CanScreen5, a global repository for #breast, #cervical and #colorectal #cancer #screening programs

https://www.nature.com/articles/s41591-023-02315-6

#Glutamate dehydrogenase1 supports #HIF1α stability to promote #colorectal #tumorigenesis under #hypoxia

An siRNA screen identifies αKG metabolic enzyme #GDH1 as acetylation-dependent control factor for intestinal cancer progression

https://www.embopress.org/doi/10.15252/embj.2022112675

Thermal ablation as an alternative to partial hepatectomy as observed in the retrospective #colorectal #cancer liver #metastases AMCORE registry from the Netherlands shows similar outcome results for lesions of the size of 3cm or smaller #ECIO2023 as presented by H. Schulz
https://pubmed.ncbi.nlm.nih.gov/34199556/

TODAY!🗓️ Mar. 7, 10pm Sagamihara Time

Prof. Takeshi Naitoh, will talk to you about "When is the optimal timing of metabolic surgery and which is the suitable procedure?"

Free🌐at: https://aischannel.com/coffee-with/takeshi-naitoh

#IamAIS #colorectal

📢Januarys review of the recent #randomizedclinicaltrials now available!

Focus on: #HPB #UpperGI #Colorectal

Keep up to date with recent results ⬇️ https://www.bjsacademy.com/academy/scientific-surgery/randomized-clinical-trials

#LeadingSurgicalEducation #SoMe4Surgery
@BJSurgery @BJSOpen @young_bjs

I'm posting this link, as I DIDN'T do my first test when it arrived. Two years later, I DID do the test and found I had stage 3 bowel cancer. Please return your tests folks. The lifetime risk for men is 1 in 15, and women 1 in 18!

Please boost - it could save lives.

#colorectal cancer
#screeningkits
#cancer

https://twitter.com/NHSuk/status/1627586186813243392?t=1gpPfHBdTiLfQj5Keg4P0A&s=08

📢Decembers review of the recent #randomizedclinicaltrials now available!

Focus on: #GeneralSurgery #Breast #Colorectal #Trauma #Vascular

Keep up to date with recent results ⬇️ https://www.bjsacademy.com/academy/scientific-surgery/randomized-clinical-trials

#LeadingSurgicalEducation #SoMe4Surgery
@BJSurgery @BJSOpen @young_bjs

RT @jnkath
Great start for 2023! Our new paper is out in @NatureMedicine, led by @twittlabs from @uni_mainz. We use a multi-modal deep learning pipeline to predict outcomes in #colorectal #cancer. @EKFZdigital @NCT_UCC_DD @NCT_HD. Shout out to @AI4Pathology who pioneered this field. https://twitter.com/twittlabs/status/1612725457606115328

#oncology #immunology #immunotherapy #genetherapy #cancer #cancerawareness #cancerresearch #oncologist #oncología #oncologyresearch #clinicaltrial #clinicalresearch #oncology #immunology #immunotherapy #genetherapy #cancer #cancerawareness #cancerresearch #medicine #research #Mednewsweek #gicancer #gioncology #colorectalcancer #colorectalcancerawarenessmonth #colorectalcancerawareness #colorectal #colonoscopy #coloncancer

#colorectalcancerawarenessmonth #colorectalcancerawareness #colorectal #dvt #pe #thombosis #thrombopoiesis #clot #gicare #gioncology #gicancer #coronavirus #COVID19 #COVIDVaccination #Covid_19 #pandemic #pandemiclife #COVID #sars_cov_2 #covid19research

#colorectalcancerawareness #colorectal #dvt #pe #thombosis #thrombopoiesis #clot
#gicare #gioncology #gicancer #coronavirus #COVID19 #COVIDVaccination #Covid_19 #pandemic #pandemiclife #COVID #sars_cov_2 #covid19research #SARSCoV2virus #coronatherapy #coronaupdates #pandemic2020 #SARSCoV2 #CoronaVirusUpdates

Part 2 of Novembers review of the recent #randomizedclinicaltrials now available!

