Bee venom is a unique cluster of regulatory peptides. Bee venom kills HIV while sparing healthy cells

Nanoparticles containing the bee venom peptide melittin are capable of destroying the human immunodeficiency virus while leaving surrounding tissue intact.

This was reported in the March issue of Antiviral Therapy by scientists from the School of Medicine at the University of Washington.

The researchers say their discovery is a big step toward creating a new vaginal gel designed to prevent the spread of HIV.

Dr. Joshua Hood, an official at the university, said: "We hope that in areas particularly vulnerable to HIV, people will be able to use this gel to stop the spread of the epidemic."

Melittin destroys viruses and some cancer cells.

Melittin is a powerful protein toxin found only in bee venom. It is capable of punching holes in the protective shell that surrounds HIV and some other viruses. Free melittin in sufficiently large quantities can become a powerful weapon against various viral infections, and more.

Lead study author Dr. Samuel Wickline, professor of biomedical sciences, demonstrated nanoparticles loaded with melittin that have anti-cancer properties. Back in 2004, Croatian scientists reported in the Journal of the Science of Food and Agriculture that bee products, including bee venom, can be used to treat and prevent cancer. Data on the anti-cancer properties of bee venom are by no means new, but now scientists have revealed the secret of this medicine at the molecular level.

Normal cells remain intact during treatment - scientists have shown that nanoparticles with melittin do not damage the cell membrane of healthy cells. For this purpose, the nanoparticles were equipped with special molecular “bumpers”, which, when meeting a normal cell (its size is much larger than a viral particle), prevent the nanoparticle from attaching to its shell.

HIV is a particle that is incomparably smaller than any human cell, so “bumpers” do not limit the effect of nanoparticles on the virus. When the virus approaches the nanoparticle, it passes between the restrictors and comes into contact with a toxin that destroys HIV.

Dr. Hood explains: “Melittin on nanoparticles fuses with the viral envelope, forming small pores that lead to rupture and loss of the viral envelope.”

While most antiviral drugs inhibit the virus's ability to replicate, this drug directly attacks a vital part of the virus. The problem with traditional inhibitors of viral replication is that they do not stop the onset of the infectious process. And some strains of HIV have already developed resistance to traditional therapy, so ART does not stop their reproduction.

Dr. Hood says about this: “We have learned to attack that part of the virus that remains almost unchanged in different strains. Theoretically, the virus has no way of adapting to a new agent. It cannot radically change the structure of the membrane that protects its genetic material.”

Nanoparticles with melittin can not only prevent, but also treat HIV infection. Dr. Hood believes these nanoparticles can be used for two purposes:

Prevention of the spread of HIV (vaginal gel).
. Treatment of HIV/AIDS, including resistant infection (injections).

It is believed that such particles, after being introduced into the systemic bloodstream, are capable of clearing the patient’s blood of the virus over a period of time. But clinical trials need to be conducted to obtain evidence.

Hood admitted that the base particles used in the experiment were developed many years ago as an artificial component of blood. These nanoparticles were not very good at delivering oxygen. But it was found that the particles are able to circulate in human blood for a long time without causing any harm to the body. Thus, these structures are an excellent platform for the delivery of various antibacterial and antiviral agents.

Melittin, it turns out, attacks more than just the two-layer membrane of the infamous retrovirus. It is capable of destroying the protective shell of hepatitis viruses type B and C, which opens up another broad field for scientists for research.

The promising vaginal gel will also have spermicidal properties, which makes it also a contraceptive drug. An ideal multifaceted remedy for backward countries where there are big problems with both HIV and contraception. However, Dr. Hood's study will not examine contraceptive effects.

Dr Hood said: 'We're now looking at this gel as a bold option for couples where one partner is HIV positive but they want to have sex and have children. Nanoparticles with melittin themselves are absolutely harmless to sperm, so it is possible to create a gel that protects against HIV, but without a contraceptive effect.”

Dr. Hood's research has so far been conducted on laboratory cells in an artificial environment. However, nanoparticles are easy to produce, and it is now possible to supply sufficient quantities of the drug for clinical trials in humans.

Konstantin Mokanov

Melitin, a polypeptide with surfactant properties, is capable of destroying the human immunodeficiency virus without causing harm to surrounding living cells. This is reported by scientists from the University of Washington (USA) from the pages of the March issue of the journal Antiviral Therapy.

