#oncogenesi

[medicomunicare]

Il DNA extracromosomiale: "il nemico in casa" che può essere sfruttato per trattare i tumori più aggressivi

DNA normale e speciale: focus sul DNA extracromosomiale Il nostro DNA è solitamente immagazzinato in strutture chiamate cromosomi che si trovano in quasi tutte le cellule del corpo. Garantiscono che quando le cellule si dividono, il loro DNA venga copiato accuratamente in nuove cellule. Tuttavia, il DNA extracromosomico (ecDNA) esiste al di fuori dei cromosomi in piccoli cerchi di materiale…

[mistfunk]

Mistigram: this texty screen, a touch of Bosch at the beach, is the handiwork of @adelfaure , designed as album art for #EarthlyDelight by #Oncogenesis. This piece was included in the new music-themed MIST0224 artpack collection.

[bpod-bpod]

Unexpected Indication

Like a burly bouncer with a hidden talent for ballet, there’s more to telomeres than meets the eye. They are repeating sections of DNA that sit at the end of strands, protecting the inner regions by degrading a little each time a cell replicates. They eventually diminish sufficiently to cause cell damage as we age. It was recently discovered that, counter to previous beliefs, these lengths of DNA can code for two small proteins, VR and GL. Researchers synthesised these to study their impacts, and then found them more frequently in cancer cells (pictured, VR in green, human cancer cells in red) and in people with telomere-related diseases. A blood test for these proteins might be a route to early cancer diagnosis, and as the levels rise over time, the potent proteins might be an indicator of a person’s biological age (a more significant indicator of health than chronological age).

Written by Anthony Lewis

Image from work by Taghreed M. Al-Turki and Jack D. Griffith

Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Image copyright held by the original authors

Research published in Proceedings of the National Academy of Science (PNAS), September 2023

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[neosciencehub]

Our Research Targets as Many Traits of Cancer as Possible Through Pseudogenes

Our Research Targets as Many Traits of Cancer as Possible Through Pseudogenes @neosciencehub #neosciencehub #science #research #pseudogenes #cancer #NSH #EMBL #NCI #NIH #biology #Genomics #healthcare #DNA #oesophagel #IISER #AI #NCI #

Meet GovadaPravallika, a promising mind who has pursued her Masters in Science from the esteemed Indian Institute of Science Education and Research (IISER), Pune, one of only six such institutions in India. Currently, she is delving deeper into the realm of Cancer Biology and Genomics for her PhD. She took a leap in her world of genetics and genomics and published a radical research- “Stage II…

[residancylog]

September 16th | Signal transduction | 26 days.

Dear Lenin,

I’ve finally gathered the courage to share these subtle updates with you. Truth be told, I was hesitant to document even a fragment of this still-undefined/ undifferentiated journey! — like a trembling bird in my palms, waiting to take flight.

Yesterday, I sat at my desk, not feeling grumpy for once, and immersed myself in clinical oncology. I pinned a few notes to the wall—I had never done that before intentionally you believe that? then I worked through a quiet decent number of questions, and they felt manageable. I tried to keep the momentum going, by diving into blood diseases but found myself wandering through the winding paths of pathology and oncogenesis. I didn’t quite finish, but today, if Allah wills, I will.

Pray for me, will you! I’ll tell you about my last week soon enough, but for now, did you know already that tissue is, indeed, the issue?

Kindley yours.

[medicineforcare]

Resihance

Resihance

Regorafenib   is a multi-kinase inhibitor used primarily for the treatment of cancer. It is particularly effective in targeting angiogenesis (the formation of new blood vessels), which plays a crucial role in cancer growth and metastasis. Below is a detailed overview of Regorafenib:

Mechanism of Action:

Regorafenib inhibits multiple protein kinases involved in tumor angiogenesis, oncogenesis, and the tumor microenvironment. Specifically, it targets:

VEGFR (Vascular Endothelial Growth Factor Receptor) – involved in blood vessel formation.

PDGFR (Platelet-Derived Growth Factor Receptor) – involved in the growth and survival of cells.

