Stomach cancer, or gastric cancer, represents a significant global health burden with diverse etiological factors and varied clinical manifestations. This article provides a comprehensive review of the epidemiology, pathogenesis, diagnosis, treatment options, and prognosis of stomach cancer, with a focus on integrating recent advances in research and clinical practice. Stomach cancer is the fifth most common malignancy worldwide and the third leading cause of cancer-related deaths. The disease predominantly affects older adults, with a higher prevalence in Eastern Asia, Eastern Europe, and South America. This article aims to elucidate the complex interactions between genetic predispositions, environmental factors, and lifestyle choices in the development of stomach cancer.
Stomach cancer arises from multiple etiological factors. Helicobacter pylori Infection is the strongest known risk factor, linked to about 89% of gastric adenocarcinomas. Consumption of smoked, salted, and pickled foods increases risk, whereas fresh fruits and vegetables may offer protective effects. Genetic predispositions, including mutations in the E-cadherin gene and familial clustering, are noted. Smoking, alcohol use, and chronic gastritis also contribute to higher risk.
The development of stomach cancer involves several stages:
A. Chronic Inflammation: Initiated primarily by *H. pylori*, leading to atrophic gastritis and intestinal metaplasia.
B. Genetic Alterations: Accumulation of genetic mutations that lead to dysplasia and eventually adenocarcinoma.
C. Environmental Influences: Interactions with dietary carcinogens and smoking that exacerbate genetic predispositions.
Clinical Manifestations: Symptoms of stomach cancer are often vague and can include:
Early Stages: Indigestion, stomach discomfort, and mild nausea.
Advanced Stages: Weight loss, vomiting, blood in the stool, and severe pain.
Diagnosis involves multiple modalities:
Endoscopy and Biopsy: Gold standard for diagnosis, allowing direct visualization and histological examination.
Imaging: Ultrasound, CT scans, and PET scans help assess the spread and stage of the cancer.
Laboratory Tests: Blood tests to check for anemia and tumor markers.
Treatment depends on the stage and extent of the disease:
Surgical Resection: Gastrectomy, either partial or total, is common in early stages.
Chemotherapy and Radiotherapy: Used pre- and post-operatively to reduce tumor size and manage metastases.
Targeted Therapies: Emerging treatments focusing on specific genetic markers and pathways.
The prognosis of stomach cancer is dependent on the cancer’s stage at diagnosis:
Early Detection: Associated with a significantly better prognosis, with five-year survival rates over 65%.
Advanced Disease: Poor prognosis with survival rates dropping below 30%.
Preventive strategies include:
Dietary Modifications: Reducing intake of carcinogenic foods and increasing consumption of fruits and vegetables.
Eradication of H. pylori: Recommended in individuals with chronic gastritis or a family history of stomach cancer.
Screening Programs: Particularly in high-risk regions, using endoscopy to detect early, treatable stages of cancer.
Stomach cancer remains a challenging malignancy with a need for improved early detection methods and more effective therapeutic strategies. Ongoing research into the molecular pathways involved offers hope for targeted therapies, which could lead to better patient outcomes.
PATHOPHYSIOLOGY OF STOMACH CANCER
The pathophysiology of stomach cancer, also known as gastric cancer, is a complex process that involves multiple stages of cellular transformation from normal gastric mucosa to malignant tumors. Here’s a detailed look at the various stages and mechanisms involved:
Stomach cancer typically begins with changes in the inner lining of the stomach. These changes are often precipitated by chronic inflammation, primarily due to persistent infections such as with Helicobacter pylori (H. pylori), which is implicated in the majority of non-cardia gastric cancers. H. pylori Infection leads to chronic gastritis characterized by the infiltration of inflammatory cells. This bacterium produces cytotoxins (e.g., CagA) and prompts the production of inflammatory cytokines (such as IL-1β and TNF-α), which cause DNA damage and promote a carcinogenic environment. It leads to Atrophic Gastritis a stage with loss of gastric glandular cells and replacement with intestinal and fibrous tissues, diminishing the stomach’s acid-producing capability and leading to a condition known as intestinal metaplasia.
As the gastric mucosa undergoes chronic inflammation, it accumulates genetic and epigenetic changes that contribute to the development of cancer. Changes happen in oncogenes (like HER2 and EGFR) and tumor suppressor genes (such as p53 and E-cadherin) which disrupt normal cell cycle control and apoptosis, leading to uncontrolled cell growth. Methylation of DNA, histone modification, and the involvement of non-coding RNAs can silence tumor suppressor genes and activate oncogene expression without altering the DNA sequence.
Gastric Dysplasia involves the abnormal growth and morphology of gastric cells, a pre-cancerous stage where cells exhibit increased proliferation, altered differentiation, and genetic instability. Dysplasia can progress to invasive carcinoma, where cancer cells break through the basement membrane and invade the gastric wall.
Adenocarcinoma is the most common type of gastric cancer, which originates from the glandular epithelium of the stomach lining. It is classified into two major histological subtypes based on Lauren classification: the intestinal type, which forms gland-like structures and is often linked to H. pylori infection and environmental factors; and the diffuse type, which consists of scattered cells that do not form structures and has a worse prognosis.
Stomach cancer can spread locally or through lymphatic and hematogenous routes to distant organs, such as the liver, lungs, and bones. This stage is characterized by the ability of cancer cells to detach, survive in circulation, adhere to distant tissues, and establish new tumors. Lymphatic Spread is the most common pathway for initial metastasis in stomach cancer, which often leads to liver and lung metastases.
The tumor microenvironment, consisting of non-cancerous cells, immune cells, and extracellular matrix, plays a crucial role in the progression and response to therapy. Stromal cells uch as fibroblasts and immune cells, can support tumor growth and metastasis through the secretion of growth factors and cytokines. Cancer cells can evade immune surveillance by expressing checkpoint proteins that inhibit immune cell function. The pathophysiology of stomach cancer is multifaceted, involving a progression from initial mucosal changes induced by chronic inflammation, through stages of genetic and epigenetic modifications leading to dysplasia and invasive carcinoma, and ultimately metastasis. Understanding these pathways is crucial for developing targeted therapies and improving patient outcomes.