Researchers believe they have made a breakthrough in creating a vaginal gel that will prevent women from contracting the virus that sometimes causes the deadly AIDS. Such a gel promises to be in demand in those places on the planet where HIV “feels” especially well, for example, in southern Africa.

Poisonous melitin is capable (in certain concentrations) of destroying the protective shells of various microbes and viruses, incl. HIV, forming channels in them. It was previously found that nanoparticles filled with bee toxin polypeptide have anticancer properties, i.e. can kill tumor cells that do not want to die on their own. Back in 2004, scientists from Croatia learned to treat cancer using products isolated from bee venom.

How does melitin manage to perforate viral membranes without affecting the membranes of healthy cells? The point is nanoparticles, the surface of which is equipped with peculiar “bumpers”. When the particles come into contact with normal cells, they are repelled by them. In turn, HIV is much smaller in size than nanoparticles, so it gets stuck between the “bumpers” on the surface of the agent, where it is exposed to the destructive effects of the toxin, which actually “undresses” the virus.

Most antiretroviral drugs suppress the ability of the virus to replicate inside infected cells. But HIV itself does not cease to be itself - the infection simply “dormants.” And some strains of the virus have generally found a way to resist drugs that inhibit the replication of the pathogen.

Melitin physically destroys HIV. Theoretically, it is impossible to adapt to this - without a bilayer lipid membrane, the virus cannot survive. If experimental nanoparticles are introduced into a patient’s blood, they should clear it of HIV. By the way, these miracles of technology were initially developed in order to obtain artificial blood, but the particles did a poor job of delivering oxygen. One good thing is that the body does not reject them and nanoparticles can circulate in the bloodstream for a long time. That is, with their help it is possible to heal not only from HIV, but also from other infections caused by pathogens with small sizes - for example, from. Also, a gel with nanoparticles has the potential to kill sperm when used as a contraceptive.

Nanoparticles containing a bee venom toxin (melittin) can destroy the human immunodeficiency virus (HIV) while leaving surrounding cells unharmed, scientists from the University of Washington School of Medicine report in the March issue of the journal Antiviral Therapy. for 2013. The researchers say their finding is an important step toward creating a vaginal gel that can prevent HIV infection from spreading in the body. HIV is the virus that causes AIDS.

Joshua L. Good, M.D., Ph.D., chief scientific officer of the medical department, said, "We hope that in places where the HIV virus is spreading very quickly, people could use this gel as a preventative measure to stop the initial infection."

Melittin also destroys some other viruses and malignant tumor cells

Melittin is a powerful toxin that has been found in bee venom. It can destroy the protective viral envelope that surrounds the human immunodeficiency virus, as well as the envelope of other viruses. Pure melittin in large quantities can cause significant harm.

Senior author, Samuel A. Wickline, MD, J. Russell Hornsby Professor of Biomedical Sciences, clearly demonstrated that nanoparticles loaded with melittin have anti-cancer properties and have the ability to kill tumor cells. The use of bee venom in antitumor therapy is not an innovation; in 2004, Croatian scientists published in the journal Science of Nutrition and Agriculture that bee products, including bee venom, may well find their use in the treatment and prevention of cancer.

Healthy cells, at the same time, remain untouched - scientists have proven that nanoparticles filled with melittin do not harm normal, healthy cells. Protective bumpers were added to the surface of the nanoparticles so that when they come into contact with normal cells (which tend to be much larger), the nanoparticles bounce off rather than attaching to them.

HIV virus cells are much smaller than nanoparticles, and they fit between the bumpers. When HIV encounters nanoparticles, it penetrates between the bumpers and comes into direct contact with their surface, which is coated with bee toxin, which in turn destroys the virus.

Good explained: “Melittin on nanoparticles fuses with the viral envelope. Melittin forms small pores, similar to an attack complex, and ruptures the membrane, extracting the virus from it.”

While most anti-HIV drugs work to stop the virus from multiplying, this drug targets a vital part of its structure. The problem with interfering with a pathogen's abilities is that it does not stop it from spreading infection. Some types of HIV have found a way to bypass the drugs that block its spread, and despite taking these drugs, it still spreads in the body.

Good says: “We're targeting the physical properties that are inherent to the HIV virus. Theoretically, the virus has no way to adapt to this impact. The virus must have a protective coating of a two-layer membrane.” Melittin nanoparticles can prevent the penetration of HIV infection and, at the same time, treat existing HIV infection in the body.

