#oncogenic pathways

[medicomunicare]

Though "poker faces", psoriasis and skin diseases show their last CARD: 1 4 Myc should be enough

Our skin, the body’s largest organ–provides the first line of defense against infections and many other threats to our health. Decades of research has shown that a wide range of diseases can occur, or become worse, when the skin cannot form an effective barrier. Millions of people are affected by eczema, psoriasis and other inflammatory skin disorders. Now, experts in human genetics and asthma…

[lifepulse]

Drug resistance in multiple myeloma: When cancer cells say "NO" to treatment

Drug resistance is like a game of cat and mouse. Cancer cells are the cat, and researchers are the mouse. The cat is always trying to find new ways to catch the mouse, but the mouse is always trying to find new ways to avoid getting caught.

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[covid-safer-hotties]

Reference saved in our archive

Covid's making it difficult for people's immune systems to suppress cancer. There was a recent small-scale mouse study showing "tumor shrinkage" in a small percentage of those transgenic mice. This is a much larger analysis of the oncogenic potential of covid in humans. Guess which story the news has been reporting.

Abstract The 2019 outbreak of SARS-CoV-2 has caused a major worldwide health crisis with high rates of morbidity and death. Interestingly, it has also been linked to cancer, which begs the issue of whether it plays a role in carcinogenesis. Recent studies have revealed various mechanisms by which SARS-CoV-2 can influence oncogenic pathways, potentially promoting cancer development. The virus encodes several proteins that alter key signaling pathways associated with cancer hallmarks. Unlike classical oncogenic viruses, which transform cells through viral oncogenes or by activating host oncogenes, SARS-CoV-2 appears to promote tumorigenesis by inhibiting tumor suppressor genes and pathways while activating survival, proliferation, and inflammation-associated signaling cascades. Bioinformatic analyses and experimental studies have identified numerous interactions between SARS-CoV-2 proteins and cellular components involved in cancer-related processes. This review explores the intricate relationship between SARS-CoV-2 infection and cancer, focusing on the regulation of key hallmarks driving initiation, promotion and progression of cancer by viral proteins. By elucidating the underlying mechanisms driving cellular transformation, the potential of SARS-CoV-2 as an oncovirus is highlighted. Comprehending these interplays is essential to enhance our understanding of COVID-19 and cancer biology and further formulating strategies to alleviate SARS-CoV-2 influence on cancer consequences.

[rookinthecrownest]

Hi everyone, I know none of you follow me for science-related content but oops, this touches on stuff I'm passionate about (science education, molecular biology) and has activated my Unskippable Dialogue. Get ready to hopefully learn something with Rookie.

Now, I get that the above tweets come from X/Twitter, and character limitations make adding any sort of meaningful nuance next to impossible - but I do want to touch on how disseminating scientific information on these websites can lead to mass proliferation of at worst, misinformation (this tweet/post is not really misinformation, because there is some truth to it) and at best, well-meaning but very reductive and over-simplified attempts to explain natural phenomena. Both are still a problem in the era of widespread medical misinformation.

Here's the thing; COVID-19 is both a fascinating virus, and a terrifying/deadly one - I'm sure I don't need to tell you all that. But the molecular pathways in question, and referenced in the above tweet, are ridiculously complex and intermingle in ways I don't have the time to really get into for now. The point is, molecular biology is an incredibly complicated field, as anyone who's taken a specialized university-level course and above can tell you (*ahem* yours truly). We can speculate on things with a reasonable amount of confidence, but we won't truly know how they work until the pathways and interactions are fully mapped out (which can take a long time!). Is COVID19 an oncogenic virus? Honestly... probably, I wouldn't be surprised at all. COVID"s been doing a lot of weird stuff since it came on the scene. I haven't done enough solid reading around the topic to say for certain. But even if it is truly oncogenic is it actually responsible for the up-tick in CRC cases in young people? The way we arrive at that answer is more complicated than what is initially presented here.

I'm being intentionally careful with my words here. You'll notice I don't use emotionally charged language or absolute statements because scientists and doctors have had to learn the hard way to pick their words carefully, because of how easily they get twisted into something they didn't actually say.

Let's take a look at the complicated relationship between CRC and COVID19.

Numero Uno: The Increasing Rates of CRC in Young Adults Has Been Well Studied Far Before COVID Entered the Picture

Rates of CRC in young adults in America (and across the world - see a worldwide systematic review here) have been rising since 1995. If you go by Cancer Care Ontario, they've noticed it in Canada since around 2005. This large cohort study from Canada done in 2019 looked at data from the National Cancer Incidence Reporting system and showed that not only was the incidence of CRC in men and women < 50 y/o increasing, it suggested the rate may even be accelerating (in 2019! Pre-COVID! BTW, it takes on average 4-12 months to get a paper published, which means this trend was observed long before the paper actually made out for peer review). Whichever number you decide to go with, both of them precede COVID by a rather large margin. There are many hypotheses about why this is and they range from gut bacteria, inflammation, diet, carcinogens, etc. But the current body of evidence points to some joint exposure for people < 50 which is causing this rise in CRC. We just don't know what that exposure is for certain. It's likely multifactorial in nature.

