should get mammograms every year. *Women 55 and older can switch to a mammogram every other year, or they can choose to continue yearly mammograms. Screening should continue as long as a woman is in good health and is expected to live at least 10 more years. *All women should understand what to expect when getting a mammogram for breast cancer screening – what the test can and cannot do." Regarding mammograms, there is a great tool which is becoming more common: digital breast tomosynthesis, also known as 3D mammography. Our 3D mammogram combines multiple X-ray images into a 3D model so the radiologist has more views of the breast, which may help in detecting cancer earlier. If you would like to schedule a mammogram, call 214-320-7000 to make an appointment.

📃Scientific paper: SRPX2 promotes cancer cell proliferation and migration of papillary thyroid cancer Abstract: Thyroid cancer is the endocrine tumor with the highest incidence at present. It originates from the thyroid follicular epithelium or follicular paraepithelial cells. There is an increasing incidence of thyroid cancer all over the world. We found that SRPX2 expression level was higher in papillary thyroid tumors than in normal thyroid tissues, and SRPX2 expression was closely related to tumor grade and clinical prognosis. Previous reports showed that SRPX2 could function by activating PI3K/AKT signaling pathway. In addition, in vitro experiments showed that SRPX2 promoted the proliferation and migration of papillary thyroid cancer (PTC). In conclusion, SRPX2 could promote the malignant development of PTC. This may be a potential treatment target for PTC. Continued on ES/IODE ➡️ https://etcse.fr/63HCj ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: SRPX2 promotes cancer cell proliferation and migration of papillary thyroid cancer Abstract: Thyroid cancer is the endocrine tumor with the highest incidence at present. It originates from the thyroid follicular epithelium or follicular paraepithelial cells. There is an increasing incidence of thyroid cancer all over the world. We found that SRPX2 expression level was higher in papillary thyroid tumors than in normal thyroid tissues, and SRPX2 expression was closely related to tumor grade and clinical prognosis. Previous reports showed that SRPX2 could function by activating PI3K/AKT signaling pathway. In addition, in vitro experiments showed that SRPX2 promoted the proliferation and migration of papillary thyroid cancer (PTC). In conclusion, SRPX2 could promote the malignant development of PTC. This may be a potential treatment target for PTC. Continued on ES/IODE ➡️ https://etcse.fr/63HCj ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

Triggering Necroptosis in Tumor Cells Can Backfire in a Cloud of IL-1a Tumor cell deaths can benefit tumors. A paradox? Not at all. If, for example, a dying tumor cell undergoes necroptosis, it can release inflammatory factors that can enhance or diminish antitumor immunity. Consequently, the idea of relying on necroptosis, an inflammatory form of cell death, as an alternative or adjunct to apoptosis, a non-inflammatory form of cell death, needs to be pursued with all due caution. To determine how necroptosis could be induced as a means of fighting cancer, scientists at the H. Lee Moffitt Cancer Center and Research Institute have been studying necroptosis activation, which involves the necroptosis mediators RIPK3 and MLKL. In a new study, the scientists, who were led by Brian Ruffell, PhD, found to their surprise that RIPK3 and MLKL were dispensable for tumor growth in genetic and implantable models of breast or lung cancer. What’s more, the scientists determined that inducing necroptosis within established breast tumors generated a myeloid-suppressive microenvironment that inhibits T-cell function, promotes tumor growth, and reduces survival. https://hubs.li/Q02ZD0QB0

🔍 Did you know that prostate cancer is the second most common cancer among men and a leading cause of cancer-related deaths in the USA? With September being Prostate Cancer Awareness Month, it’s crucial to emphasize the importance of early detection. 💡 At Virdx, the virtual diagnostics unit of QuantCo we’re on a mission to revolutionize cancer diagnostics. Starting with prostate cancer, we’re making non-invasive, dignified, and actionable diagnostics a reality through advancements in magnetic resonance physics, machine learning, and software engineering. 📘 Learn more: Prostate Cancer Foundation’s Top 10 Facts https://lnkd.in/dBbVKvna #quantco #ProstateCancerAwareness #MensHealth #AI #HealthcareInnovation Ken Herrmann Jens Kleesiek Jacob Matthew Murray Boris Hadaschik Edward Steiner Henning Reis (MD, PD Dr. med.) QuantCo Prostate Cancer Foundation Prostate Cancer UK

Cancer cells exhibit uncontrolled division due to genetic mutations that disrupt the normal regulatory mechanisms governing cell growth and death. Unlike healthy cells, which divide in a controlled manner to maintain tissue health, cancer cells bypass these controls, leading to rapid and unchecked proliferation. This relentless division results in the formation of tumors and can facilitate the spread of cancer to other parts of the body. Understanding the mechanisms behind cancer cell division is crucial for developing effective treatments. For instance, chemotherapy targets rapidly dividing cells by damaging their DNA or interfering with the cell division process, thereby inhibiting tumor growth. Advancements in research continue to shed light on the complexities of cancer cell division, offering hope for more targeted and effective therapies in the future.