Good believes that melittin loaded into nanoparticles has potential for two types of treatment:

Vaginal gel to prevent the spread of HIV infection in the body.
Treatment of pre-existing HIV infection, i.e. individually pharmacoresistant treatment.

In theory, if nanoparticles are injected into a patient's bloodstream, they should be able to clear HIV infection from the blood.

Good said: “The main particle we use in these experiments was developed many years ago as an artificial blood product. It doesn't do a very good job of delivering oxygen, but it circulates safely in the body and gives us a good platform that we can adapt to fight different types of infections."

Melittin randomly attacks bilayer membranes, making it a potent drug used in drug therapy beyond treating HIV infection. Hepatitis B and C viruses, among a number of other viruses, are based on the same type of protective shell and can be destroyed by introducing nanoparticle-loaded melittin into the body.

The gel also has the potential to affect sperm, the researchers explain, using it as a possible contraceptive agent.

Goode said: “We've also seen this process in couples where only one partner has HIV and they really want children. These particles themselves are safe for sperm, for the same reason they are completely safe for vaginal cells.”

This study was conducted on cells in a laboratory setting. That being said, nanoparticles are easy to produce, and sufficient quantities of particles can certainly be provided for future human research.

Latest HIV Research

Over the past few years, scientists have made great strides in improving the treatment of HIV/AIDS and developing strategies to prevent the disease.

Researchers from Johns Hopkins Children's Center, the University of Mississippi Medical Center, and the University of Massachusetts Medical School reported that a baby treated with antiretroviral therapy was functionally cured thirty hours after birth. Functional treatment means that no viral replication is detected in the body after antiretroviral therapy.

Developing antiretroviral therapy for HIV comes at a cost - researchers at Harvard University in the US report that scaling up antiretroviral therapy in a remote South African province of KwaZulu-Natal reduced the risk of HIV transmission to sexual partners by 96%.

"Nanoparticles containing the bee venom toxin melittin can destroy the human immunodeficiency virus (HIV) while leaving surrounding cells unharmed," scientists from the University of Washington School of Medicine said in March 2013.

The researchers say their finding is a major step toward creating a vaginal gel that could prevent the spread of HIV. Joshua L. Good, MD, scientific director, said:

"We hope that in places where HIV has spread, people could use this gel as a preventive measure to stop the initial spread of infection."

Melittin destroys some viruses and malignant tumor cells

Melittin is a powerful toxin found in bee venom. This toxin is capable of affecting the protective membrane surrounding HIV. However, do not forget that in large doses, mellitin can cause serious damage to the body. Senior author, Samuel A. Wickline, MD, J. Russell Hornsby Professor of Biomedical Sciences, showed that nanoparticles loaded with melittin have anti-cancer properties and have the potential to kill tumor cells. The connection between bee venom and antitumor treatment is not new. In 2004, Croatian scientists reported in the journal the Science of Food and Agriculture that honey. bee products, including poison, may well find application in the treatment and prevention of cancer. Normal cells remain unaffected - Scientists have shown that nanoparticles filled with melittin do not harm normal, healthy cells. Protective elements were added to the surface of the nanoparticles so that when they come into contact with normal cells (which tend to be much larger), the nanoparticles bounce off rather than attaching.

Scientists have discovered a powerful toxin in bee venom that could ultimately play a crucial role in preventing the spread of HIV infection.

Since the human immunodeficiency virus is very small in size, nanoparticles come into contact with them, damaging its surface, and the bee toxin destroys the virus itself.

Melittin nanoparticles can prevent and completely cure HIV infections.

Scientists believe that melittin can be used to treat HIV infection in the following ways:

Vaginal gel to prevent the spread of HIV infection.
As a therapy for existing cases of HIV infection, in particular drug-resistant ones.
Theoretically, if nanoparticles are injected into a patient's bloodstream, they should clear HIV from the blood.

Theoretically, if nanoparticles are injected into a patient's bloodstream, they should be able to clear HIV from the blood. Scientist Good says, "The main particles we use in these experiments were developed many years ago as an artificial blood product. It's not the best way to deliver oxygen, but it circulates safely in the body and gives us a good platform to adapt and fight against different types of infections." Melittin attacks bilayer membranes indiscriminately, making it potentially suitable for drug therapy beyond HIV infection. Hepatitis B and C have the same type of protective shell and can be targeted and destroyed by administering melittin.