Particular focus: #GeneralSurgery #UpperGI #Colorectal #HPB

Keep up to date with recent results ➡️ https://www.bjsacademy.com/academy/scientific-surgery/randomized-clinical-trials

#LeadingSurgicalEducation #SoMe4Surgery
@BJSurgery @BJSOpen @young_bjs

RT @TsengJennifer@twitter.com

@rheum_cat@twitter.com @doctorORbust@twitter.com Not nearly as pretty as yours @rheum_cat@twitter.com and yes @doctorORbust@twitter.com stopped by in the flesh!@BMCSurgery #surgonc #endocrinesurg #colorectal teams appreciated your aesthetics and your yummy treats! @The_BMC@twitter.com @BUMedicine@twitter.com #holidaybaking @TeviahSachs@twitter.com @F_ThurstonDrake@twitter.com @akobzherz@twitter.com & more!

🐦🔗: https://twitter.com/TsengJennifer/status/1602755359537610762

Today's 📌#surgicalopenlassroom—#MSCRS Virtual Coloproctology Congress —SYMPOSIUM 1 / PELVIC FLOOR—Dr. Francis Seow-Choen presents: Traumatic Anal Sphincter Injury, Immediate Or Late Repair? + Q&A

▶ Watch the full video at: https://my.mtr.cool/spzoerbiorf 
 #colorectal #MedEd

@LaraClette @cortomaltese J'ai toujours #Colorectal pour #ColoreTonFil, j'espère qu'il n'y a pas un message 😐🤔

@explainpaper

Tumoral Immune Cell Exploitation in Colorectal Cancer Metastases Can Be Targeted Effectively by Anti-CCR5 Therapy in Cancer Patients

Niels Halama, Inka Zoernig, Anna Berthel, Christoph Kahlert, Fee Klupp, Meggy Suarez-Carmona,Thomas Suetterlin, Karsten Brand, Juergen Krauss, Felix Lasitschka, Tina Lerchl, Claudia Luckner-Minden, Alexis Ulrich, Moritz Koch, Juergen Weitz, Martin Schneider, Markus W. Buechler, Laurence Zitvogel,
Thomas Herrmann, Axel Benner, Christina Kunz, Stephan Luecke, Christoph Springfeld, Niels Grabe, Christine S. Falk, and Dirk Jaeger

Targeting Tumor-Promoting Microenvironment Through CCR5 Blockade in #Colorectal #Cancer #Liver Metastases

#Cancer progression is a process in which cancer cells and #immune cells interact with each other in a way that can lead to the growth and spread of cancer. In #colorectal cancer, when the cancer has spread to other parts of the body, it is called #metastasis and it is very difficult to treat. Treatments such as PD-1/PD-L1 blockade and #chemokine modulation have been successful in modifying the interactions between the immune system and cancer, leading to the rejection or suppression of progression. Cancer cells can also alter the immune microenvironment, leading to #immunosuppression and #immune evasion. In this research paper, the authors studied the microenvironment in #CRC #liver metastases and identified a network of #tumor cells and immune cells that exploit the CCL5-CCR5 axis. They then investigated and characterized the effects of blocking the CCL5-CCR5 axis.

the microenvironment of #liver metastases of #colorectal cancer (#CRC).

the environment induces migration of T lymphocytes, which produce a #cytokine called CCL5. This CCL5 then supports tumor growth and spread by influencing macrophages and #tumor cells. The environment is immunosuppressive and the tumor cells are exploiting the host's #immune cells to their advantage. In other words, the tumor cells are using the host's immune cells to help them grow and spread.

the effects of CCR5 blockade on the #tissue level.

Tumor #cell death and a specific pattern of #cytokine and #chemokine modulation are observed in the #ExplantModel and in #tumor biopsies from a #ClinicalTrial. Macrophages are the key for these anti-tumoral effects, as they produce IFNs and reactive oxygen species which cause tumor cell death. #CCR5 blockade induces a phenotypic shift in the macrophages, which is referred to as a switch from an M2 to an M1 phenotype. This repolarization also reduces levels of CD163+ cells, reshaping the #myeloid cell composition in the microenvironment. The influx of new effector cells due to CCR5 inhibition can shift the effects of CCL5 towards beneficial effects, such as reduction of #immunosuppression , #angiogenesis, and #chemotherapy resistance.

The microenvironment of the invasive margin of #liver metastases.