GENETIC FACTORS INVOLVED IN STOMACH CANCER
The genetic factors involved in stomach cancer are complex, involving a range of inherited mutations, acquired genetic alterations, and interactions with environmental factors. Understanding these genetic components is crucial for identifying at-risk individuals and developing targeted therapies. Certain hereditary conditions are associated with an increased risk of developing gastric cancer. Hereditary Diffuse Gastric Cancer (HDGC) syndrome is primarily caused by mutations in the CDH1 gene, which codes for the protein E-cadherin. E-cadherin plays a crucial role in cell-cell adhesion and tissue architecture. Mutations lead to a loss of function, contributing to cell detachment, increased invasiveness, and cancer progression. Gastric Adenocarcinoma and Proximal Polyposis of the Stomach (GAPPS) is a rare genetic condition characterized by the development of numerous polyps in the upper stomach and an increased risk of gastric cancer, though the specific genetic mutations are still under investigation. Lynch Syndrome, known as hereditary non-polyposis colorectal cancer (HNPCC), is a condition that increases the risk of many types of cancer, including stomach cancer, due to mutations in mismatch repair genes (MLH1, MSH2, MSH6, PMS2).
Stomach cancer often involves various genetic mutations and polymorphisms that affect cell growth, DNA repair, and apoptosis. TP53 is a tumor suppressor gene that is frequently mutated in gastric cancer, leading to loss of function and uncontrolled cell division. TP53 mutations are associated with poor prognosis and are common in many cancer types.
KRAS and BRAF are oncogenes, mutations of which can activate signaling pathways that promote cell proliferation and survival. While less common in gastric cancer compared to other cancers, they are critical markers for targeted therapy. PIK3CA and PTEN are genes are involved in the PI3K/Akt signaling pathway, which regulates cell growth and survival. Mutations and alterations in these genes can contribute to gastric cancer development. Epigenetic modifications, such as DNA methylation and histone modification, play a significant role in gastric carcinogenesis by silencing tumor suppressor genes and activating oncogenes. Hypermethylation of promoters of specific genes like CDH1 (in addition to mutations) and MLH1 can lead to their silencing, which is commonly observed in gastric cancer.
MicroRNAs (miRNAs) are small non-coding RNAs that can act as oncogenes or tumor suppressors and are involved in the post-transcriptional regulation of gene expression. Altered miRNA expression profiles have been observed in gastric cancer, affecting various aspects of tumor development and metastasis.
Gastric cancer often exhibits chromosomal instability (CIN), which includes amplifications, deletions, or rearrangements of chromosomes. HER2 gene is overexpressed in about 20% of gastric cancers, especially in the gastroesophageal junction cancer, leading to enhanced signaling for cell growth and survival. HER2 status is a critical factor for targeted therapy using trastuzumab. LOH genes at several chromosomal loci including 1p, 3p, 4q, 5q, 6q, 9p, 17p, and 18q is common in gastric cancer, which can affect multiple tumor suppressor genes.
The genetic landscape of stomach cancer is diverse and involves a myriad of inherited and acquired genetic alterations. A detailed understanding of these genetic factors not only helps in identifying individuals at increased risk but also opens avenues for personalized treatment strategies. Ongoing genetic research continues to uncover the complexities of gastric cancer, aiming to improve diagnostic precision and therapeutic outcomes.
ROLE OF HELICOBACTER PYLORI IN STOMACH CANCER
Helicobacter pylori (H. pylori) is a gram-negative, microaerophilic bacterium predominantly found in the human stomach. It has been implicated in various gastrointestinal diseases, including peptic ulcers, chronic gastritis, and gastric cancers. This article provides a comprehensive overview of H. pylori, discussing its discovery, pathogenic mechanisms, associated clinical conditions, diagnostic methods, and current treatment regimens.
Since its discovery in 1982 by Barry Marshall and Robin Warren, H. pylori has revolutionized our understanding of the pathogenesis of gastric diseases. It is estimated that approximately half of the world’s population is infected with H. pylori, making it one of the most prevalent infections globally. Despite its widespread occurrence, only a minority of infected individuals develop serious gastric diseases. This article aims to elucidate the biological and clinical aspects of H. pylori and its significant impact on human health.
H. pylori is characterized by its ability to survive and proliferate in the harsh acidic environment of the stomach, The bacterium is spiral-shaped, which facilitates its mobility in the gastric mucosa. H. pylori produces urease, an enzyme that catalyzes the conversion of urea to ammonia and carbon dioxide, thereby neutralizing stomach acid around the bacterium and enabling its survival. The pathogenic effects of H. pylori are primarily due to its ability to induce inflammation and damage in the gastric lining. Virulence Factors includes cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) which play crucial roles in the bacterium’s ability to cause disease. It is strongly linked to the development of duodenal and gastric ulcers, gastritis, and is a risk factor for gastric cancer, specifically adenocarcinoma and MALT lymphoma.
The majority of individuals infected with H. pylori are asymptomatic. However, clinical manifestations can include severe stomach pain, bloating, indigestion, weight loss, abdominal pain, nausea, and anemia. There may be dyspepsia and increased risk of developing gastric mucosa-associated lymphoid tissue (MALT) lymphoma.
Accurate diagnosis of H. pylori infection is crucial for effective management:
Non-Invasive Tests: Urea breath test, stool antigen test, and blood antibody
Non-Invasive Tests: Endoscopy with biopsy for histological examination, culture, or rapid urease testing.
The increasing antibiotic resistance of H. pylori has become a significant challenge, reducing the efficacy of standard treatment regimens. Research into vaccine development and alternative therapies is ongoing. Preventive strategies focus on improving sanitation and hygiene to reduce transmission, particularly in developing countries where the infection rate is highest. H. pylori remains a major public health challenge due to its association with serious gastrointestinal diseases. Continued research into its pathogenesis, along with the development of more effective treatments and potential vaccines, is essential for reducing its impact worldwide.
ROLE OF SMOKED, SALTED AND PICKLED FOODS IN STOMACH CANCER
The consumption of smoked, salted, and pickled foods plays a significant role in the development of stomach cancer through various chemical interactions and effects on the gastric environment. These dietary habits have been particularly implicated in regions with high rates of gastric cancer, such as East Asia and Eastern Europe. Understanding the chemistry behind these food preparations and their carcinogenic potential is crucial for public health measures and dietary recommendations.
When foods are smoked, salted, or pickled, nitrosamines can form as a result of reactions between nitrogenous compounds (from proteins) and nitrites added as preservatives. Nitrosamines are potent carcinogens that have been shown to induce gastric tumors in animal models and are suspected to have similar effects in humans. Smoking foods leads to the formation of Polycyclic Aromatic Hydrocarbons (PAHs), which are also carcinogenic. PAHs are formed during the incomplete combustion of organic material and can adhere to the surface of smoked meats and fish.