This study was carried out in cells under laboratory conditions. However, nanoparticles are easy to produce and are available in sufficient quantities for human studies.

. Concerns about unmanageable side effects (such as constipation, nausea, or confusion. Concerns about pain medication addiction. Non-adherence to prescribed pain medications. Financial barriers. Health care system concerns: Low priority for cancer pain management. Most appropriate treatment may be too expensive for patients and their families Tight regulation of controlled substances Problems with affordability or access to treatment Opiates not available over the counter to patients Unavailable medications Flexibility is key to cancer pain management Because patients vary in diagnosis, stage of the disease, response to pain and personal preferences, then it is necessary to be guided by these particular features. More details in the following articles: ">Pain in cancer 6

to cure or at least stabilize the development of cancer. Like other therapies, the choice to use radiation therapy to treat a specific cancer depends on a number of factors. These include, but are not limited to, the type of cancer, the patient's physical condition, the stage of the cancer, and the location of the tumor. Radiation therapy (or radiotherapy is an important technology for shrinking tumors. High energy waves are directed at the cancerous tumor. The waves cause damage to cells, disrupting cellular processes, preventing cell division, and ultimately lead to the death of malignant cells. The death of even part of the malignant cells leads to One significant disadvantage of radiation therapy is that the radiation is not specific (that is, it is not directed exclusively at cancer cells for cancer cells and can also harm healthy cells. The response of normal and cancer tissue to therapy The response of tumor and normal tissue to radiation depends on their growth pattern before the start of therapy and during treatment. Radiation kills cells through interaction with DNA and other target molecules. Death does not occur instantly, but occurs when cells try to divide, but as a result of exposure to radiation, a failure occurs in the division process, which is called abortive mitosis. For this reason, radiation damage occurs more quickly in tissues containing cells that divide quickly, and cancer cells are the ones that divide quickly. Normal tissues compensate for the cells lost during radiation therapy by speeding up the division of remaining cells. In contrast, tumor cells begin to divide more slowly after radiation therapy, and the tumor may shrink in size. The extent of tumor shrinkage depends on the balance between cell production and cell death. Carcinoma is an example of a type of cancer that often has a high rate of division. These types of cancer tend to respond well to radiation therapy. Depending on the dose of radiation used and the individual tumor, the tumor may begin to grow again after stopping therapy, but often more slowly than before. To prevent the tumor from growing back, radiation is often given in combination with surgery and/or chemotherapy. Goals of Radiation Therapy Curative: For curative purposes, radiation exposure is usually increased. Reaction to radiation ranges from mild to severe. Symptom relief: This procedure is aimed at relieving cancer symptoms and prolonging survival, creating a more comfortable living environment. This type of treatment is not necessarily performed with the intention of curing the patient. Often this type of treatment is prescribed to prevent or eliminate pain caused by cancer that has metastasized to the bones. Radiation instead of surgery: Radiation instead of surgery is an effective tool against a limited number of cancers. Treatment is most effective if the cancer is found early, while it is still small and non-metastatic. Radiation therapy may be used instead of surgery if the location of the cancer makes surgery difficult or impossible to perform without serious risk to the patient. Surgery is the preferred treatment for lesions that are located in an area where radiation therapy may be more harmful than surgery. The time required for the two procedures is also very different. Surgery can be performed quickly after diagnosis; Radiation therapy may take weeks to be fully effective. There are pros and cons to both procedures. Radiation therapy may be used to save organs and/or avoid surgery and its risks. Radiation destroys rapidly dividing cells in the tumor, while surgical procedures may miss some of the cancerous cells. However, large tumor masses often contain oxygen-poor cells in the center that do not divide as quickly as cells near the surface of the tumor. Because these cells do not divide rapidly, they are not as sensitive to radiation therapy. For this reason, large tumors cannot be destroyed using radiation alone. Radiation and surgery are often combined during treatment. Useful articles for a better understanding of radiation therapy: ">Radiation Therapy 5