There was no relevant Th1, Th2, or Th17 #cytokine signature present in any of the samples. However, the authors did find that #chemokines and #macrophage-related cytokines were significantly increased at the invasive margin. Chemokines are molecules that help to attract #immune cells to the area, and macrophage-related cytokines are molecules that help to regulate the activity of #macrophages, which are a type of immune cell. 98% of the CD3+ #lymphocyte s in the resection specimens were positive for PD-1, which is a molecule that helps to regulate the activity of the immune system.

#CCL5 is a protein produced by T cells, which are a type of white blood cell. #CCR5 is a receptor found on metastatic tumor cells, which are cancer cells that have spread from the primary #tumor to other parts of the body. In this research paper, it was found that CCL5 has #pleiotropic tumor-promoting effects on #tumor cells and tumor-associated #macrophage s. This means that CCL5 has multiple effects on both the cancer cells and the macrophages, which are a type of white #blood #cell, that are associated with the #tumor. CCL5 was produced mainly by T cells located at the invasive margin and #peritumoral stroma of metastases, and that CCR5 was dominantly expressed by metastatic tumor cells. CCL5 also had effects on tumor #CellProliferation, invasive tumor #CellBehavior, and increased production of matrix #metalloproteinas es by tumor-associated macrophages. Finally, they found that CCR5 inhibition had an effect on key molecules of #epithelial to #mesenchymal transition ( #EMT ).

The researchers wanted to test the effects of #CCR5 blockade, which is a way of blocking the CCR5 receptor on cells, using a drug called maraviroc. They used human #tumor #explantmodel s, which are samples of #tissue from advanced #CRC patients with #liver metastases. Maraviroc led to morphologically overt tumor #CellDeath in the #explants, which means that the tumor cells died and changed in appearance. The researchers then tested the hypothesis that #macrophage s, (type of white blood cell), were required for the tumor cell death-inducing effects of CCR5 blockade. They used clodronate #liposome s to deplete CD163+ TAMs, ( #macrophage s associated with tumors) and found that combining clodronate with CCR5 inhibition abrogated the immediate tumor cell death-inducing effects of #CCR5 inhibition. This confirmed the role of macrophages in this process. IFN-g induced stromal CD163+ #macrophage #cell death and led to a reconfiguration of the #myeloid cell compartment. Inhibition of macrophage-derived reactive oxygen species could partially block the anti-tumoral effects of CCR5 inhibition. Finally, they tested the effects of CCL5/CCR5 inhibition and found that both a CCL5 neutralizing antibody and a CCR5 blocking #antibody had similar functional effects to maraviroc.

A #ClinicalTrial (MARACON) was conducted to test the effects of a drug called maraviroc on patients with advanced-stage #metastatic colorectal #cancer. The #trial involved taking biopsies of the patients before and after treatment with maraviroc, and the results showed that the drug had beneficial effects on the tumor-promoting #microenvironment and led to objective clinical responses. These responses included induction of central #TumorNecrosis, reduction of tumor cell death, and reduction of key #cytokine s and growth factors that promote tumor growth. The drug was also found to be very well tolerated, with mild elevation of #liver enzymes being the most common side effect. Finally, the trial showed that partial responses were achieved in patients with previously refractory disease.

CCR5 blockade, is a type of #therapy used to treat #cancer.

The MARACON clinical trial, showed that CCR5 blockade had a positive effect on the tumor microenvironment and led to a higher response rate in subsequent chemotherapies. The authors suggest that this effect is not limited to the #liver metastases, but is a systemic feature. They also suggest that the local presence of multiple layers of #immune subversion in cancers depends on the individual tissue, #treatment, tumor type, and the difference between primary #tumor and metastatic lesion. The authors also found that the results of the #ClinicalTrial were in line with the results of a fully human organotypic tumor #ExplantModel, which is a simple model with a straightforward approach. The authors also note that the survival data from the trial is not conclusive due to the limited number of patients, but that the objective treatment responses are very encouraging. They suggest that CCR5 blockade may be a promising approach and needs to be evaluated further scientifically and clinically.