Salt has a direct damaging effect on the gastric mucosa, leading to increased cell turnover and a higher susceptibility to carcinogens. High salt conditions in the stomach also promote the activity of H. pylori, exacerbating its pathogenic effects and further increasing cancer risk. Excessive salt intake can also lead to hyperchlorhydria (excessive acid in the stomach), which exacerbates the development of gastritis and eventually can lead to gastric cancer.
Preservation techniques such as pickling often involve acidic environments, which can alter the microbiome of the stomach. Such changes can reduce the competition for H. pylori, facilitating its survival and increasing its pathogenic potential.
The chemical processes involved in the preparation of smoked, salted, and pickled foods are crucial for understanding their carcinogenic potential:
1. Formation of Nitrosamines: Nitrites, commonly used as preservatives in these foods, can react with amines (from proteins) under acidic conditions (such as those found in the stomach) to form N-nitroso compounds, including nitrosamines. This reaction can occur directly in the stomach after consumption of nitrite-containing foods.
2. Production of PAHs: Smoking foods involves exposing them to smoke from burning materials (wood, coal, etc.), which contain numerous volatile and semi-volatile compounds, including PAHs. PAHs are absorbed by the food and ingested.
3. Acidic Environments in Pickling: Pickling often involves vinegar or other acidic solutions. These acidic conditions can contribute to an environment where the DNA-damaging agents (like nitrosamines and reactive oxygen species) are more active, potentially leading to increased mutation rates in gastric cells.
Numerous epidemiological studies have shown a correlation between the consumption of smoked, salted, and pickled foods and an increased risk of stomach cancer. This risk is particularly pronounced in areas where these food preservation methods are commonplace and often coincide with lower intake of fresh fruits and vegetables, which have protective effects against cancer due to their antioxidant content. The dietary habits of consuming smoked, salted, and pickled foods significantly contribute to the development of stomach cancer due to the presence of carcinogens like nitrosamines and PAHs, along with the promotion of conditions favorable to H. pylori survival and activity. Reducing the intake of these foods and increasing the consumption of fresh, non-processed foods can help mitigate the risk of gastric cancer. Public health strategies aimed at dietary modification and awareness are essential for reducing the global burden of this disease.
ROLE TOBACCO SMOKING AND ALCOHOL USE IN STOMACH CANCER
Smoking, alcohol use, and chronic gastritis are well-established risk factors for stomach cancer, each contributing through distinct pathways and mechanisms. These factors can independently and synergistically damage gastric tissues, promote inflammation, and lead to genetic alterations that increase the likelihood of developing gastric cancer. Understanding these mechanisms is crucial for public health efforts aimed at reducing the incidence of this serious disease.
Tobacco smoke contains a multitude of carcinogenic compounds, including nitrosamines and polycyclic aromatic hydrocarbons (PAHs), which can directly interact with the gastric mucosa. These compounds cause DNA damage, which, if unrepaired, leads to mutations and can initiate cancer development. Smoking has been shown to increase gastric acid secretion and decrease the secretion of bicarbonate in the duodenum, which can exacerbate conditions like gastritis and promote the development of gastric ulcers, both of which are risk factors for stomach cancer. Smoking impairs the overall immune response, which could reduce the body’s ability to combat Helicobacter pylori infection, a major cause of chronic gastritis and a risk factor for gastric cancer.
Alcohol consumption, especially at high levels, can irritate and damage the gastric mucosa directly. This damage can lead to inflammation and make the gastric lining more susceptible to cancer-causing agents. Metabolism of alcohol results in the production of acetaldehyde, a toxic chemical and potent carcinogen. Acetaldehyde can bind to DNA and proteins, leading to mutations and disruptions in cellular processes. Chronic alcohol use can lead to deficiencies in essential nutrients such as vitamins A, C, E, and folate, which play roles in maintaining DNA integrity and immune function. Deficiencies in these nutrients may increase susceptibility to cancer.
Chronic gastritis, often caused by prolonged Helicobacter pylori infection, leads to ongoing inflammation of the gastric lining. Chronic inflammation is associated with the production of reactive oxygen and nitrogen species that can cause oxidative DNA damage, promoting mutations. Over time, chronic inflammation can lead to atrophic gastritis, a condition characterized by the thinning of the stomach lining and loss of glandular cells. This can progress to intestinal metaplasia, a precancerous condition in which stomach cells transform into intestinal-type cells, increasing the risk of gastric cancer. Chronic gastritis can alter the production of gastric acid, either increasing or decreasing acid secretion, which can affect the stomach’s microbiome and its susceptibility to further damage and malignancy.
The combined effects of smoking, alcohol use, and chronic gastritis significantly elevate the risk of stomach cancer. Each of these factors contributes to a cycle of damage, inflammation, and cellular changes that can culminate in cancer. Public health measures that promote smoking cessation, responsible alcohol consumption, and effective management of gastritis, especially H. pylori infection, are vital for reducing the incidence of stomach cancer. Additionally, awareness programs highlighting the risks associated with these behaviors and medical conditions can help mitigate the burden of this serious disease.
LIFESTYLE AND ENVIRONMENTAL FACTORS IN STOMACH CANCER
Environmental factors and lifestyle choices play a significant role in the development of stomach cancer, influencing both the risk and progression of the disease. These factors interact with genetic predispositions and can either exacerbate or mitigate the risk associated with inherent genetic factors. Understanding these environmental and lifestyle contributions is crucial for prevention and management strategies.
Dietary Habits
High Intake of Salted, Smoked, and Pickled Foods: As mentioned earlier, these foods contain high levels of nitrosamines and other carcinogens like polycyclic aromatic hydrocarbons, which can damage the gastric mucosa and increase cancer risk.
Low Intake of Fruits and Vegetables: A diet lacking in fresh fruits and vegetables results in lower intake of antioxidants (such as vitamins A, C, and E), which protect against cellular damage from free radicals. Antioxidants help neutralize reactive oxygen species, reducing the risk of mutation and cancer development.
Consumption of Red and Processed Meats: These foods are high in heme iron and have been linked to higher rates of stomach cancer, possibly due to the production of carcinogenic N-nitroso compounds.
Obesity and Physical Inactivity
Obesity often leads to increased abdominal pressure and might contribute to the development of hiatal hernia, which can cause reflux and subsequent damage to the gastric lining. Additionally, obesity changes the levels of various hormones and adipokines, which can promote inflammation and potentially lead to cancer. Obesity is more strongly associated with cancer at the gastric cardia (the part closest to the esophagus) than non-cardia gastric cancer.