Meanwhile, interestingly, the incidence of CRC in adults > 50 are decreasing (with the largest decline seen in people 80-89 y/o) and this is likely due to highly effective population-based screening programs implemented by both the United States Preventative Services Task Force (USPSTF) & it's Canadian equivalent, the Canadian Task Force on Preventative Healthcare (CTFPH). Both of these bodies meet and review recommendations for population-level healthcare by examining the current body of evidence and updating said recommendations (things like prostate cancer screening, breast cancer screening, etc.).

But those recommendations are not always updated very frequently. It takes time to gather experts, review large swathes evidence, and then get those recommendations out to clinicians.

For reference, in 2002 the USPSTF recommended all adults age 50 and above receive regular CRC screening. This was not updated until May 2021, to lower the age to 45, as the USPSTF incorporated the alarming data on the rise of CRC cases in younger people into their recommendations.

In Canada, CRC screening for average-risk adults still starts at age 50. Because like I said, changes on population-based screening programs take time and face a lot of bureaucratic red tape, especially in a place like Canada where screening is part of taxpayer funded universal healthcare.

The ultimate point is IT TAKES TIME FOR THESE RECOMMENDATIONS TO BE IMPLEMENTED, so even if USPSTF aged down their screening, they did it based on data we already had.

Numero Dos: Confounding Factors & CRC Diagnosis During COVID Pandemic

The COVID19 pandemic caused a massive disruption to regular CRC screening in many countries. This lead to less colonoscopies being performed. According to the American College of Surgeons, surgical cases of CRC fell by 17.3% during the first year of the pandemic. Those who did present with CRC in 2020, tended to present at a later/more advanced stage than those who were diagnosed in 2019. And this makes sense - COVID starts, world shuts down, no one's doing colonoscopies or people are avoiding healthcare centres to decrease their risk of exposure, etc. etc. Less people are screened, more cases are missed or present at an advanced un-resectable/incurable stage.

But that doesn't answer the question - could COVID19 itself responsible for the upshift in CRC in young adults?

This retrospective study of over 3000 patients newly diagnosed with CRC between 2017 and 2021 attempted to answer that question. Unfortunately, they didn't stratify based on age, so it doesn't really answer our question. Still, this study from South Korea found no statistically significant difference in the proportion of Stage IV CRC patients between pre-COVID (2017-2019) and COVID (2020). They did, however, find (consistent with what was mentioned from the ACS earlier) that those in the COVID group who did present in Stage IV were more likely to be unresectable at presentation and have poorer prognosis compared to those in the pre-COVID arm. I think there was another small retrospective study from Spain that essentially showed something similar-but-not-quite. They did specify that their data for early onset CRC (EOCRC), but it showed that there was no major difference in frequency of diagnosis or stage at presentation for EOCRC. The authors hypothesized this to be due to young people getting more aggressive treatment right off the bat because they are more robust/able to handle it. And again, it was a small study so take it with the biggest grain of salt. Study's here if you wanna read it.

Now, the disruption of care during the pandemic is a fairly large confounding variable in and of itself. Even if we do see a sharp rise in the post-pandemic era of EOCRC, how can we be sure that's truly due to infection with COVID19, and not our healthcare systems catching up on missed cases? That's going to be exceedingly difficult to parse out.

"But Rookie, it's been 5 years since the start of the pandemic, surely we should have noticed something by now" and that is a great question dear reader. Let me tell you a little thing about colon cancer screening intervals that will hopefully make what I'm about to say make more sense.

If you were to get a screening colonoscopy today, and it came back totally normal, you wouldn't need another one for about 10 years. Why 10 years? Well, CRC is a fairly slow growing cancer. The likelihood of you getting full-blown Stage IV metastatic CRC 2 years after a completely normal colonoscopy without so much as a sessile polyp is veeeery low and incredibly unlikely. Colon cancer starts as polyps. But not all polyps (if they are found) are cancerous or pre-cancerous. Secondly, of those precancerous polyps, it still takes time for them to actually undergo malignant transformation. Can there be factors that accelerate that? Yeah, sure. But on average it takes 10-15 years for those polyps to turn into something worrisome.

What my long-winded explanation is trying to say, is that we are gonna need at least 5-10 more years of collecting good quality data, meta-analyses and systematic reviews, before we can truly attribute COVID19 to an upshift of CRC in young adults because, as mentioned previously, the trend was already on its way up before COVID came around.

Numero Tres: The Molecular Pathways involved in Oncogenesis are Ridiculously Fucking Complicated, Like No Seriously

This one goes without saying, but molecular biology is hard. There's about a million different pathways, and their interactions grow increasingly complex as we get more information on them by the day.

Here is a simplified diagram proposing to explain the oncogenic potential of COVID19 from a really good paper you can read here. And I do mean very simplified (I've seen much worse in my textbooks *sobs*).