Skin reactions with targeted therapy Skin problems Shortness of breath Neutropenia Nervous system disorders Nausea and vomiting Mucositis Menopausal symptoms Infections Hypercalcemia Male sex hormone Headaches Hand-foot syndrome Hair loss (alopecia Lymphedema Ascites Pleurisy Edema Depression Cognitive problems Bleeding Loss of appetite Restlessness and anxiety Anemia Confusion Delirium Difficulty swallowing Dysphagia Dry mouth Xerostomia Neuropathy For specific side effects, read the following articles: "> Side effects36

cause cell death in various directions. Some of the drugs are natural compounds that have been identified in various plants, while other chemicals are created in the laboratory. Several different types of chemotherapy drugs are briefly described below. Antimetabolites: Drugs that can affect the formation of key biomolecules inside the cell, including nucleotides, the building blocks of DNA. These chemotherapeutic agents ultimately interfere with the process of replication (production of the daughter DNA molecule and therefore cell division. Examples of antimetabolites include the following drugs: Fludarabine, 5-Fluorouracil, 6-Thioguanine, Ftorafur, Cytarabine. Genotoxic drugs: Drugs that can damage DNA: By causing this damage, these agents interfere with DNA replication and cell division. Examples of drugs: Busulfan, Carmustine, Epirubicin, Idarubicin. Spindle inhibitors (or mitosis inhibitors: These chemotherapy agents are aimed at preventing proper cell division , interacting with cytoskeletal components that allow one cell to divide into two parts. As an example, the drug paclitaxel, which is obtained from the bark of the Pacific Yew and semi-synthetically from the English Yew (Taxus baccata. Both drugs are prescribed as a series of intravenous injections. Others Chemotherapeutic agents: These agents inhibit (slow down cell division through mechanisms that are not covered in the three categories listed above. Normal cells are more resistant to drugs because they often stop dividing under conditions that are not favorable. However, not all normal dividing cells escape the effects of chemotherapy drugs, which is evidence of the toxicity of these drugs. Cell types that tend to rapidly those dividing, such as in the bone marrow and in the lining of the intestines, tend to suffer the most. Death of normal cells is one of the common side effects of chemotherapy. For more information about the nuances of chemotherapy, see the following articles: ">Chemotherapy 6