Occupational and Environmental Exposures
Certain occupations, such as those involving exposure to coal dust, metal dust, and chemicals used in the rubber and plastics industry, have been associated with an increased risk of stomach cancer. Although more commonly linked to other types of cancer, exposure to high levels of radiation can also increase stomach cancer risk.
Environmental factors and lifestyle choices significantly influence the risk of developing stomach cancer. Many of these risk factors are modifiable, suggesting that changes in diet, reduction in smoking and alcohol use, management of body weight, and avoidance of harmful exposures can substantially decrease the risk of this disease. Public health strategies focusing on lifestyle modifications, early detection, and eradication of H. pylori infection could effectively reduce the incidence and mortality associated with stomach cancer.
ENZYMES INVOVED IN MOLECULAR PATHOLOGY OF STOMACH CANCER
The molecular pathology of stomach cancer involves a complex interplay of various enzymes that contribute to tumorigenesis through their actions on specific substrates, their regulatory functions, and their modulation by activators and inhibitors. Here is an overview of some key enzymes involved in the molecular pathology of stomach cancer, along with their substrates, functions, activators, and inhibitors:
1. Matrix Metalloproteinases (MMPs)
Substrates: Extracellular matrix components such as collagen, laminin, and fibronectin.
Functions: MMPs are involved in the degradation of the extracellular matrix, facilitating tumor invasion and metastasis. They also play a role in angiogenesis and the modulation of the tumor microenvironment.
Activators: MMPs are activated by various factors including inflammatory cytokines (e.g., TNF-α, IL-1β), growth factors, and oncogenic signaling pathways.
Inhibitors: Tissue inhibitors of metalloproteinases (TIMPs) are natural inhibitors of MMPs. Synthetic inhibitors include Marimastat and other broad-spectrum MMP inhibitors.
2. Cyclooxygenase-2 (COX-2)
Substrates: Arachidonic acid.
Functions: COX-2 converts arachidonic acid into prostaglandins, which are involved in inflammation and pain. In cancer, COX-2 is associated with promoting tumor growth, angiogenesis, and suppression of apoptosis.
Activators: COX-2 expression can be induced by inflammatory cytokines, growth factors, and oncogenes.
Inhibitors: Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin and selective COX-2 inhibitors (coxibs) are effective in reducing COX-2 activity.
3. Telomerase
Substrates: Telomeric DNA.
Functions: Telomerase adds repetitive nucleotide sequences to the ends of chromosomes, thereby maintaining telomere length and enabling cancer cells to replicate indefinitely.
Activators:Telomerase activity is typically low in most somatic cells but is activated in cancer cells by mutations, increased expression of its catalytic subunit (hTERT), and through pathways involving MYC and Wnt signaling.
Inhibitors: Telomerase inhibitors include synthetic oligonucleotides, small molecule inhibitors, and immunotherapeutic approaches targeting hTERT.
4. Catenins (β-Catenin)
Substrates: Acts as a part of the cadherin protein complex for cell-cell adhesion and is also involved in the Wnt signaling pathway.
Functions: In the Wnt pathway, β-catenin translocates to the nucleus and activates transcription of genes promoting cell proliferation and survival. Its dysfunction is linked to increased cell motility and tumor invasiveness.
Activators: Wnt ligands, mutations in APC or β-catenin itself, which prevent its degradation.
Inhibitors: Compounds that stabilize the destruction complex (APC, Axin, GSK3β) or prevent β-catenin from entering the nucleus.
5. Helicase (e.g., Helicobacter pylori-induced)
Substrates: DNA and RNA substrates during replication and transcription.
Functions: Helicases unwind double-stranded DNA and RNA, which is crucial for replication, repair, and transcription. In the context of H. pylori infection, certain bacterial factors such as CagA can modulate host cell DNA unwinding and processing enzymes, contributing to genomic instability.
Activators: Generally activated by ATP and other nucleoside triphosphates.
Inhibitors: Specific helicase inhibitors are being researched, including those that inhibit the replication machinery of cells.
The enzymes involved in the molecular pathology of stomach cancer play crucial roles in the progression and metastasis of the disease. Targeting these enzymes with specific inhibitors can offer therapeutic benefits, while understanding their regulation by activators provides insights into cancer biology and potential preventive strategies. Further research is necessary to develop targeted therapies that can effectively modulate these enzymes in the context of stomach cancer.
ACIDITY OF STOMACH MICROENVIRONMENT
The acidity of the stomach microenvironment plays a pivotal role in the molecular pathology of stomach cancer, influencing various cellular processes, the behavior of cancer cells, and the effectiveness of treatments. The stomach’s natural acidic environment is primarily maintained by the secretion of hydrochloric acid from gastric parietal cells, which helps in digestion and acts as a barrier to pathogens. However, alterations in this acidity can contribute to the development and progression of stomach cancer in several key ways:
Chronic exposure to high levels of gastric acid can damage the mucosal lining of the stomach, leading to chronic inflammation and gastritis. Over time, chronic gastritis can progress to atrophic gastritis, a condition where the gastric glands are lost, leading to reduced acid production. These changes increase the risk of gastric cancer by promoting an environment conducive to DNA damage and cellular transformation.
The acidic environment of the stomach is a critical factor in the survival and colonization of Helicobacter pylori. H. pylori can modulate gastric acidity by inducing gastritis, which over time leads to a more neutral pH due to atrophic changes. This bacterium further exacerbates the inflammatory response and promotes genetic instability, both of which are significant risk factors for gastric cancer.
2. Role in Cellular Metabolism and Cancer Cell Survival
Cancer cells often exhibit altered metabolism, known as the Warburg effect, where they rely more on glycolysis for energy production even in the presence of oxygen. The resulting production of lactic acid contributes to the acidity of the tumor microenvironment. This acidity can promote invasion and metastasis by activating proteases that degrade the extracellular matrix and by facilitating angiogenesis.
Cancer cells in the stomach can adapt to the acidic microenvironment, which might otherwise be inhospitable. These adaptations include changes in the expression of pH regulators like the proton pumps and bicarbonate transporters, allowing cancer cells to maintain intracellular pH that supports survival and growth, while the extracellular matrix remains acidic.
3. Influence on Immune Surveillance
Immune Suppression: The acidic microenvironment has been shown to suppress the function of various immune cells, including T-cells and natural killer cells. This suppression aids cancer cells in evading immune surveillance, a crucial factor for tumor progression and metastasis.
4. Effect on Therapeutic Efficacy
The effectiveness of certain chemotherapeutic agents and targeted therapies can be influenced by the acidity of the stomach. For instance, some drugs are unstable in acidic conditions, which can reduce their efficacy before they reach their target sites within cancer cells.