RAF kinases (including BRAF) – involved in cell proliferation and survival.

By blocking these pathways, Regorafenib reduces tumor growth and the spread of cancer.

Indications:

Regorafenib is used in the treatment of several cancers, including:

Colorectal Cancer: It is used in metastatic colorectal cancer (mCRC) that has progressed after standard therapy.

Gastrointestinal Stromal Tumors (GIST): It is prescribed for GIST after imatinib and sunitinib treatment have failed.

Hepatocellular Carcinoma (HCC): For patients with advanced liver cancer who have been previously treated with sorafenib.

Common Side Effects:

Fatigue

Hand-foot skin reaction (redness, swelling, pain in palms and soles)

Diarrhea

Hypertension (high blood pressure)

Nausea and vomiting

Abdominal pain

Decreased appetite

Weight loss

Serious Side Effects:

Liver toxicity: Regorafenib can lead to severe liver damage, including elevated liver enzymes, jaundice, and, in rare cases, liver failure.

Bleeding: Regorafenib can increase the risk of severe bleeding, especially in patients with cancer that has spread to the liver.

Cardiovascular complications: It can lead to high blood pressure and may increase the risk of heart attack or stroke.

Gastrointestinal perforation: A rare but potentially life-threatening complication.

Monitoring and Precautions:

Liver function should be monitored regularly because of the risk of liver toxicity.

Blood pressure should be checked frequently to detect any early signs of hypertension.

Skin reactions should be monitored closely, as they can affect the patient's quality of life.

Kidney function should also be assessed periodically, especially in patients at risk of kidney damage.

Pharmacokinetics:

Absorption: Regorafenib is well absorbed after oral administration but should be taken with a low-fat meal to ensure proper absorption.

Metabolism: The drug is metabolized in the liver primarily through CYP3A4, and its active metabolites also play a role in its efficacy.

Excretion: Regorafenib and its metabolites are excreted primarily through feces, with a small portion eliminated through urine.

[crimsonpublisherscancerstudy]

Deciphering the Ras/MAPK Signaling Pathway in the Progression and Treatment of Hepatocellular Carcinoma_Crimson Publishers

Abstract

Hepatocellular Carcinoma (HCC) is a serious health issue and its frequency is rapidly escalating throughout the world therefore researchers have focused more attention to the Ras/MAPK signaling pathway. The signaling pathways are linked to develop tumors and the Ras/MAPK pathway is one of these pathways, activated in 60% of HCCs with poor prognosis. A number of different proteins causes the abnormal regulation of the MAPK pathway in HCC. Ras, a small GTPase and Raf are the most commonly mutated oncogene supports the critical function of this pathway in oncogenesis. The genetic mutations leading to effector molecule to permanently activated in the Ras/MAPK signaling cascades. The inappropriate activation of this pathway is primarily due to the downregulation of various Ras/MAPK pathway inhibitors including RASSF proteins, GAPs, DUSP1, Spred and Sprouty proteins. The post-transcriptional or epigenetic processes downregulate these cancer suppressor genes. The aim of current study on the primary mutations resulting in aberrant activation of Ras/MAPK pathway and their role on the initiation and progression of HCC. It also offers an update on the various inhibitors to target this central signaling pathway including various Ras, Raf, MEK inhibitors in the context of HCC. Finally, we evaluate the available options for treatment in this context.

Read more about this article:

For more articles in Novel Approaches in Cancer Study

[lboogie1906]

Dr. Erle S. Robertson (1964) is a professor at the University of Pennsylvania School of Medicine and program director of the Abramson Cancer Centre’s Tumour Virology Programme. He is a leading expert in the field of viral oncology. He has served on many national and international committees. He directs a laboratory that focuses on the mechanisms of oncogenesis mediated by infectious agents.

He received his BS in Microbiology from Howard University and his Ph.D. in Microbiology and Molecular Genetics from Wayne University. He transferred to Harvard Medical School to complete his postdoctoral training. He was an Associate Professor in the Department of Microbiology and Immunology at the University of Michigan Medical School before moving to the University of Pennsylvania. He is a Professor of Microbiology, Director of the Tumour Virology Training Programme, and Associate Director of Research in the Department of Otolaryngology. He leads a virology lab with more than 10 post-doctoral fellows and has authored more than 200 publications, including 8 books.