The authors describe a variety of different molecular signalling pathways through which COVID19 can exert oncogenic potential and I'm not going to go through all of them because this isn't meant to be a biology lesson, but one of those pathways involves the erythropoietin-producing hepatocellular carcinoma (Eph) receptor. It belongs to a family of receptor tyrosine kinases (RTKs), which are implicated in various types of cancers due to their roll in controlling cell division, metabolism, cell survival, etc. These receptors are found in different tissues and organs - one of which is the colon! The authors think that virus' Spike Protein can impact downstream signalling cascades by stimulating this receptor. This is BAD, because disturbing these very tightly controlled signalling pathways can lead to oncogenesis, or cancer progression (in many different ways ranging from oxidative stress to inhibition of tumour suppressing proteins).

So, we have a plausible mechanism for which COVID19 infection can potentially drive up CRC rates in young people, great. But having a plausible mechanism isn't enough to definitively say anything about COVID19's role in this particular type of cancer. And that is why the original tweet rubbed me the wrong way!

This shit is so ridiculously complicated and the original tweet is making it seem like this is already a largely accepted idea rather than an ever-evolving field of research. Also, they say we've known this since 2022, but in 2022, the paper they referenced wasn't even peer reviewed yet when it hit the mainstream.

Oh, and finally, this is unrelated, but if you're going to tweet 'Did doctors forget about the oncogenic potential of viruses' (objectively untrue, we are all incredibly familiar because we had it drilled into us) be sure you understand who you're tweeting at.

For those who don't know, Dr. Patrick Soon-Shiong is a bit of a legend in the medical community. Not only did he perform the first whole pancreatic transplant at UCLA in the 80's, but he literally invented a cancer drug, Abraxane, for the treatment of pancreatic cancer.

Yeah I can't imagine tweeting that to a dude who invented a cancer drug. Trust me, Dr Soon-Shiong is not likely to have forgotten about the oncogenic potential of viruses. And he even recently acknowledged the oncogenic potential of COVID19 and said they're working on more research. Lol.

Sorry for the rant. Hopefully you did indeed learn something with me, you fine folks!

[blueweave]

Europe Genomic Cancer Panel and Profiling Market size by value at USD 2.62 billion in 2023. During the forecast period between 2024 and 2030, BlueWeave expects Europe Genomic Cancer Panel and Profiling Market size to expand at a CAGR of 9.10% reaching a value of USD 4.71 billion by 2030. The Genomic Cancer Panel and Profiling Market across Europe is propelled by the advancements in genomic sequencing technologies, rising cancer incidence, increased adoption of precision oncology, investments in research and development, and collaborative efforts between industry stakeholders. These factors collectively contribute to the substantial growth potential of the European Genomic Cancer Panel and Profiling Market.

Sample @ https://www.blueweaveconsulting.com/report/europe-genomic-cancer-panel-and-profiling-market/report-sample

Opportunity - Advancements in Technology

Next-generation sequencing (NGS) technologies represent a transformative advancement in genomic analysis, fundamentally changing the landscape of cancer profiling. These cutting-edge platforms revolutionize the decoding of genetic information, providing unparalleled speed, accuracy, and cost-effectiveness compared to traditional methods. NGS enables simultaneous analysis of multiple genes within a single run, allowing for comprehensive profiling of cancer genomes and detection of various genetic alterations, including point mutations, insertions, deletions, and copy number variations. This thorough interrogation aids in identifying driver mutations and oncogenic pathways, paving the way for personalized treatment strategies tailored to each patient's unique genetic profile.

[delveinsight12]

Understanding c-MET Non-Small Cell Lung Cancer Market: Causes, Symptoms, Diagnosis, and Treatment Options

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, comprising approximately 85% of all lung cancer cases. Within the realm of NSCLC, c-MET-positive tumors represent a significant subset associated with specific molecular and clinical characteristics. This article provides a detailed exploration of c-MET-positive NSCLC, including its causes, signs and symptoms, diagnostic approaches, and treatment options, drawing insights from the latest market research and developments.

c-MET, also known as hepatocyte growth factor receptor (HGFR), is a proto-oncogene that plays a crucial role in cell growth, migration, and invasion. In NSCLC, the c-MET gene can become dysregulated, leading to aberrant signaling pathways that promote tumor growth and metastasis. Overexpression or mutation of the c-MET gene has been implicated in aggressive tumor behavior and resistance to standard therapies.

c-MET-positive NSCLC often presents with distinct clinical features and may require specialized treatment approaches to effectively manage the disease. Identifying and targeting c-MET alterations is essential for optimizing therapeutic strategies and improving patient outcomes.

Causes of c-MET Non-Small Cell Lung Cancer

The exact causes of c-MET-positive NSCLC are multifaceted and involve a combination of genetic and environmental factors:

1. Genetic Mutations: Mutations or amplifications in the c-MET gene can lead to the overexpression of the c-MET protein, driving tumor growth and progression. These genetic alterations can result from inherited genetic predispositions or acquired mutations.

2. Environmental Factors: Exposure to carcinogens, such as tobacco smoke, asbestos, and environmental pollutants, is a well-established risk factor for lung cancer. These environmental factors can contribute to the development of genetic mutations and aberrant signaling pathways, including those involving c-MET.