The acidity of the stomach microenvironment is a significant factor in the molecular pathology of stomach cancer, influencing everything from the initial mutagenic conditions that increase cancer risk to the survival, proliferation, and metastasis of cancer cells. Understanding these dynamics helps in tailoring interventions that might include buffering agents, proton pump inhibitors, or drugs that target metabolic adaptations of cancer cells to the acidic conditions. Additionally, modifying this acidic microenvironment could improve the efficacy of existing treatments and support the development of new therapeutic strategies.
ROLE OF HORMONES IN STOMACH CANCER
Hormones play various roles in the development and progression of stomach cancer, influencing cell growth, differentiation, and the gastric environment. Here’s an overview of key hormones involved in stomach cancer, their targets, and their functions:
1. Gastrin
Targets: Gastrin primarily targets the enterochromaffin-like cells and parietal cells in the stomach.
Functions: Gastrin is a hormone that stimulates the secretion of gastric acid by the parietal cells of the stomach, essential for digestion. It also promotes the growth of the gastric mucosa and gastric epithelial cells. In stomach cancer, hypergastrinemia (excess gastrin) can stimulate the growth of gastric cancer cells through the activation of the gastrin/cholecystokinin-2 receptor pathway. This pathway can lead to increased cell proliferation and decreased apoptosis, contributing to cancer progression.
2. Ghrelin
Targets: Ghrelin targets growth hormone secretagogue receptors (GHSR), predominantly located in the brain but also found in gastric tissues.
Functions: Known as the “hunger hormone,” ghrelin regulates appetite and energy balance but is also involved in modulating cellular proliferation and apoptosis in the gastric mucosa. In gastric cancer, ghrelin levels are often altered, and its role is complex, potentially having both protective and promotive effects on tumor growth depending on the cancer stage and cellular context.
3. Leptin
Targets: Leptin acts primarily on leptin receptors (Ob-R) expressed in various tissues, including the stomach.
Functions: Leptin is primarily known for regulating energy intake and expenditure, including appetite and hunger, metabolism, and behavior. However, leptin also promotes angiogenesis and proliferation in various cellular contexts. In stomach cancer, leptin can promote cancer progression by enhancing cell proliferation, angiogenesis, and reducing apoptosis through pathways involving JAK/STAT, MAPK, and PI3K/Akt signaling.
4. Estrogen
Targets: Estrogen receptors (ERα and ERβ) which are found in some gastric cancer cells.
Functions: Estrogen has been shown to have a complex role in gastric cancer. Depending on the receptor subtype, estrogen can either promote or inhibit tumor growth. ERβ typically exerts protective effects and is often downregulated in gastric cancer, whereas ERα has been implicated in promoting gastric cancer cell proliferation.
5. Insulin-like Growth Factor (IGF)
Targets: IGF-1 receptor (IGF-1R) on various tissues, including gastric cells.
Functions: IGF-1 promotes cell growth and survival and is involved in cancer development. In gastric cancer, IGF-1 signaling can enhance tumor growth and metastasis by promoting cell proliferation and inhibiting apoptosis through the PI3K/Akt and MAPK pathways.
The hormonal regulation in gastric cancer involves a complex interplay of hormones that affect cell proliferation, apoptosis, and the tumor microenvironment. Understanding these hormonal pathways provides insights into potential therapeutic targets for treating or managing stomach cancer. Hormone-based therapies, such as hormone receptor antagonists or hormone modulating treatments, could offer new avenues for intervention in stomach cancer, particularly for tumors that express specific hormone receptors prominently.
ROLE OF HEAVY METALS IN STOMACH CANCER
Heavy metals, including arsenic, cadmium, lead, and nickel, have been implicated in the molecular pathology of stomach cancer through various mechanisms. Exposure to these metals can occur via contaminated food, water, or air, and occupational exposure is also significant in certain industries.
1. Arsenic
Mechanisms of Action: DNA Damage: Arsenic can induce DNA damage directly through the production of reactive oxygen species (ROS) and indirectly by impairing DNA repair mechanisms. This can lead to mutations and genomic instability, key events in the carcinogenic process.
Epigenetic Alterations: Arsenic exposure has been associated with epigenetic changes such as DNA methylation, histone modifications, and miRNA expression alterations. These changes can affect gene expression critical for cell cycle regulation, apoptosis, and DNA repair.
Inflammation: Chronic inflammation, a known risk factor for cancer, can be exacerbated by arsenic exposure, further promoting tumorigenesis.
Epidemiological Evidence: Long-term exposure to arsenic, particularly through drinking water, has been linked to an increased risk of stomach cancer in several studies.
2. Cadmium
Induction of Oxidative Stress: Cadmium exposure increases oxidative stress by generating reactive oxygen species, leading to cell damage and apoptosis resistance.
Disruption of Cellular Processes: Cadmium can interfere with essential cellular functions, including cell signaling, cell adhesion, and DNA repair, through its ability to bind to proteins and enzymes, replacing other essential metals like zinc.
Epidemiological Evidence: Occupational exposure to cadmium has been associated with a higher risk of stomach cancer, particularly in individuals with certain genetic susceptibilities that affect metal metabolism.
3. Lead and Nickel
Oxidative Stress and DNA Damage: Similar to arsenic and cadmium, lead and nickel can induce oxidative stress, contributing to DNA damage and affecting cellular antioxidant defenses.
Hormonal Disruption: Nickel, in particular, has been shown to interfere with hormone signaling pathways, potentially affecting cellular growth and proliferation in ways that promote cancer development.
Epidemiological Evidence: There is suggestive evidence linking exposure to these metals with gastric cancer, though the data is less extensive than for arsenic and cadmium.
Heavy metals contribute to the molecular pathology of stomach cancer through direct and indirect mechanisms, including oxidative stress, DNA damage, epigenetic modifications, and the disruption of cellular processes. These effects cumulatively increase the risk of genetic mutations and malignant transformation of gastric cells. Public health measures to reduce exposure to heavy metals, particularly in high-risk areas and industries, are crucial for preventing stomach cancer and other health issues associated with these toxic substances.
VITAMINS AND MICROELEMENTS
Vitamins and microelements play significant roles in the prevention and potentially the progression of stomach cancer. Their effects are multifaceted, ranging from antioxidant protection and DNA repair to influencing cell growth and immune function. Deficiencies or excesses in certain vitamins and minerals can affect gastric health and may alter the risk of developing stomach cancer.