RT @EKing719@twitter.com

What do you get when you cross a #SexualHealth focused #urologist and a #colorectal surgeon?
Stay tuned for what @AshleyGWinter@twitter.com and I have in store!! #Colowellness @Colo_Wellness@twitter.com @odelahealth@twitter.com

🐦🔗: https://twitter.com/EKing719/status/1601314720727769088

The Uprising of Mitochondrial DNA Biomarker in Cancer

Advances in predictive #diagnostic and #precisionmedicine, can lead to powerful discoveries and treatments for patients. #Cancer cells acquire functional capabilities to survive, proliferate, and circulate due to an enabling characteristic called genomic instability. Genomic maintenance systems have the ability to spot and repair any #DNA defects, while cancer cells increase the rates of mutation that orchestrate tumorigenesis. Chromosomal instability (CIN) is one of the most frequent changes observed in cancer cells, which often results from aberrations in chromosome structures and numbers. The second section of the paper focuses on #biomarkers, which are substances, structures, or processes that can influence or predict the incidence and outcome of a disease. There are three classifications of biomarkers: exposure, effect, and susceptibility. Biomarkers of exposure measure exogenous chemicals or their metabolites within an organism, while biomarkers of effect measure alterations of endogenous factors caused by exposure to an exogenous agent. Biomarkers of susceptibility measure genetic polymorphism predisposition of individuals and their external multifactorial influencers. Surrogate endpoints are often used to substitute clinical endpoints, and biomarkers can be used as a screening tool for an early indicator of #malignancy-risk development. They can also be used as diagnostic aids and prognostic biomarkers, as well as predictive biomarkers to identify the sensitivity and/or resistance of cancer patients towards specific agents or #medical product exposure.

The communication between the nucleus and mitochondria of a cell is known as intergenomic #crosstalk and it is bidirectional, meaning it can go both ways. It is important for regulating energy metabolism and tumor suppression. The communication is achieved by pathways such as anterograde #signaling and retrograde signaling. Anterograde signaling is when the nucleus controls gene transcription and cytoplasmic mRNA translation in response to external signals. Retrograde signaling is when mitochondrial dysfunction or loss of mitochondrial #membrane potential triggers communication with the nuclear genetic compartment. This communication is important for #homeostasis adaptation and can detect any nuclear damage or nuclear stress.

#Mitochondria are organelles found in cells that are responsible for producing energy. They are believed to have originated from a #singlecell-ed organism and are made up of two membranes. They contain their own genetic material, called #mtDNA, which is made up of 16569 nucleotide base pairs. mtDNA mutations can lead to mitochondrial dysfunction, which can cause #onco-genic events, such as #tumor cell reprogramming and metabolic shifts. #Mitoepigenetics is the study of how #epigenetics mechanisms regulate mtDNA transcription and replication, and it is believed to be involved in cancer progression.

The interconnection between #carcinogenesis (the development of cancer) and mitochondria (the energy-producing organelles in cells) was first proposed in 1973. Since then, there have been many studies done on this topic, using DNA scanning technologies to detect mutations and deletions. Mitochondrial DNA (mtDNA) is beneficial for carcinogenic studies because it consists of 37 genes with no introns, meaning most mutations will occur in coding regions. Additionally, mtDNA has a small size, is easy to extract, has no genetic rearrangements, and has fast mutation rates, which makes it useful for molecular research. It also has a high copy number, meaning only minimal #tissue samples are needed for analysis. Large-scale deletions are commonly known to be responsible for mitochondrial diseases, and are thought to be the cause of various diseases and cancers.

Two types of mtDNA deletions, 3.4 kb and 4977 bp are associated with various types of cancer. The 3.4 kb deletion was patented by Parr et al. [97] and is used to detect cancer in individuals. It is also used to determine different #prostate tissue types, either benign, malignant, or proximal to malignant [100]. The 4977 bp deletion is primarily associated with #aging and is a common deletion with missing mtDNA nucleotide sequences starting at 8470 to 13447 np [106]. It has been studied in various types of cancer, such as #breastcancer, #colorectal, gastric, hepatocellular, and #brain tumors, and is thought to be associated with external environmental factors, genetic predisposition, and ethnicity.