3. Preexisting Lung Conditions: Chronic lung conditions, such as chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis, can increase the risk of developing lung cancer. These conditions may contribute to the dysregulation of c-MET signaling.

4. Family History: A family history of lung cancer or other cancers can increase the risk of developing NSCLC, including c-MET-positive tumors. Genetic predisposition and familial cancer syndromes may play a role in c-MET dysregulation.

Signs and Symptoms

The symptoms of c-MET-positive NSCLC are similar to those of other NSCLC subtypes, though the presence of c-MET alterations may influence the disease's clinical behavior. Common signs and symptoms include:

1. Persistent Cough: A chronic cough that does not improve with treatment may be an early sign of lung cancer. In c-MET-positive NSCLC, the cough may become more severe and persistent.

2. Shortness of Breath: Difficulty breathing or shortness of breath can occur as the tumor grows and obstructs the airways or lung tissue.

3. Chest Pain: Patients may experience localized chest pain or discomfort, which can be caused by the tumor's growth or invasion into surrounding tissues.

4. Hemoptysis: Coughing up blood or blood-streaked sputum may indicate advanced disease or tumor invasion.

5. Weight Loss and Fatigue: Unexplained weight loss and persistent fatigue are common systemic symptoms of cancer, including c-MET-positive NSCLC.

6. Recurrent Infections: Frequent respiratory infections or pneumonia may occur as the tumor obstructs or damages the lung tissue.

To know more about c-MET NSCLC Treatment market, visit: https://www.delveinsight.com/report-store/cmet-mnsclc-market

Diagnosis of c-MET Non-Small Cell Lung Cancer

The diagnosis of c-MET-positive NSCLC involves a combination of imaging studies, biopsy, and molecular testing:

1. Imaging Studies:

   - Chest X-Ray: A preliminary imaging test that can reveal abnormalities in the lungs, such as masses or nodules.

   - Computed Tomography (CT) Scan: Provides detailed cross-sectional images of the chest and can help identify the size, location, and extent of the tumor. CT scans are often used for staging and assessing tumor spread.

   - Positron Emission Tomography (PET) Scan: PET scans can detect areas of increased metabolic activity associated with cancer, aiding in the detection of metastases.

2. Biopsy:

   - Bronchoscopy: A procedure in which a flexible tube with a camera is inserted through the airways to obtain tissue samples from the tumor.

   - Needle Biopsy: A needle is used to extract tissue samples from the tumor, often guided by imaging techniques.

3. Molecular Testing:

   - c-MET Gene Testing: Identifies mutations or amplifications in the c-MET gene that are associated with tumor growth and progression. This testing is essential for determining the appropriate targeted therapy.

   - Next-Generation Sequencing (NGS): Provides comprehensive genetic analysis to identify various mutations and alterations in the tumor, including c-MET.

Treatment Options for c-MET Non-Small Cell Lung Cancer

Treatment for c-MET-positive NSCLC often involves a combination of standard therapies and targeted approaches to address the specific molecular characteristics of the tumor:

1. Surgery: Surgical resection is often the first-line treatment for localized NSCLC. The goal is to remove the tumor and affected lung tissue. However, surgery may not be suitable for all patients, particularly those with advanced or metastatic disease.

2. Radiation Therapy: Radiation therapy uses high-energy rays to target and destroy cancer cells. It may be used as an adjuvant treatment following surgery or as a primary treatment for inoperable tumors.

3. Chemotherapy: Systemic chemotherapy involves the use of drugs to kill cancer cells throughout the body. It is often used for advanced or metastatic NSCLC and may be combined with other treatments.

4. Targeted Therapy:

   - c-MET Inhibitors: Specific drugs targeting the c-MET pathway, such as crizotinib, cabozantinib, and tepotinib, are used to inhibit abnormal c-MET signaling and reduce tumor growth. These therapies are tailored to patients with c-MET gene mutations or amplifications.

   - Combination Therapies: Combining c-MET inhibitors with other targeted agents or immunotherapies may enhance treatment efficacy and overcome resistance.

5. Immunotherapy: Immune checkpoint inhibitors, such as pembrolizumab and nivolumab, can help stimulate the immune system to recognize and attack cancer cells. While not specific to c-MET, these therapies may be used in conjunction with targeted treatments.

6. Clinical Trials: Participation in clinical trials may provide access to new and experimental treatments that are not yet widely available. Clinical trials are essential for advancing treatment options and improving outcomes for patients with c-MET-positive NSCLC.

Market Insights

The market for c-MET-positive NSCLC treatments reflects the growing demand for targeted therapies and advancements in personalized medicine:

- Market Size and Growth: The global market for c-MET-positive NSCLC treatments is expanding, driven by increasing prevalence, advances in molecular diagnostics, and the development of targeted therapies. Key market segments include pharmaceuticals, diagnostic tools, and personalized treatment solutions.