Vitamins
1. Vitamin C (Ascorbic Acid)
Role: Vitamin C is a potent antioxidant that can neutralize free radicals, reducing oxidative stress, a risk factor for cancer. It may also inhibit the formation of carcinogenic compounds like nitrosamines in the stomach.
Epidemiological Evidence: High dietary intake of vitamin C from fruits and vegetables is associated with a reduced risk of stomach cancer.
2. Vitamin E
Role: As an antioxidant, vitamin E protects cellular membranes from oxidative damage. It also modulates immune function and inhibits cell proliferation in cancerous cells.
Epidemiological Evidence: Some studies suggest that higher levels of vitamin E intake may be protective against stomach cancer, although results can vary.
3. Vitamin A and Carotenoids
Role: Vitamin A and its precursors, carotenoids, are involved in immune function enhancement and maintenance of healthy mucous membranes in the stomach. They also have antioxidant properties.
Epidemiological Evidence: Higher dietary intake of carotenoids has been linked to a lower risk of gastric cancer.
4. Folate (Vitamin B9)
Role: Folate is crucial for DNA synthesis and repair. A deficiency in folate can lead to DNA mutations and chromosomal damage, increasing cancer risk.
Epidemiological Evidence: Adequate folate intake is associated with a reduced risk of stomach cancer, particularly in environments with high exposure to carcinogens.
Microelements
1. Selenium
Role: Selenium functions as a cofactor for antioxidant enzymes like glutathione peroxidases. It helps in DNA repair and supports immune surveillance against cancerous cells.
Epidemiological Evidence: Low selenium levels have been associated with an increased risk of stomach cancer.
2. Zinc
Role: Zinc is essential for numerous biological functions, including DNA synthesis, cell division, and normal cellular homeostasis. It also has antioxidant properties and can support the immune system.
Epidemiological Evidence: Zinc deficiency may be linked to increased gastric inflammation and cancer risk.
3. Iron
Role: Iron is crucial for cellular metabolism and oxygen transport. However, excess iron can lead to increased oxidative stress and DNA damage.
Epidemiological Evidence: High body iron stores have been implicated in increased risk of stomach cancer, likely due to iron’s role in catalyzing the formation of reactive oxygen species.
The roles of vitamins and microelements in stomach cancer highlight the importance of a balanced diet rich in essential nutrients for cancer prevention. Adequate intake of antioxidants like vitamin C, E, selenium, and carotenoids can protect against the development of stomach cancer by reducing oxidative damage and enhancing DNA repair and immune function. Moreover, maintaining proper levels of these nutrients might help mitigate the risk factors associated with gastric carcinogenesis. Public health strategies that promote nutritional education and ensure dietary sufficiency could significantly impact stomach cancer incidence rates globally.
ROLE OF PHYTOCHEMICALS IN STOMACH CANCER
Phytochemicals, naturally occurring compounds found in plants, play significant roles in the prevention and potential treatment of stomach cancer. These bioactive substances are present in fruits, vegetables, grains, and other plant-based foods and are recognized for their health-promoting properties, including anti-inflammatory, antioxidant, and anticancer effects. Here’s an overview of how specific phytochemicals influence stomach cancer:
1. Flavonoids
Examples: Quercetin, kaempferol, and catechins.
Role: Flavonoids possess strong antioxidant properties that help reduce oxidative stress, one of the factors implicated in cancer development. They also modulate signal transduction pathways involved in cell proliferation, apoptosis, and angiogenesis.
Impact: Studies have shown that a higher intake of flavonoids can reduce the risk of stomach cancer, particularly due to their ability to inhibit the growth of Helicobacter pylori, a major risk factor for gastric cancer.
2. Carotenoids
Examples: Beta-carotene, lycopene, lutein, and zeaxanthin.
Role: Carotenoids are potent antioxidants that protect cells from DNA damage. They also modulate immune responses and inhibit the proliferation of cancer cells.
Impact: Epidemiological studies suggest that diets rich in carotenoids are associated with a reduced risk of stomach cancer.
3. Glucosinolates
Examples: Found in cruciferous vegetables like broccoli, cauliflower, and Brussels sprouts.
Role: Upon consumption, glucosinolates are converted into isothiocyanates and indoles through enzymatic reactions involving the enzyme myrosinase. Isothiocyanates have been shown to inhibit carcinogenesis and metastasis by inducing apoptosis and blocking the activation of carcinogens.
Impact: Regular consumption of cruciferous vegetables has been linked to a lower risk of stomach and other cancers.
4. Polyphenols
Examples: Resveratrol, curcumin, and ellagic acid.
Role: Polyphenols have multiple mechanisms of action, including the inhibition of inflammation, neutralization of free radicals, and modulation of key pathways involved in cell growth, apoptosis, and angiogenesis.
Impact: These compounds can prevent the initiation and progression of gastric cancer. For instance, resveratrol and curcumin have been studied for their anti-inflammatory and anticancer properties, showing potential in reducing gastric cancer risk.
5. Saponins
Examples: Found in beans, legumes, and some root vegetables.
Role: Saponins possess cholesterol-lowering properties, immune-stimulating effects, and may inhibit tumor growth. They can induce apoptosis and inhibit cell proliferation.
Impact: Although less studied than other phytochemicals, saponins contribute to the overall anticancer effects observed in diets rich in a variety of plant-based foods.
6. Allicin
Examples: Found in garlic and onions.
Role: Allicin has antimicrobial properties that may be effective against H. pylori. It also has anti-inflammatory and antioxidant effects, reducing the risk of cancer by inhibiting the proliferation of cancer cells and inducing apoptosis.
Impact: Consumption of garlic and onions has been associated with a decreased risk of stomach cancer, attributed largely to compounds like allicin.
The intake of phytochemical-rich foods is strongly linked to reduced risks of stomach cancer. These compounds interact with biological pathways to reduce inflammation, prevent DNA damage, and inhibit the growth and spread of cancer cells. Public health recommendations increasingly advocate for diets rich in fruits, vegetables, and whole grains, not only for their nutrient content but also for their phytochemical properties that offer protective effects against cancer and other diseases.
ROLE OF MODERN CHEMICAL DRUGS IN CAUSING STOMACH CANCER
The relationship between modern chemical drugs and the causation of stomach cancer is a complex and multi-faceted issue. Some medications have been found to potentially increase the risk of developing stomach cancer, often as a consequence of their long-term effects on the stomach lining, gastric acid production, or overall gastric environment. Here’s an overview of several types of drugs that have been associated with an increased risk of stomach cancer:
1. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) and Aspirin
Role and Mechanism: NSAIDs, including aspirin, are widely used for pain relief and inflammation reduction. While they can protect against certain types of cancer, such as colorectal cancer, their role in stomach cancer is more ambiguous. NSAIDs can cause irritation of the stomach lining, leading to gastritis and ulcers. Chronic injury may contribute to cancer risk in susceptible individuals.