The text is discussing different types of deletions in mtDNA (mitochondrial DNA) that are associated with cancer. The 5.1.3 section is talking about the 3895 bp deletion, which was first observed in 1991 in two patients with progressive external #ophthalmoplegia. It was then found to be 10 times less frequent than the 4977 bp deletion. A study involving 104 age-matched subjects showed that the 3895 bp deletion was more frequent in those with usually sun-exposed skin and nonmelanoma skin cancer. The 4576 bp deletion was then discussed, which was found to be an indicator for breast cancer in a study involving 39 breast cancer patients. The 4576 bp deletion was not found in 23 normal patients without breast cancer. The text then moves on to discuss mtDNA copy number, which is the amount of mtDNA in each cell. It is suggested that mtDNA copy number changes may lead to mitochondrial instability and regulate energy metabolism, which can initiate #tumorigenesis. Studies have also shown that mtDNA copy number changes can be used as a predictive biomarker for #chemotherapy response.

Cell-free mtDNA (cf-mtDNA) is a type of mitochondrial DNA that is released into the #blood circulation due to disruption of the normal mitochondrial life cycle. It is believed to activate the Toll-like receptor 9 (TLR9) pathway, which can cause #inflammation and potentially lead to cancer. It has been used to diagnose cancer and sepsis, and as a biomarker for metabolic syndrome and predicting the risk of future diabetes. It is also being studied as a #noninvasive liquid #biopsy for cancer, as higher levels of cf-mtDNA have been found in cancer patients compared to healthy controls. Research is being conducted to find the potential link between cf-mtDNA and various cancers, as it is a preferable biomarker due to its higher mtDNA copy number, simpler structure, and shorter length.

Mitochondrial Microsatellite Instability (#mtMSI) is a type of genetic mutation that occurs in the mitochondrial genome. It is caused by short tandem repeats (mononucleotide or dinucleotide) of 1 to 6 base pairs that are scattered throughout the mitochondrial genome. These variations can lead to frameshift mutations, which can be caused by DNA polymerase γ, an enzyme that is responsible for oxidative damage. Mammalian mitochondria also have an inefficient mismatch repair system, which can lead to mtMSI formation. The most commonly reported mtMSI is located in the D-loop region, which is a mutational hotspot in primary tumors. It is a highly polymorphic homopolymeric C stretch, which is involved in R-loop formation, a stable RNA-DNA hybrid that triggers mtDNA replication. D310 alteration has been suggested as a new cancer detection tool and a potential early premalignant cancer marker. Another potential marker is D16184, which is located in the hypervariable region I and is involved in mtDNA biogenesis. Studies have reported the presence of D16184 in various cancer types, such as gastric and endometrial carcinoma. Somatic mtDNA alterations have also been correlated to cancer, with evidence showing that mtDNA changes can contribute to the development or progression of cancer. One example of a somatic mtDNA alteration is A12308G, which is located in the variable loop next to the anticodon stem of tRNA Leu (CUN). This alteration has been suggested as a potential diagnostic tool for #colorectalcancer and as a risk factor for prostate and #renalcancer. A10398G has also been studied in relation to cancer, although the results have been conflicting.

Mitochondrial biomarkers are molecules that can be used to detect cancer in its early stages. A commercial kit (PCMT) has been developed to help with this detection. However, even if cancer is detected early, it can still be difficult to treat if the symptoms have not yet developed. Therefore, researchers are looking into gene therapy and other mitochondrial interventions as potential treatments for cancer. They can use current advancements in vitro mitochondrial intervention to identify the pathogenicity and therapeutic potential of a particular mtDNA mutation. One method proposed is to transfer artificial healthy mitochondria to remove damaged mtDNA without genetic manipulation. Other studies have looked at the levels of mtDNA biomarkers in cancerous and non-cancerous samples, as well as the levels of mtDNA methylation and mtRNA in cancerous tissues.