His laboratory is involved in research into oncogenesis caused by viruses. Areas of investigation include basic molecular mechanisms that contribute to understanding the role of oncogenic human gamma herpes viruses.

His team is involved in many studies aimed at understanding the role of the microbiome in cancer and the dysbiotic activities that may contribute to neoplastic events. His group is developing a drug discovery program with lead compounds that are now being used to develop more efficient analogs that are less toxic, have better solubility for administration, and are more bioavailable in preclinical animal studies.

Kaposi’s sarcoma came to public attention in the early 1990s as one of the most obvious AIDS-defining diseases. In 1994, Chang and Moore identified KSHV as the causative agent associated with Kaposi’s sarcoma. KSHV was identified as the second human oncogenic herpesvirus with collinear homology to EBV and infects human B cells and endothelial cells. The mechanism of KSHV-mediated oncogenesis is not well characterized. #africanhistory365 #africanexcellence

[medicomunicare]

Fattori di trascrizione: i "direttori d'orchestra" cellulari della salute umana

Fattori di trascrizione e salute umana I fattori di trascrizione sono proteine essenziali che regolano l’espressione genica, influenzando la trascrizione del DNA in RNA messaggero (mRNA), che è il primo passo della produzione di proteine. Essi si legano a sequenze specifiche di DNA, chiamate promotori o enhancer, per attivare o reprimere la trascrizione dei geni. Sono cruciali per il controllo di…

[screamingforchaos]

i have the final exams of my first year of med school in 4 days!!!

feels so surreal lol. i had preliminary exams for this about a month ago and like for the duration between those two i was really burnt out like i genuinely was so mentally exhausted i could not give a fuck

i made a list of topics i was supposed to study today and one for tomorrow too and I'm making my way through the list.

I'm also watching youtube blogs about people who also have med school exams to feel less terrified and alone

anyways, here's my list for today, by the end of today I'm hoping i check everything off of it :))

carbohydrate metabolism

cardiovascular system

oncogenesis

nutrition

hormones of the gastrointestinal tract

General physiology

a part of neurophysiology

[ramtracking]

Spatiotemporally resolved colorectal oncogenesis in mini-colons ex vivo [ Colorectal cancer ]

Spatiotemporally resolved colorectal oncogenesis in mini-colons ex vivo [News Summary] Three-dimensional organoid culture technologies have revolutionized cancer research by allowing for more realistic and scalable… The tiny colons were grown from mouse stem cells, but human versions could one day be used to test new drugs for colorectal cancer,… In the fight to cure cancer, scientists need…

[neosciencehub]

Pseudogenes in Esophageal Carcinoma

Unveiling the Shadows: New Frontier in Cancer Biology Cancer research is continually evolving, branching into areas previously unexplored or deemed less significant. A prime example of this evolution is the study of pseudogenes and their impact on cancer, specifically esophageal carcinoma. How do the Pseudogenes Drive Cancer Progression in the Oesophagus? Pseudogenes are DNA sequences that…

[tepat-side]

I wake up, and think of 100 things to do. That’s too much, so I’ll just do 50. I spend an hour thinking which ones to do. When I’ve decided, I start the first task. I plan 2 hours for it. It takes me all day. At the end, it’s 90% finished. The next day, I decide to finish it. I only have 10% more to do, I should be able to finish it in an hour or two. But I can’t remember where I was, so it takes another day to do the last 10%. Once I’ve finished, I realize how I could have actually done it in 2 hours, and besides, that wasn’t the most important thing I had to do and I should have done something else instead. ’m exhausted now and can’t do anything but surf the net. I read about an important new discovery in genetics. This could be really important to understanding oncogenesis, I think. I add “cure cancer” to my to-do list. Now I have 51 things I have 101 things to do because I thought of 50 more things to do while I was finishing task 1.