and non-small cell lung cancer. These types are diagnosed based on how the cells look under a microscope. Based on the established type, treatment options are selected. To understand the prognosis of the disease and survival rate, I present statistics from open US sources for 2014 on both types of lung cancer together: New cases of the disease (prognosis: 224210 Number of projected deaths: 159260 Let us consider in detail both types, specifics and treatment options.">Lung cancer 4
in the United States in 2014: New cases: 232,670 Deaths: 40,000 Breast cancer is the most common non-skin cancer among women in the United States (open sources, an estimated 62,570 cases of pre-invasive disease (in situ, With 232,670 new cases of invasive disease and 40,000 deaths, fewer than one in six women diagnosed with breast cancer will die from the disease, compared with an estimated 72,330 American women who will die from lung cancer in 2014. Breast Cancer glands in men (yes, yes, there is such a thing, it accounts for 1% of all cases of breast cancer and mortality from this disease. Widespread screening has increased the incidence of breast cancer and changed the characteristics of detected cancer. Why has it increased? Yes, because the use of modern methods has made it possible to detect incidence of low-risk cancers, premalignant lesions and ductal cancer in situ (DCIS). Population-based studies in the US and UK show an increase in DCIS and the incidence of invasive breast cancer since 1970, this is associated with the widespread use of postmenopausal hormone therapy and mammography. In the last decade, postmenopausal women have refrained from using hormones and the incidence of breast cancer has decreased, but not to the level that can be achieved with the widespread use of mammography. Risk and protective factors Increasing age is the most important risk factor for breast cancer. Other risk factors for breast cancer include the following: Family medical history o Underlying genetic susceptibility Sex mutations in the BRCA1 and BRCA2 genes, and other breast cancer susceptibility genes Alcohol consumption Breast tissue density (mammographic) Estrogen (endogenous: o Menstrual history (onset of menstruation / late menopause o No history of childbirth o Older age at first birth History of hormone therapy: o Combination of estrogen and progestin (HRT Oral contraception) Obesity Lack of exercise Personal history of breast cancer Personal history of proliferative forms of benign breast disease Radiation exposure to the breast Of all Of women with breast cancer, 5% to 10% may have germline mutations in the BRCA1 and BRCA2 genes.Studies have found that specific BRCA1 and BRCA2 mutations are more common among women of Jewish descent. Men who carry a BRCA2 mutation also have an increased risk of developing breast cancer. Mutations in both the BRCA1 and BRCA2 genes also create an increased risk of developing ovarian cancer or other primary cancers. Once BRCA1 or BRCA2 mutations have been identified, it is advisable for other family members to undergo genetic counseling and testing. Protective factors and measures to reduce the risk of developing breast cancer include the following: Estrogen use (especially after a hysterectomy Establishing an exercise habit Early pregnancy Breastfeeding Selective estrogen receptor modulators (SERMs) Aromatase inhibitors or inactivators Reducing the risks of mastectomy Reducing the risk of oophorectomy or removal ovarian Screening Clinical trials have found that screening asymptomatic women with mammography, with or without clinical breast examination, reduces mortality from breast cancer.Diagnosis If breast cancer is suspected, the patient usually undergoes the following steps: Confirmation of the diagnosis Evaluation Stage of disease Choice of therapy The following tests and procedures are used to diagnose breast cancer: Mammography Ultrasound Breast magnetic resonance imaging (MRI, when clinically indicated Biopsy Contralateral breast cancer Pathologically, breast cancer can be multicentric and bilateral defeat. Bilateral disease is somewhat more common in patients with invading focal carcinoma. Over 10 years after diagnosis, the risk of primary breast cancer in the contralateral breast ranges from 3% to 10%, although endocrine therapy may reduce this risk. Development of second breast cancer is associated with an increased risk of distant recurrence. If the BRCA1/BRCA2 gene mutation was diagnosed before the age of 40, the risk of cancer of the second breast in the next 25 years reaches almost 50%. Patients diagnosed with breast cancer should undergo bilateral mammography at the time of diagnosis to rule out synchronous disease. The role of MRI in screening for contralateral breast cancer and monitoring women treated with breast conservation therapy continues to evolve. Because mammography's increased detection rate of possible disease has been demonstrated, selective use of MRI for adjunctive screening is occurring more frequently, despite the lack of randomized controlled data. Because only 25% of MRI-positive findings represent malignancy, pathological confirmation is recommended before treatment. Whether this increased rate of disease detection will lead to improved treatment outcomes is unknown. Prognostic Factors Breast cancer is usually treated with various combinations of surgery, radiation therapy, chemotherapy and hormonal therapy. Conclusions and selection of therapy may be influenced by the following clinical and pathological features (based on conventional histology and immunohistochemistry: Menopausal status of the patient. Stage of disease. Grade of primary tumor. Tumor status depending on the status of estrogen receptors (ER and progesterone receptors (PR). Histological types Breast cancer is classified into different histological types, some of which have prognostic significance. For example, favorable histological types include colloid, medullary and tubular cancer. Uses of molecular profiling in breast cancer include the following: ER and PR status testing. Receptor testing HER2/Neu status. Based