@explainpaper

@cancer

@mitochondria

@mito

@dna

@mtdna

@precisionmedicine

@diagnostics

@mtmsi

@aging

@Ophthalmoplegia

@Tumorigenesis

@Blood

@Inflammation

@Biopsy

@Chemotherapy

@Colorectalcancer

@Renalcancer

@Brain

@Breastcancer

The Uprising of Mitochondrial DNA Biomarker in Cancer

Advances in predictive #diagnostic and #precisionmedicine, can lead to powerful discoveries and treatments for patients. #Cancer cells acquire functional capabilities to survive, proliferate, and circulate due to an enabling characteristic called genomic instability. Genomic maintenance systems have the ability to spot and repair any #DNA defects, while cancer cells increase the rates of mutation that orchestrate tumorigenesis. Chromosomal instability (CIN) is one of the most frequent changes observed in cancer cells, which often results from aberrations in chromosome structures and numbers. The second section of the paper focuses on #biomarkers, which are substances, structures, or processes that can influence or predict the incidence and outcome of a disease. There are three classifications of biomarkers: exposure, effect, and susceptibility. Biomarkers of exposure measure exogenous chemicals or their metabolites within an organism, while biomarkers of effect measure alterations of endogenous factors caused by exposure to an exogenous agent. Biomarkers of susceptibility measure genetic polymorphism predisposition of individuals and their external multifactorial influencers. Surrogate endpoints are often used to substitute clinical endpoints, and biomarkers can be used as a screening tool for an early indicator of #malignancy-risk development. They can also be used as diagnostic aids and prognostic biomarkers, as well as predictive biomarkers to identify the sensitivity and/or resistance of cancer patients towards specific agents or #medical product exposure.

The communication between the nucleus and mitochondria of a cell is known as intergenomic #crosstalk and it is bidirectional, meaning it can go both ways. It is important for regulating energy metabolism and tumor suppression. The communication is achieved by pathways such as anterograde #signaling and retrograde signaling. Anterograde signaling is when the nucleus controls gene transcription and cytoplasmic mRNA translation in response to external signals. Retrograde signaling is when mitochondrial dysfunction or loss of mitochondrial #membrane potential triggers communication with the nuclear genetic compartment. This communication is important for #homeostasis adaptation and can detect any nuclear damage or nuclear stress.

#Mitochondria are organelles found in cells that are responsible for producing energy. They are believed to have originated from a #singlecell-ed organism and are made up of two membranes. They contain their own genetic material, called #mtDNA, which is made up of 16569 nucleotide base pairs. mtDNA mutations can lead to mitochondrial dysfunction, which can cause #onco-genic events, such as #tumor cell reprogramming and metabolic shifts. #Mitoepigenetics is the study of how #epigenetics mechanisms regulate mtDNA transcription and replication, and it is believed to be involved in cancer progression.

The interconnection between #carcinogenesis (the development of cancer) and mitochondria (the energy-producing organelles in cells) was first proposed in 1973. Since then, there have been many studies done on this topic, using DNA scanning technologies to detect mutations and deletions. Mitochondrial DNA (mtDNA) is beneficial for carcinogenic studies because it consists of 37 genes with no introns, meaning most mutations will occur in coding regions. Additionally, mtDNA has a small size, is easy to extract, has no genetic rearrangements, and has fast mutation rates, which makes it useful for molecular research. It also has a high copy number, meaning only minimal #tissue samples are needed for analysis. Large-scale deletions are commonly known to be responsible for mitochondrial diseases, and are thought to be the cause of various diseases and cancers.

Two types of mtDNA deletions, 3.4 kb and 4977 bp are associated with various types of cancer. The 3.4 kb deletion was patented by Parr et al. [97] and is used to detect cancer in individuals. It is also used to determine different #prostate tissue types, either benign, malignant, or proximal to malignant [100]. The 4977 bp deletion is primarily associated with #aging and is a common deletion with missing mtDNA nucleotide sequences starting at 8470 to 13447 np [106]. It has been studied in various types of cancer, such as #breastcancer, #colorectal, gastric, hepatocellular, and #brain tumors, and is thought to be associated with external environmental factors, genetic predisposition, and ethnicity.