- Key Players: Leading companies involved in the c-MET NSCLC market include:

   - Pfizer Inc.: Known for its development of targeted therapies and involvement in the treatment of lung cancer.

   - Roche Holdings: Engaged in the development of targeted therapies and molecular diagnostics for NSCLC.

   - Novartis Pharmaceuticals: Focuses on innovative treatments and research in oncology, including c-MET-targeted therapies.

   - AstraZeneca: Contributes to research and development of targeted and combination therapies for lung cancer.

- Research and Development: Ongoing research aims to improve understanding of c-MET signaling, develop new targeted therapies, and enhance diagnostic capabilities. Innovations in drug development and molecular diagnostics are contributing to better management and treatment outcomes for patients with c-MET-positive NSCLC.

c-MET-positive NSCLC represents a significant subset of non-small cell lung cancer with distinct molecular and clinical characteristics. Understanding the causes, symptoms, and treatment options is crucial for effective management of this challenging condition. Advances in targeted therapies and molecular diagnostics offer hope for improved outcomes and personalized treatment strategies. The growing market for c-MET NSCLC treatments underscores the importance of continued research and innovation in addressing this complex and impactful form of lung cancer.

Download report @ https://www.delveinsight.com/sample-request/cmet-mnsclc-market

[pharmaapimanufacturer]

Adagrasib is an advanced investigational anti-cancer agent, specifically designed as a potent and selective inhibitor of the KRAS G12C mutation, which is prevalent in various cancers such as non-small cell lung cancer (NSCLC). This API (Active Pharmaceutical Ingredient) works by irreversibly binding to the mutant KRAS protein, thereby preventing its activation and subsequent oncogenic signaling pathways. This document delves into the pharmacodynamics, detailed mechanism of action, and emerging clinical applications of Adagrasib, offering insights into its potential role in targeted cancer therapies.

[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

[healthcarehubhh]

Neurofibromatosis Treatment Drugs Industry Growth

Neurofibromatosis (NF) is a genetic disorder that causes tumors to form on nerve tissues. There are two main types - NF1 and NF2. NF1, also known as von Recklinghausen disease, is the more common form affecting around 1 in 3000 people. The main symptoms include light brown spots on the skin, tumors on or under the skin (neurofibromas), and Lisch nodules on the iris. NF2 is rarer and causes bilateral vestibular schwannomas (tumors on the eighth cranial nerve), which can lead to hearing loss and balance problems if not treated. Other features may include meningiomas (tumors of the meninges) and ependymomas (tumors of the central nervous system). Medical Management of NF1 For NF1, the treatment approach depends on the symptoms. If neurofibromas are small and cause no problems, only monitoring is needed. However, larger or painful neurofibromas may require surgery to remove them. Magnetic resonance imaging (MRI) scans are useful to monitor the growth of tumors. Children with NF1 are closely followed to watch for the development of optic pathway gliomas, which can affect vision if not treated. Medical therapy focuses on managing complications like high blood pressure, learning disabilities, and bone abnormalities. Targeted Neurofibromatosis Treatment Drugs Therapies In recent years, research has led to the development of targeted drug therapies that interfere with molecular pathways driving tumor growth in NF. One such pathway involves the RAS family of oncogenes, which are mutated in a high percentage of NF1 tumors. Selumetinib (Koselugo) is a MEK inhibitor drug approved by the FDA to treat inoperable plexiform neurofibromas in patients with NF1. By blocking the MEK protein, it helps control tumor growth. Another RAS pathway drug, sotorasib (Lumakras), showed efficacy against KRAS G12C mutant solid tumors in a clinical trial and may offer an option for NF patients with specific mutations. Several other MEK and RAF inhibitors are under investigation for NF. Medical Management of NF2 For NF2, treatment goals are to halt tumor growth and preserve hearing and neurological function as long as possible. Surgery continues to play a major role by removing tumors causing symptoms. Stereotactic radiosurgery uses focused beams of radiation to control residual or growing tumors without the risks of open surgery. Monitoring with serial MRIs helps determine when intervention is needed. The multikinase inhibitor sorafenib was shown to slow tumor growth in an NF2 clinical trial and represents a potential medical option. However, effective drug therapies are still quite limited for systemic treatment of NF2. Research Directions Ongoing research aims to discover new drugs that more specifically target signaling pathways driving NF tumor formation and growth. Candidate pathways include PI3K-AKT-mTOR, Hedgehog, Notch, Wnt, and Hippo signaling. Therapies modulating these cascades are in preclinical testing. Immunotherapies are another area of investigation since NF tumors can express tumor antigens that may stimulate anti-tumor immune responses. Combining targeted drugs with immunotherapy is a strategy to make treatments more effective. Advances in gene therapy also offer hope that someday, mutations causing NF could be directly corrected. Progress is being made, but more work is still required to develop curative options for these currently incurable genetic tumor predisposition syndromes.