Impact: The risk associated with NSAIDs is generally related to higher doses and prolonged use. The potential for these drugs to cause gastric mucosal damage might increase the risk of cancer, though they can also have protective effects due to their anti-inflammatory properties.
2. Proton Pump Inhibitors (PPIs)
Role and Mechanism: PPIs are used to treat conditions like gastroesophageal reflux disease (GERD) and ulcers by significantly reducing stomach acid production. Long-term use of PPIs has been linked to various gastric alterations, including changes in the stomach’s microbiota, decreased acid which could allow for the proliferation of harmful bacteria, and potential hypergastrinemia (excess gastrin levels).
Impact: Some studies suggest that prolonged use of PPIs may increase the risk of stomach cancer, particularly in individuals with chronic Helicobacter pylori infection. The increased gastrin levels can stimulate gastric cell proliferation, potentially leading to cancerous changes.
3. Antibiotics
Role and Mechanism: While antibiotics are essential for treating infections, their overuse or misuse can lead to alterations in the gastric microbiome. This disruption can influence the development of gastric diseases, including cancer, by affecting the balance of protective versus harmful bacteria.
Impact: Repeated antibiotic use can disrupt gastric ecology, potentially increasing the risk of Helicobacter pylori-associated diseases, including gastritis and gastric cancer.
4. Chemotherapy Drugs
Role and Mechanism: Chemotherapy drugs are used to treat various cancers, including stomach cancer, but their toxicity can also affect normal cells, including those in the gastric mucosa.
Impact: Some chemotherapy agents can cause gastric mucosal damage as a side effect, which might predispose to gastric cancer in a small subset of patients, particularly when combined with other risk factors.
The potential of modern chemical drugs to contribute to the causation of stomach cancer highlights the importance of careful prescription practices, consideration of patient history, and monitoring during drug therapy. It’s essential for healthcare providers to balance the benefits of these medications against potential risks, especially for individuals at higher risk of developing stomach cancer. Furthermore, this underscores the need for ongoing research to clarify the mechanisms by which these drugs might influence cancer risk and to develop safer therapeutic alternatives.
IMPORTANT BIOLOGICAL LIGANDS INVOLVED IN STOMACH CANCER
In the molecular pathology of stomach cancer, numerous biological ligands and their respective functional groups play pivotal roles. These ligands interact with cellular receptors, enzymes, and other molecules, influencing crucial processes such as cell proliferation, apoptosis, angiogenesis, and metastasis.
1. Growth Factors and Cytokines
Epidermal Growth Factor (EGF)
Functional Group: EGF-like domain
Role: Promotes cell proliferation and survival; frequently overexpressed in gastric cancer cells.
Transforming Growth Factor-beta (TGF-β)
Functional Group: Cysteine knot motif
Role: Dual role in cancer; suppresses tumor growth in early stages but promotes metastasis and angiogenesis in advanced stages.
Vascular Endothelial Growth Factor (VEGF)
Functional Group: Cystine knot growth factor superfamily
Role: Stimulates angiogenesis, critical for tumor growth and metastasis.
Interleukin-6 (IL-6)
Functional Group: Four α-helices; belongs to the helical cytokine family
Role: Drives chronic inflammation and contributes to tumor growth and progression.
2. Hormones
Gastrin
Functional Group: Amidated C-terminus
Role: Stimulates gastric acid secretion and promotes growth of the gastric mucosa and possibly gastric tumors.
Leptin
Functional Group: Four α-helices, similar to cytokines
Role: Linked to cell proliferation and reduced apoptosis in cancer cells.
3. Enzymes and Their Inhibitors
Matrix Metalloproteinases (MMPs)
Functional Group: Zinc-binding motif (HEXXHXXGXXH)
Role: Degradation of the extracellular matrix, facilitating tumor invasion and metastasis.
Tissue Inhibitors of Metalloproteinases (TIMPs)
Functional Group: N-terminal domain that binds to MMP
Role: Regulate MMP activity; imbalance can lead to increased invasion and metastasis.
4. Adhesion Molecules
E-cadherin
Functional Group: Calcium-binding motifs
Role: Mediates cell-cell adhesion; loss of function is associated with increased invasiveness and metastasis.
Integrins
Functional Group: RGD (Arg-Gly-Asp) sequence that binds to extracellular matrix components
Role: Mediate cell-extracellular matrix interactions; involved in signaling that promotes survival, migration, and invasion.
5. Receptors
HER2/neu (ErbB2)
Functional Group: Cysteine-rich extracellular domain
Role: Receptor tyrosine kinase involved in signaling pathways that enhance cell proliferation and survival.
FGF Receptors (FGFRs)
Functional Group: Immunoglobulin-like domains in extracellular region
Role: Involved in cell division, growth, and differentiation.
These biological ligands, through their specific functional groups, interact with cellular pathways to influence the pathology of stomach cancer. Targeting these ligands or their interactions offers potential therapeutic strategies for treating stomach cancer. For instance, monoclonal antibodies or small molecule inhibitors that block the activity of growth factors like VEGF or receptors like HER2 have been developed and are used in clinical settings. Understanding these interactions and the structural domains involved continues to be a crucial area of research in developing more effective treatments for gastric cancer.
MOLECULAR IMPRINTS THERAPEUTICS CONCEPTS OF HOMEOPATHY
MIT HOMEOPATHY represents a rational and updated approach towards theory and practice of therapeutics, evolved from redefining of homeopathy in a way fitting to the advanced knowledge of modern biochemistry, pharmacodynamics and molecular imprinting. It is based on the new understanding that active principles of potentized homeopathic drugs are molecular imprints of drug molecules, which act by their conformational properties. Whereas classical approach of homeopathy is based on ‘similarity of symptoms’ rather than diagnosis, MIT homeopathy proposes to make prescriptions based on disease diagnosis, molecular pathology, pharmacodynamics, as well as knowledge of biological ligands and functional groups involved in the disease process. Even though this approach may appear to be somewhat a serious departure from the basics of homeopathy, once you understand the scientific explanation of ‘similia similibus curentur’ provided by MIT, you will realize that this is actually a more updated and scientific version of homeopathy.