The text is discussing different types of deletions in mtDNA (mitochondrial DNA) that are associated with cancer. The 5.1.3 section is talking about the 3895 bp deletion, which was first observed in 1991 in two patients with progressive external #ophthalmoplegia. It was then found to be 10 times less frequent than the 4977 bp deletion. A study involving 104 age-matched subjects showed that the 3895 bp deletion was more frequent in those with usually sun-exposed skin and nonmelanoma skin cancer. The 4576 bp deletion was then discussed, which was found to be an indicator for breast cancer in a study involving 39 breast cancer patients. The 4576 bp deletion was not found in 23 normal patients without breast cancer. The text then moves on to discuss mtDNA copy number, which is the amount of mtDNA in each cell. It is suggested that mtDNA copy number changes may lead to mitochondrial instability and regulate energy metabolism, which can initiate #tumorigenesis. Studies have also shown that mtDNA copy number changes can be used as a predictive biomarker for #chemotherapy response.

Cell-free mtDNA (cf-mtDNA) is a type of mitochondrial DNA that is released into the #blood circulation due to disruption of the normal mitochondrial life cycle. It is believed to activate the Toll-like receptor 9 (TLR9) pathway, which can cause #inflammation and potentially lead to cancer. It has been used to diagnose cancer and sepsis, and as a biomarker for metabolic syndrome and predicting the risk of future diabetes. It is also being studied as a #noninvasive liquid #biopsy for cancer, as higher levels of cf-mtDNA have been found in cancer patients compared to healthy controls. Research is being conducted to find the potential link between cf-mtDNA and various cancers, as it is a preferable biomarker due to its higher mtDNA copy number, simpler structure, and shorter length.

Mitochondrial Microsatellite Instability (#mtMSI) is a type of genetic mutation that occurs in the mitochondrial genome. It is caused by short tandem repeats (mononucleotide or dinucleotide) of 1 to 6 base pairs that are scattered throughout the mitochondrial genome. These variations can lead to frameshift mutations, which can be caused by DNA polymerase γ, an enzyme that is responsible for oxidative damage. Mammalian mitochondria also have an inefficient mismatch repair system, which can lead to mtMSI formation. The most commonly reported mtMSI is located in the D-loop region, which is a mutational hotspot in primary tumors. It is a highly polymorphic homopolymeric C stretch, which is involved in R-loop formation, a stable RNA-DNA hybrid that triggers mtDNA replication. D310 alteration has been suggested as a new cancer detection tool and a potential early premalignant cancer marker. Another potential marker is D16184, which is located in the hypervariable region I and is involved in mtDNA biogenesis. Studies have reported the presence of D16184 in various cancer types, such as gastric and endometrial carcinoma. Somatic mtDNA alterations have also been correlated to cancer, with evidence showing that mtDNA changes can contribute to the development or progression of cancer. One example of a somatic mtDNA alteration is A12308G, which is located in the variable loop next to the anticodon stem of tRNA Leu (CUN). This alteration has been suggested as a potential diagnostic tool for #colorectalcancer and as a risk factor for prostate and #renalcancer. A10398G has also been studied in relation to cancer, although the results have been conflicting.

Mitochondrial biomarkers are molecules that can be used to detect cancer in its early stages. A commercial kit (PCMT) has been developed to help with this detection. However, even if cancer is detected early, it can still be difficult to treat if the symptoms have not yet developed. Therefore, researchers are looking into gene therapy and other mitochondrial interventions as potential treatments for cancer. They can use current advancements in vitro mitochondrial intervention to identify the pathogenicity and therapeutic potential of a particular mtDNA mutation. One method proposed is to transfer artificial healthy mitochondria to remove damaged mtDNA without genetic manipulation. Other studies have looked at the levels of mtDNA biomarkers in cancerous and non-cancerous samples, as well as the levels of mtDNA methylation and mtRNA in cancerous tissues.

@explainpaper

@cancer

@mitochondria

@mito

@dna

@mtdna

@precisionmedicine

@diagnostics

@mtmsi

@aging

@Ophthalmoplegia

@Tumorigenesis

@Blood

@Inflammation

@Biopsy

@Chemotherapy

@Colorectalcancer

@Renalcancer

@Brain

@Breastcancer

If the risk of CRC within 1 year is 5% after bacteremia with a specific bacteria, the number needed to screen with a colorectal study to identify 1 case of CRC is 20.
#Colorectal #screening of all patients with species-specific bacteremia is likely to identify additional patients at risk for CRC with adenomas or other premalignant conditions