on these results, breast cancer is classified as: Hormone receptor positive. HER2 positive. Triple negative (ER, PR, and HER2/Neu negative. Although some rare inherited mutations, such as BRCA1 and BRCA2, predispose to the development of breast cancer in carriers of the mutation, however, prognostic data on carriers of the BRCA1 / BRCA2 mutation are contradictory; these women are simply at greater risk of developing second breast cancer. But it is not a fact that this can happen. Hormone replacement therapy After careful consideration, patients with severe symptoms may be treated with hormone replacement therapy. Follow-up The frequency of surveillance and the appropriateness of screening after completion of primary treatment for stage I, stage II, or stage III breast cancer remain controversial. Data from randomized trials show that periodic follow-up with bone scans, liver ultrasound, chest x-rays and blood tests for liver function does not improve survival or quality of life at all compared with routine health checks. Even when these tests allow early detection of relapse of the disease, this does not affect the survival of patients. Based on these data, limited screening and annual mammography may be an acceptable continuation for asymptomatic patients who have been treated for stage I to III breast cancer. More detailed information in the articles: "> Mammary cancer5
, ureters, and proximal urethra are lined by a specialized mucosa called transitional epithelium (also called urothelium. Most cancers that form in the bladder, renal pelvis, ureters, and proximal urethra are transitional cell carcinomas (also called urothelial carcinomas, derived from transitional epithelium Transitional cell bladder cancer can be low-grade or full-grade: Low-grade bladder cancer often recurs in the bladder after treatment, but rarely invades the muscle walls of the bladder or spreads to other parts of the body.Patients rarely die from bladder cancer low grade. Full grade bladder cancer usually recurs in the bladder and also has a strong tendency to invade the muscle walls of the bladder and spread to other parts of the body. High grade bladder cancer is considered more aggressive than low grade bladder cancer and much more more likely to result in death. Almost all deaths from bladder cancer are due to high-grade cancer. Bladder cancer is also divided into muscle-invasive and non-muscle-invasive disease, based on invasion of the muscle lining (also referred to as the detrusor muscle, which is located deep in the muscle wall of the bladder. Muscle-invasive disease is much more likely to spread to other parts of the body and is typically treated by either removing the bladder or treating the bladder with radiation and chemotherapy.As noted above, high-grade cancers are much more likely to be muscle-invasive cancers than low-grade cancers.Thus, Muscle-invasive cancer is generally considered to be more aggressive than non-muscle-invasive cancer.Non-muscle-invasive disease can often be treated by removing the tumor using a transurethral approach and sometimes chemotherapy or other procedures in which a drug is injected into the urinary cavity bladder with a catheter to help fight cancer. Cancer can arise in the bladder in the setting of chronic inflammation, such as a bladder infection caused by the parasite haematobium Schistosoma, or as a result of squamous metaplasia; The incidence of squamous cell carcinoma of the bladder is higher in the setting of chronic inflammation than otherwise. In addition to transitional carcinoma and squamous cell carcinoma, adenocarcinoma, small cell carcinoma, and sarcoma can form in the bladder. In the United States, transitional cell carcinomas account for the vast majority (more than 90% of bladder cancers. However, a significant number of transitional cell carcinomas have areas of squamous cell or other differentiation. Carcinogenesis and Risk Factors There is compelling evidence of the influence of carcinogens on the occurrence and development of bladder cancer. The most common risk factor for developing bladder cancer is cigarette smoking. It is estimated that up to half of all bladder cancer cases are caused by smoking and that smoking increases the risk of developing bladder cancer at two to four times the baseline risk. Smokers with less functional polymorphisms N-acetyltransferase-2 (known as a slow acetylator) has a higher risk of developing bladder cancer compared to other smokers, apparently due to a decreased ability to detoxify carcinogens. Certain occupational hazards have also been linked to bladder cancer, and higher rates of bladder cancer have been reported due to textile dyes and rubber in the tire industry; among artists; leather processing industry workers; from shoemakers; and aluminum, iron and steel workers. Specific chemicals associated with bladder carcinogenesis include beta-naphthylamine, 4-aminobiphenyl, and benzidine. Although these chemicals are now generally banned in Western countries, many other chemicals that are still used today are also suspected of causing bladder cancer. Exposure to the chemotherapy agent cyclophosphamide has also been associated with an increased risk of bladder cancer. Chronic urinary tract infections and infections caused by the parasite S. haematobium are also associated with an increased risk of developing bladder cancer, and often squamous cell carcinoma. Chronic inflammation is believed to play a key role in the process of carcinogenesis in these conditions. Clinical features Bladder cancer usually presents with simple or microscopic hematuria. Less commonly, patients may complain of frequent urination, nocturia, and dysuria, symptoms that are more common in patients with carcinoma. Patients with urothelial cancer of the upper urinary tract may experience pain due to obstruction by the tumor. It is important to note that urothelial carcinoma is often multifocal, necessitating examination of the entire urothelium if a tumor is detected. In patients with bladder cancer, imaging of the upper urinary tract is essential for diagnosis and follow-up. This