[divyabodhwani23]

Accelerating Advancement: Navigating the Landscape of the EZH2 Inhibitors Market from 2024 to 2030

The EZH2 Inhibitors Market is a burgeoning sector within the pharmaceutical industry, propelled by advancements in cancer research and targeted therapy development. EZH2, or enhancer of zeste homolog 2, is a histone methyltransferase enzyme involved in epigenetic regulation, specifically in the addition of methyl groups to histone proteins. Dysregulation of EZH2 activity has been implicated in various cancers, making it an attractive target for therapeutic intervention. In this market analysis, we explore the key drivers, challenges, trends, and opportunities shaping the EZH2 Inhibitors Market.

𝐆𝐞𝐭 𝐟𝐫𝐞𝐞 𝐒𝐚𝐦𝐩𝐥𝐞: https://www.marketdigits.com/request/sample/4673

One of the primary drivers of the EZH2 Inhibitors Market is the increasing understanding of epigenetic mechanisms in cancer biology. Epigenetic alterations, including aberrant histone methylation mediated by EZH2, play a critical role in cancer initiation, progression, and metastasis. Targeting EZH2 with selective inhibitors offers a promising strategy for disrupting these epigenetic alterations and inhibiting tumor growth. As researchers unravel the complexities of EZH2 signaling pathways and their implications for cancer pathogenesis, the demand for EZH2 inhibitors as potential anticancer agents continues to grow.

The EZH2 Inhibitors Market is valued at USD 492.3 million in 2024 and projected to reach USD 3,244.7 million by 2030, experiencing a Compound Annual Growth Rate (CAGR) of 26.6% during the forecast period spanning 2024-2032.

Moreover, the EZH2 Inhibitors Market benefits from the growing prevalence of EZH2-altered cancers across various malignancies. EZH2 overexpression or gain-of-function mutations have been identified in several cancer types, including lymphoma, leukemia, prostate cancer, breast cancer, and solid tumors. These genetic alterations drive oncogenic processes, such as cell proliferation, survival, invasion, and metastasis, making EZH2 an attractive therapeutic target for precision medicine approaches. The expanding patient population with EZH2-altered cancers fuels the demand for effective EZH2 inhibitors that can provide therapeutic benefits and improve clinical outcomes.

Major vendors in the global EZH2 Inhibitors Market are Daichi Sankyo Co. Ltd., Epizyme Inc., Merck KGaA, Pfizer Inc., Eternity Bioscience, Kainos Medicine, Morphosys AG, Jiangsu Hengrui Pharmaceuticals Co. Ltd, Others Prominent Players.

In addition to targeting EZH2 directly, combination therapies involving EZH2 inhibitors and other anticancer agents are emerging as a promising approach to enhance treatment efficacy and overcome drug resistance. Preclinical and clinical studies have demonstrated synergistic effects when EZH2 inhibitors are combined with chemotherapy, targeted therapies, immunotherapy, or other epigenetic modifiers. By exploiting complementary mechanisms of action and therapeutic vulnerabilities in cancer cells, combination therapies hold potential for achieving durable responses and overcoming therapeutic resistance in EZH2-altered cancers.

However, the EZH2 Inhibitors Market also faces challenges and limitations that may hinder its growth and adoption. One of the main challenges is the development of selective and potent EZH2 inhibitors with favorable pharmacokinetic properties and acceptable safety profiles. Designing small molecules that specifically target the catalytic activity of EZH2 while sparing other methyltransferases and off-target effects remains a significant hurdle in drug discovery and development. Additionally, addressing acquired resistance mechanisms and optimizing treatment regimens to maximize clinical benefits represent ongoing challenges in the clinical translation of EZH2 inhibitors.

Furthermore, regulatory approval and market access for EZH2 inhibitors require robust clinical evidence demonstrating their safety, efficacy, and therapeutic utility in EZH2-altered cancers. Conducting clinical trials with appropriate patient selection criteria, biomarker validation, and endpoint assessment is essential for establishing the clinical value of EZH2 inhibitors and obtaining regulatory approvals. Moreover, reimbursement considerations, pricing strategies, and market dynamics influence the commercialization and accessibility of EZH2 inhibitors for patients with EZH2-altered cancers.

In conclusion, the EZH2 Inhibitors Market represents a promising frontier in cancer therapeutics, driven by advances in understanding the role of EZH2 in cancer biology and the development of targeted therapy approaches. While challenges and limitations exist, ongoing research efforts, collaborative partnerships, and technological innovations hold promise for overcoming these hurdles and advancing the clinical development and commercialization of EZH2 inhibitors. By harnessing the potential of EZH2 inhibitors as precision medicine agents, stakeholders in the oncology community can contribute to improving patient outcomes and addressing unmet medical needs in EZH2-altered cancers.

[superkalafragilisticiexpectitall]

All credit to William Makis MD

NEW ARTICLE: Thymoquinone (Black Seed Oil / Nigella Sativa) and CANCER - New Research - 5 papers reviewed Black seed oil (Nigella Sativa) has a phytochemical compound with advanced anti-cancer properties called Thymoquinone.

