Chemotherapy / M2 MC Cancer Research Results

Chemo, Chemotherapy: Click to Expand ⟱
Features: treatment category
Chemotherapy is a treatment approach that uses drugs to target and kill rapidly dividing cells, primarily cancer cells. However, because many normal cells also divide quickly (such as those in the bone marrow, digestive tract, and hair follicles), chemotherapy can also affect these cells, leading to a range of side effects.

Main Classes of Chemotherapy Agents and Examples
Alkylating Agents:
-work by adding alkyl groups to DNA, which interferes with the DNA’s structure and prevents replication.
Examples: Cyclophosphamide, Ifosfamide, Melphalan, Chlorambucil, Busulfan.

Anti-metabolites:
-interfere with DNA and RNA synthesis by substituting for the normal building blocks of nucleic acids.
Examples: Methotrexate, 5-Fluorouracil (5-FU), Cytarabine, Gemcitabine, 6-Mercaptopurine.

Anti-microtubule Agents:
-interfere with the structures that separate chromosomes during cell division (mitosis). Examples: Paclitaxel, Docetaxel, Vincristine, Vinblastine.

Topoisomerase Inhibitors:
-target the enzymes topoisomerase I and II, which control the changes in DNA structure required for replication.
Examples: Etoposide (topoisomerase II inhibitor), Irinotecan (topoisomerase I inhibitor), Topotecan.

Cytotoxic Antibiotics:
-intercalate into DNA, inhibiting the replication of cancer cells.
Examples: Doxorubicin, Daunorubicin, Bleomycin, Mitoxantrone.

Platinum-Based Agents:
-contain platinum and cause cross-linking of DNA, which interferes with DNA repair and replication. Examples: Cisplatin, Carboplatin, Oxaliplatin.

Many chemotherapy agents exert their effects, at least in part, by inducing oxidative stress in cancer cells. They can increase ROS levels through several mechanisms:
-Direct generation of free radicals.
-Disruption of mitochondrial function, leading to increased production of ROS.
-Interference with the cell’s antioxidant systems.

-May want to avoid antioxidants 7 days bef
ore and 7 days after chemo.
Examples: NAC, Glutathione, Alpha Lipoic Acid, Vitamin E
-anti-oxidants known to have pro-oxidant effects (like Quercetin, Curcumin, etc.) should not be taken 2-3 days before and after chemo
-pro-oxidants known to bring good benefit to chemo can be continued during chemo. Examples are: Omega 3, Aremisia Annua, Silver NanoParticles.


M2 MC, M2 macrophage conversion: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
M2 macrophages (M2 MC) are a subtype of macrophages that are generally associated with anti-inflammatory responses, tissue repair, and the promotion of tumor growth.
Strategies to reprogram M2 macrophages into a more pro-inflammatory M1 phenotype or to inhibit their function are being explored in cancer therapies.
M2 macrophages can play a dual role, promotion/suspression.
M2 macrophages are a subtype of macrophages that are generally associated with anti-inflammatory responses, tissue repair, and the promotion of tumor growth. The conversion of macrophages from the M1 (pro-inflammatory) to the M2 (anti-inflammatory) phenotype is a critical process in the tumor microenvironment and has significant implications for cancer progression.

M2 macrophages are generally considered protumorigenic. They secrete various cytokines and growth factors that promote tumor cell proliferation, angiogenesis, and tissue remodeling. Additionally, they can suppress the activity of cytotoxic T cells and natural killer (NK) cells, further aiding tumor immune evasion.


Scientific Papers found: Click to Expand⟱
1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1)

HO-1↓, 1,   OXPHOS↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3)

ATP↑, 1,   Insulin↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

Glycolysis↓, 1,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death(tgid=5)

MAPK↓, 1,   TumCD↑, 1,  

Autophagy & Lysosomes(tgid=9)

ATG3↑, 1,   Beclin-1↑, 1,   LAMP2↑, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10)

DNAdam↑, 1,   P53↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

HDAC↓, 1,   IGF-1↓, 1,   STAT5↓, 1,  

Migration(tgid=13)

Treg lymp↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

M2 MC↓, 1,  

Drug Metabolism & Resistance(tgid=21)

ChemoSen↑, 1,   Dose↝, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22)

BG↓, 1,   GutMicro↑, 2,  

Functional Outcomes(tgid=23)

ChemoSideEff↓, 1,  

Infection & Microbiome(tgid=24)

CD8+↑, 1,  
Total Targets: 28

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: M2 MC, M2 macrophage conversion
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:233  Target#:177  State#:%  Dir#:%
wNotes=on sortOrder:rid,rpid

 

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