As we know, “Similia Similibus Curentur” is the fundamental therapeutic principle of homeopathy, upon which the entire practice is constructed. Modern biochemistry says, if the functional groups of the disease-causing molecules and drug molecules are similar, they can bind to similar molecular targets and elicit similar symptoms. As per MIT perspective, homeopathy employs this concept to identify the similarity between pathogenic and drug molecules by observing the symptoms they induce. Through “Similia Similibus Curentur,” Hahnemann actually sought to harness the principle of competitive inhibitions to develop a novel therapeutic method. If symptoms induced in healthy individuals by a drug taken in its molecular form mirror those in a diseased individual, applying the drug in a molecularly imprinted form could potentially cure the disease.
Symptoms of both the disease and the drug appear similar when the disease-causing and drug substances contain similar chemical molecules with similar functional groups, which bind to similar biological targets, producing similar molecular inhibitions and leading to errors in the same biochemical pathways. These similar chemical molecules can compete to bind to the same molecular targets. Disease molecules produce disease by competitively binding with biological targets, mimicking natural ligands due to their conformational similarity. Drug molecules, by sharing conformational similarities with disease molecules, can displace them through competitive relationships, thereby alleviating the pathological inhibitions they cause.
Molecular imprints of similar chemical molecules can act as artificial binding agents for similar substances, neutralizing them due to their mutually complementary conformations. It is evident that Hahnemann observed this competitive relationship between substances affecting living organisms by producing similar symptoms. Limited by the scientific knowledge of his time, he could not fully explain that two different substances produce similar symptoms only if both contain chemical molecules with functional groups or moieties of similar conformations, enabling them to bind to similar biological targets and induce similar molecular inhibitions, leading to deviations in the same biological pathways.
Understanding the ‘similarity’ between drug-induced symptoms and disease symptoms should extend to the ‘similarity’ in molecular inhibitions caused by drug molecules and disease-causing molecules, stemming from the ‘similarity’ of their functional groups. Samuel Hahnemann, the pioneer of homeopathy, formulated his principles during a time when modern biochemistry had not yet emerged. This historical context explains why Hahnemann was unable to describe his observations using contemporary biochemical concepts. Despite these limitations, his foresight into their therapeutic implications was nothing short of genius.
Homeopathy, or “Similia Similibus Curentur,” is a therapeutic approach grounded in the identification of drug molecules that, due to their similar functional groups, are capable of competing with disease-causing molecules for binding to biological targets. This methodology relies on observing the similarity of symptoms produced by the disease and those the drug can induce in healthy individuals, thereby deactivating the disease-causing molecules through the binding action of molecular imprints derived from the drug. The future recognition of homeopathy as a scientific discipline hinges on our ability to demonstrate to the scientific community that “Similia Similibus Curentur” is based on the naturally occurring phenomenon of competitive relationships between chemically similar molecules, as explained in modern biochemistry. Once this connection is clearly established, homeopathy’s status as a scientific practice will inevitably be recognized.
Only way the medicinal properties of a drug substance could be transmitted to and preserved in a medium of water-ethanol mixture during homeopathic ‘potentization’ without any single drug molecule remaining in it is by preserving the conformational details of its functional groups by a process of ‘molecular imprinting’, since the conformational properties of functional groups of drug molecules play a decisive role in biomolecular interactions.
Active principles of homeopathy drugs potentized above 12 c are molecular imprints of ‘functional groups’ of drugs molecules used as templates for potentization process. When introduced into living system as therapeutic agent, these molecular imprints act as artificial binding pockets for the pathogenic molecules having functional groups that are similar to the template molecules used for potentization. As we know, a state of pathology arises when some endogenous or exogenous molecules having functional groups similar to those of natural ligands of a biological target competitively bind to that target and produce molecular inhibitions. Removing these molecular inhibitions amounts to cure. Once you understand this biological mechanism, you will realize that molecular imprints of natural ligands also can act as therapeutic agents by binding to pathogenic molecules that compete with the natural ligands.
Biological ligands are molecules that bind specifically to a target molecule, typically a larger protein. This interaction can regulate the protein’s function or activity in various biological processes. Ligands can be of different types, including small molecules, peptides, nucleotides, and others. In biochemistry and pharmacology, understanding ligands and their interactions with proteins is crucial for drug design and for understanding cellular signalling pathways.
Biological ligands can interact with a variety of molecular targets in the body, each playing a critical role in influencing physiological processes. Ligands can activate or inhibit enzymes, which are proteins that catalyze biochemical reactions. For example, many drugs act as enzyme inhibitors to slow down or halt specific metabolic pathways that contribute to disease.
According to MIT homeopathic perspective, biological ligands potentized above 12c will contain molecular imprints of constituent functional groups. Molecular imprints of drugs that compete with natural biological ligands for same biological targets also could be used, as both of their functional groups will be similar. These molecular imprints could be used as artificial binding pockets to deactivate any pathogenic molecule that create biomolecular inhibitions by binding to the biological target molecules by their functional groups. As per this approach, therapeutics involves identifying the biological ligands implicated in a particular disease condition, preparing their molecular imprints by homeopathic potentization, and administering those molecular imprints as disease-specific formulations.
Endogenous or exogenous pathogenic molecules mimic as authentic biological ligands by conformational similarity and competitively bind to their natural target molecules producing inhibition of their functions, thereby creating a state of pathology. Molecular imprints of such biological ligands as well as those of any molecule similar to the competing molecules can act as artificial binding pockets for the pathogenic molecules and remove the molecular inhibitions, and produce a curative effect. This is the simple biological mechanism involved in Molecular Imprints Therapeutics or homeopathy. Potentization is the technique of preparing molecular imprints, and ‘similarity of symptoms’ is the tool used for identifying the biological ligands, their competing molecules, and the drug molecules ‘similar’ to them.
Based on the identification of molecular targets by detailed study of pathogenic molecules, biological ligands and functional groups involved in the molecular pathology of stomach cancer, MIT homeopathy recommends following drugs in 30 c potency to be included in the prescriptions for STOMACH CANCER:
Leptin 30, Gastrin 30, Interleukin-6 30, Vascular endothelial growth factor 30, Epidermal growth factor 30, Transforming growth factor beta 30, Helicobacter pylori 30, Aspirin 30, Folic acid 30, Arsenic Alb 30, Cadmium sulph 30, Insulin like growth factor 30, Diethylstilbesterol 30, Gastrin 30, Pepsinum 30, Acid Mur 30, Beta catenin 30, Tobacco smoke 30, Acetic acid 30, Nitrosamines 30, Riboneucleic acid 30, TNF alpha 30, E Cadherin 30, Niccolum 30, Plumbum Met 30
REDEFINING HOMEOPATHY 
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