I review 5 recent peer-reviewed papers about Thymoquinone's anti-cancer properties- inducing apoptosis- inhibiting proliferation- inhibiting angiogenesis (VEGF)- inhibiting cancer signaling pathways (NFkB)- inhibiting metastasis (MMP)Black Seed Oil & Thymoquinone have very unique properties, that may ALSO be relevant to people who have COVID-19 mRNA Vaccine Induced Turbo Cancer.1. Pfizer & Moderna mRNA Vaccine Spike protein can damage tumor suppressor p53 which may lead to cancer.

Black Seed Oil upregulates p53 and several other tumor suppressor genes like p21 and PTEN.2. COVID-19 Vaccines may contain oncogenic microRNAs or ONCOMIRS (anagrams include "Omicron" and "Moronic", which I'm sure is just a coincidence noticed only by conspiracy theorists) Black Seed Oil & Thymoquinone regulate a large number of microRNAs:- downregulate Oncogenic miR-21- downregulate Oncogenic miR-10- upregulate tumor suppressor miR-34a Wikipedia: "miR-21 is considered to be a typical 'onco-miR', miR-21 is one of the most frequently upregulated miRNAs in solid tumours, miR-21 is associated with a wide variety of cancers including: breast, ovaries, cervix, colon, lung, liver, brain, esophagus, prostate, pancreas and thyroid"

The big question is: are microRNAs involved in COVID-19 mRNA Vaccine Induced Turbo Cancer? Sadly, many who develop Turbo Cancer will not live long enough to find out.Pfizer = Co-miRNA-ty (miRNA is microRNA) Much more in my article...don't miss this forbidden topic! Article Link in photo to avoid shadowban, just re-type the URL in the 1st photo at the top, into your browser to access

@HighWireTalk

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@TheChiefNerd

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[creativeblogwritingideas]

The Basics of DNA Methylation

DNA methylation is a fundamental epigenetic mechanism that plays a pivotal role in regulating gene expression and maintaining cellular function. Understanding the basics of DNA methylation is essential for comprehending its significance in various biological processes and its potential implications in health and disease.

What is DNA Methylation?

DNA methylation entails the attachment of a methyl cluster (CH3) to the cytosine constituent of DNA, predominantly happening at CpG dyads, where cytosine is succeeded by guanine. This alteration is facilitated by proteins termed DNA methyltransferases (DNMTs). Methylation at CpG positions has the potential to impact gene behavior by either encouraging gene suppression or aiding gene activation, contingent upon the site and surroundings within the genetic material.

Regulation of Gene Expression

DNA methylation serves as a critical mechanism for regulating gene expression patterns without altering the underlying DNA sequence. Hypermethylation of promoter regions typically results in gene repression by blocking the binding of transcription factors, RNA polymerase, and other regulatory proteins essential for gene activation. Conversely, hypomethylation of gene promoters often correlates with increased gene expression.

Inheritance and Stability

DNA methylation patterns are established during early development and are typically faithfully maintained through cell divisions, contributing to cellular identity and function. However, DNA methylation is also subject to dynamic changes influenced by various factors such as environmental exposures, aging, and disease processes. These alterations can have profound effects on gene expression profiles and cellular phenotypes.

Epigenetic Regulation

DNA methylation is a key player in the broader landscape of epigenetic regulation, which encompasses heritable changes in gene expression that do not involve alterations to the DNA sequence itself. Alongside other epigenetic modifications such as histone modifications and non-coding RNAs, DNA methylation orchestrates complex regulatory networks governing diverse biological processes, including development, differentiation, and disease susceptibility.

Clinical Implications and Genetic Methylation Tests

Understanding aberrant DNA methylation patterns is crucial for unraveling the molecular mechanisms underlying various diseases, including cancer, neurodevelopmental disorders, and autoimmune conditions. Genetic methylation tests, which analyze the methylation status of specific genomic regions, have emerged as valuable diagnostic and prognostic tools in clinical settings.

Cancer and DNA Methylation

In cancer, widespread changes in DNA methylation patterns contribute to tumorigenesis by disrupting the normal regulation of gene expression. Hypermethylation of tumor suppressor genes and hypomethylation of oncogenes are common events associated with the development and progression of cancer. Genetic methylation tests enable the detection of these aberrant methylation signatures, aiding in cancer diagnosis, prognosis, and treatment selection.

Neurodevelopmental Disorders

Aberrant DNA methylation patterns have also been implicated in neurodevelopmental disorders such as autism spectrum disorders and intellectual disabilities. Altered methylation profiles of genes involved in neuronal development, synaptic function, and neurotransmitter signaling pathways may contribute to the pathogenesis of these conditions. Genetic methylation tests offer insights into the epigenetic signatures associated with neurodevelopmental disorders, potentially informing personalized treatment strategies.

Conclusion

DNA methylation is a fundamental mechanism of epigenetic regulation with profound implications for gene expression, cellular function, and disease pathogenesis. Advances in genetic methylation tests have revolutionized our ability to interrogate DNA methylation patterns, providing valuable insights into health and disease states. Continued research in this field promises to uncover new therapeutic targets and diagnostic biomarkers, ultimately improving patient care and outcomes.