can be achieved using urethroscopy, retrograde pyelogram in cystoscopy, intravenous pyelogram, or computed tomography (CT urogram). In addition, patients with transitional cell carcinoma of the upper urinary tract have a high risk of developing bladder cancer; these patients require periodic cystoscopy and observation of the contralateral upper urinary tract. Diagnosis When bladder cancer is suspected, the most useful diagnostic test is cystoscopy. Radiological studies such as computed tomography or ultrasound do not have sufficient sensitivity to be useful in detecting bladder cancer. Cystoscopy may be performed in a urology department clinic. If cancer is detected during cystoscopy, the patient is usually scheduled for a bimanual examination under anesthesia and a repeat cystoscopy in the operating room so that transurethral tumor resection and/or biopsy can be performed. Survival In patients who die of bladder cancer , there are almost always metastases from the bladder to other organs. Low-grade bladder cancer rarely grows into the muscle wall of the bladder and rarely metastasizes, so low-grade (stage I) bladder cancer patients very rarely die from the cancer. However, they may experience multiple recurrences that should be treated resection. Almost all deaths from bladder cancer occur among patients with high-grade disease, which has a much greater potential to invade deep into the muscular walls of the bladder and spread to other organs. Approximately 70% to 80% of patients with newly diagnosed bladder cancer bladder have superficial bladder tumors (i.e., stage Ta, TIS, or T1. The prognosis of these patients depends largely on the grade of the tumor. Patients with high-grade tumors have a significant risk of dying from the cancer, even if it is not muscle-invasive cancer Those patients with high-grade tumors who are diagnosed with superficial, non-muscle-invasive bladder cancer in most cases have a high chance of cure, and even in the presence of muscle-invasive disease, sometimes the patient can be cured. Studies have shown that in some patients with distant metastases, oncologists achieved long-term complete responses after treatment with a combination chemotherapy regimen, although most of these patients have metastases limited to their lymph nodes. Secondary Bladder Cancer Bladder cancer tends to recur, even if it is non-invasive at the time of diagnosis. Therefore, standard practice is to perform urinary tract surveillance after a diagnosis of bladder cancer. However, no studies have yet been conducted to evaluate whether surveillance affects progression rates, survival, or quality of life; although there are clinical trials to determine the optimal follow-up schedule. Urothelial carcinoma is thought to reflect a so-called field defect, in which the cancer arises due to genetic mutations that are widely present in the patient's bladder or throughout the urothelium. Thus, people who have had a resected bladder tumor often subsequently have ongoing tumors in the bladder, often in other locations than the primary tumor. Similarly, but less frequently, they may develop tumors in the upper urinary tract (i.e., renal pelvis or ureter). An alternative explanation for these patterns of recurrence is that cancer cells that are destroyed when the tumor is excised may reimplant in another site in the urothelium. Support for this second theory is that tumors are more likely to recur lower than in the opposite direction from the initial cancer.Upper tract cancer is more likely to recur in the bladder than bladder cancer is to reproduce in the upper urinary tract. The rest is in the following articles: "> Bladder cancer4
, as well as an increased risk of metastatic disease. The degree of differentiation (staging) of a tumor has an important influence on the natural history of the disease and on the choice of treatment. An increase in the incidence of endometrial cancer has been found in association with long-term, unopposed estrogen exposure (increased levels. In contrast, combination therapy (estrogen + progesterone prevents an increase in the risk of developing endometrial cancer associated with a lack of resistance to the effects of estrogen specifically. Receiving a diagnosis is not the best time. However, you should know - endometrial cancer is a treatable disease. Monitor the symptoms and everything will be fine! In some patients, it may play a role "activator" of endometrial cancer is a prior history of complex hyperplasia with atypia. An increase in the incidence of endometrial cancer has also been found in association with treatment of breast cancer with tamoxifen. According to researchers, this is due to the estrogenic effect of tamoxifen on the endometrium. Because of this increase, patients who Patients prescribed therapy with tamoxifen must undergo regular examinations of the pelvic region and must be attentive to any abnormal uterine bleeding. Histopathology The distribution pattern of malignant endometrial cancer cells depends in part on the degree of cellular differentiation. Well differentiated tumors, as a rule, limit their spread to the surface of the uterine mucosa; myometrial expansion occurs less frequently. In patients with poorly differentiated tumors, invasion of the myometrium is much more common. Invasion of the myometrium is often a precursor to lymph node involvement and distant metastases, and often depends on the grade of differentiation. Metastasis occurs in the usual way. Spread to the pelvic and para-aortic nodes is common. When distant metastases occur, it most often occurs in: Lungs. Inguinal and supraclavicular nodes. Liver. Bones. Brain. Vagina. Prognostic factors Another factor that is associated with ectopic and nodal spread of the tumor is the participation of the capillary-lymphatic space in histological examination. The three prognostic groupings of clinical stage I were made possible by careful operative staging. Patients with stage 1 tumors involving only the endometrium and no evidence of intraperitoneal disease (i.e., adnexal extension) are at low risk (">Endometrial Cancer 4