question: Why do antibiotics make some cancer patients feel better?
comment: Did they know he had cancer? There are some antibiotics that can treat cancer (known as antitumor antibiotics). The anthracyclines (doxorubicin, daunorubicin) are a popular class of antitumor antibiotics. They aren't used to treat infections though, just cancers.
passages: Several trials have examined modified and unmodified tetracyclines for the treatment of human cancers; of those, very promising results were achieved with CMT-3 for patients with Kaposi Sarcoma.
  
  Section::::Structure-activity relationship.
   BULLET::::- 1972 – minocycline
  
  BULLET::::- 1972 – pristinamycin
  
  BULLET::::- 1973 – fosfomycin
  
  BULLET::::- 1974 – talampicillin
  
  BULLET::::- 1975 – tobramycin
  
  BULLET::::- 1975 – bacampicillin
  
  BULLET::::- 1975 – ticarcillin
  
  BULLET::::- 1976 – amikacin
  
  BULLET::::- 1977 – azlocillin
  
  BULLET::::- 1977 – cefadroxil
  
  BULLET::::- 1977 – cefamandole
  
  BULLET::::- 1977 – cefoxitin
  
  BULLET::::- 1977 – cefuroxime
  
  BULLET::::- 1977 – mezlocillin
  
  BULLET::::- 1977 – pivmecillinam
  
  Section::::From 1978.
  
  BULLET::::- 1979 – cefaclor
  
  BULLET::::- 1980 – cefmetazole
  
  BULLET::::- 1980 – cefotaxime
  
  BULLET::::- 1980 – piperacillin
  
  BULLET::::- 1981 – co-amoxiclav (amoxicillin/clavulanic acid)
  
  BULLET::::- 1981 – cefoperazone
  
  BULLET::::- 1981 – cefotiam
  
  BULLET::::- 1981 – cefsulodin
  
  BULLET::::- 1981 – latamoxef
   Patients were monitored by an electromyogram with readings collected on day 1 at 0 hours (pre-dose), every two hours for eight hours, then every four hours for sixteen hours. This was repeated on day 8 at 0 hours (pre-dose), every two hours for eight hours, and then every four hours for sixteen ours, at 36 hours after dose, and the final reading at 48 hours.  
  
  The results concluded that there were no changes in cardiac repolarisation (differences in QT wave value).
  
  Section::::Medical Applications.:Lung Cancer Non-Small Cell Cancer.
   Chemotherapeutic drugs have a hard time penetrating tumors to kill them at their core because these cells may lack a good blood supply. Researchers have been using anaerobic bacteria, such as "Clostridium novyi", to consume the interior of oxygen-poor tumours. These should then die when they come in contact with the tumor's oxygenated sides, meaning they would be harmless to the rest of the body. A major problem has been that bacteria do not consume all parts of the malignant tissue. However, combining the therapy with chemotheraputic treatments can help to solve this problem.
   BULLET::::- 1987 – rifaximin, the first ansamycin
  
  BULLET::::- 1988 – azithromycin
  
  BULLET::::- 1988 – flomoxef
  
  BULLET::::- 1988 – isepamycin
  
  BULLET::::- 1988 – midecamycin
  
  BULLET::::- 1988 – rifapentine
  
  BULLET::::- 1988 – teicoplanin
  
  BULLET::::- 1989 – cefpodoxime
  
  BULLET::::- 1989 – enrofloxacin
  
  BULLET::::- 1989 – lomefloxacin
  
  BULLET::::- 1989 – moxifloxacin
  
  BULLET::::- 1990 – arbekacin
  
  BULLET::::- 1990 – cefodizime
  
  BULLET::::- 1990 – clarithromycin
  
  BULLET::::- 1991 – cefdinir
  
  BULLET::::- 1992 – cefetamet
  
  BULLET::::- 1992 – cefpirome
  
  BULLET::::- 1992 – cefprozil
  
  BULLET::::- 1992 – ceftibuten
  
  BULLET::::- 1992 – fleroxacin
  
  BULLET::::- 1992 – loracarbef
  
  BULLET::::- 1992 – piperacillin/tazobactam
  
  BULLET::::- 1992 – rufloxacin
  
  BULLET::::- 1993 – brodimoprim
   One of the most recent methods that is being developed for the delivery of anti-angiogenesis factors to tumour regions in cancer sufferers is using genetically modified bacteria that are able to colonize solid tumors in vivo. This method involves genetically engineering bacterial species such as "Clostridium", "Bifidobacteria" and "Salmonella" by adding the genes for anti-angiogenic factors such as endostatin or IP10 chemokine and removing any harmful virulence genes. A target can also be added to the outside of the bacteria so that they are sent to the correct organ in the body. The bacteria can then be injected into the patient and they will locate themselves to the tumor site, where they release a continual supply of the desired drugs in the vicinity of a growing cancer mass, preventing it from being able to gain access to oxygen and ultimately starving the cancer cells. This method has been shown to work both in vitro and in vivo in mice models, with very promising results. It is expected that this method will become commonplace for treatment of various cancer types in humans in the future.
   BULLET::::- 1981 – netilmicin
  