[healthcaretechnologynews]

Biomarker driven segments of NSCLC - Yet to saturate with new approvals

Industry experts think that NSCLC space is rushed with so many approvals, yet it is a hot space for researchers, as NSCLC market has huge potential and even 1% market share is a piece of hot cake for the investors.

Currently, there are a total of 5 FDA-approved TKIs for frontline treatment in EGFR- positive NSCLC.

Though, recent data on frontline Osimertinib confers the greatest progression-free survival (PFS) advantage for patients with EGFR-positive non–small cell lung cancer (NSCLC)

Experts indicated that they would look forward to the novel approaches that are trying to enhance the activity of Osimertinib by targeting other oncogenic pathways in combination with anti-EGFR therapy.

Write to us at enquire@grgonline.com to learn how GRG Health is helping clients gather more in-depth market-level information on such topics.

Chemotherapy is backbone to treat many types of cancers, and research continues to find new chemotherapy regimens in combination with novel drugs. Over a decade, NSCLC space has evolved immensely.

Even though NSCLC space has been bifurcated into many biomarkers driven patients’ segment with specific approval in these segments, still in upcoming years we will see more approvals in the space. Industry experts think that this space is rushed with so many drugs, yet it is a hot space for researchers, as NSCLC is a huge market and even a single percent market share is a piece of hot cake for the investors.

Currently there are a total of 5 FDA-approved TKIs for frontline treatment of EGFR- positive NSCLC. These include erlotinib (Tarceva), gefitinib (Iressa), afatinib (Gilotrif), Dacomitinib (Vizimpro), and Osimertinib (Tagrisso).

We have seen a lot of exciting data over the past couple years with regard to these agents as monotherapy or in combination. Despite the sequential efficacy of these FDA-approved EGFR TKIs, frontline Osimertinib confers the greatest progression-free survival (PFS) advantage for patients with EGFR-positive non–small cell lung cancer (NSCLC) recently.

Therefore, we still expect to see several studies moving forward with results reported out in the coming years. We expect an emergence of new biomarker driven segments also (for e.g., Novel combinations, certainly targeting VEGF or MET).

There are exciting ongoing studies targeting MET following progression on Osimertinib. Experts indicated that they would look forward to the novel approaches that are trying to enhance the activity of Osimertinib by targeting other oncogenic pathways in combination with anti-EGFR therapy.

Visit our website now: https://www.grgonline.com/

[persephoneflouwers]

hello, can you please help me explain the entire pathophysiology of breast cancer? it just doesn’t makes sense to me 🥲 even though i’ve watched videos on youtube but they do not talk about what happened to the cells or tissues or pathways or mechanisms for cancer metastasis

Hi! How deep should I go with this? What is not making sense to you? It’s a huge topic and kinda hard to summarise. If I were you, I would start with the basics of a cancer cell and what happens to any neoplastic cell in human body. I can send you a few papers I just downloaded for you (just send me an email and I’ll give it to you).

I would start with definition of tumor. A cancer cell is a cell that has compromised its normal, physiological process to die and keeps growing and reproducing uncontrollably. The genetic changes that contribute to cancer tend to affect three main types of genes—proto-oncogenes, tumor suppressor genes, and DNA repair genes. These changes are sometimes called “drivers” of cancer.

Breast cancer basically evolves like this. Cancer cells develop genetic mutations - that being familiarity or acquired mutations - that basically help them proliferate possibly forever.

Breast cancer is the most common cancer in women and used to be the main type of cancer leading to death in women (i think lately lung cancer has become pretty prevalent for women too, but im not aure).

There are different types of breast cancer: BC expressing Hormone Receptor (estrogen ER+ or progesterone PR+) BC expressing Human epidermal receptor (HER2+) and the triple negative (ER- , PR-, HER2-). The treatment is based on the molecular and histological type today.

The metastasis is a whole other chapter too. Metastasis is the dissemination of cancer cells from a primary lesion to distal organs that involves a variety of cellular mechanisms: invading through, or colluding with, stroma, escaping immune surveillance by inhibiting or co-opting their anti-tumorigenic processes, evading and modulating the tissue microenvironment, and evolving resistance to therapeutic intervention. These processe happens because inside the tumor cells genetic or epigenetic processes happens. This will bring to the alteration of many intracellular signalling pathways that control autonomous cellular progression to metastasis.

But you can come back for more questions. It’s just a huge topic, I don’t know what’s your level and how many infos you need

[tumimmtxpapers]

β2-AR inhibition enhances EGFR antibody efficacy hampering the oxidative stress response machinery

The β2-Adrenergic receptor (β2-ARs) is a cell membrane-spanning G protein-coupled receptors (GPCRs) physiologically involved in stress-related response. In many cancers, the β2-ARs signaling drives the tumor development and transformation, also promoting the resistance to the treatments. In HNSCC cell lines, the β2-AR selective inhibition synergistically amplifies the cytotoxic effect of the MEK 1/2 by affecting the p38/NF-kB oncogenic pathway and contemporary reducing the NRF-2 mediated... http://dlvr.it/SwNJ8t