  BULLET::::- 1982 – ceftriaxone
  
  BULLET::::- 1982 – micronomicin
  
  BULLET::::- 1983 – cefmenoxime
  
  BULLET::::- 1983 – ceftazidime
  
  BULLET::::- 1983 – ceftizoxime
  
  BULLET::::- 1983 – norfloxacin
  
  BULLET::::- 1984 – cefonicid
  
  BULLET::::- 1984 – cefotetan
  
  BULLET::::- 1984 – temocillin
  
  BULLET::::- 1985 – cefpiramide
  
  BULLET::::- 1985 – imipenem/cilastatin, the first carbapenem
  
  BULLET::::- 1985 – ofloxacin
  
  BULLET::::- 1986 – mupirocin
  
  BULLET::::- 1986 – aztreonam
  
  BULLET::::- 1986 – cefoperazone/sulbactam
  
  BULLET::::- 1986 – co-ticarclav (ticarcillin/clavulanic acid)
  
  BULLET::::- 1987 – ampicillin/sulbactam
  
  BULLET::::- 1987 – cefixime
  
  BULLET::::- 1987 – roxithromycin
  
  BULLET::::- 1987 – sultamicillin
  
  BULLET::::- 1987 – ciprofloxacin, the first 2nd-gen fluoroquinolone
   There are an estimated 10-100 trillion multiple organisms that colonize the human body. As a side-effect of therapy, antibiotics can change the body's normal microbial content by attacking indiscriminately both the pathological and naturally occurring, beneficial or harmless bacteria found in the intestines, lungs and bladder. The destruction of the body's normal bacterial flora is thought to disrupt immunity, nutrition, and lead to a relative overgrowth in some bacteria or fungi. An overgrowth of drug-resistant microorganisms can lead to a secondary infection such as "Clostridium difficile" ("C. diff") or candidiasis ("thrush"). This side-effect is more likely with the use of broad-spectrum antibiotics, given their greater potential to disrupt a larger variety of normal human flora.
   Section::::Treatment strategies.:Types.:Cytotoxic antibiotics.
  
  The cytotoxic antibiotics are a varied group of drugs that have various mechanisms of action. The common theme that they share in their chemotherapy indication is that they interrupt cell division. The most important subgroup is the anthracyclines and the bleomycins; other prominent examples include mitomycin C, mitoxantrone, and actinomycin.
   Since bacteria prefer an anoxic environment, they are not efficient at eliminating cells on the periphery of the tumor, where oxygen supply is efficient. A combination of bacterial treatment with chemical drugs will increase chances of destroying the tumor.
  
  Section::::Harnessing evolution in therapeutics.:Oncolytic viruses.
  
  Oncolytic viruses are engineered to infect cancerous cells. Limitations of that method include immune response to the virus and the possibility of the virus evolving into a pathogen.
  
  Section::::Harnessing evolution in therapeutics.:Natural selection.
   BULLET::::- 1993 – dirithromycin
  
  BULLET::::- 1993 – levofloxacin
  
  BULLET::::- 1993 – nadifloxacin
  
  BULLET::::- 1993 – panipenem/betamipron
  
  BULLET::::- 1993 – sparfloxacin
  
  BULLET::::- 1994 – cefepime
  
  BULLET::::- 1996 – meropenem
  
  BULLET::::- 1999 – quinupristin/dalfopristin
  
  BULLET::::- 2000 – linezolid, the first oxazolidinone
  
  BULLET::::- 2001 – telithromycin, the first ketolide
  
  BULLET::::- 2003 – daptomycin
  
  BULLET::::- 2005 – tigecycline, the first glycylcycline
  
  BULLET::::- 2005 – doripenem
  
  BULLET::::- 2009 – telavancin, the first Lipoglycopeptide
  
  BULLET::::- 2010 – ceftaroline
  
  BULLET::::- 2011 – fidaxomicin
  
  BULLET::::- 2012 – bedaquiline
  
  BULLET::::- 2013 – telavancin
  
  BULLET::::- 2014 – tedizolid
  
  BULLET::::- 2014 – dalbavancin
  
  BULLET::::- 2014 – ceftolozane/tazobactam
  
  BULLET::::- 2015 – ceftazidime/avibactam
   BULLET::::- 1961 – ampicillin
  
  BULLET::::- 1961 – spectinomycin
  
  BULLET::::- 1961 – sulfamethoxazole
  
  BULLET::::- 1961 – trimethoprim, the first dihydrofolate reductase inhibitor
  
  BULLET::::- 1962 – cloxacillin
  
  BULLET::::- 1962 – fusidic acid
  
  BULLET::::- 1963 – fusafungine
  
  BULLET::::- 1963 – lymecycline
  
  BULLET::::- 1964 – gentamicin
  
  BULLET::::- 1964 – cefalotin, the first cephalosporin
  
  BULLET::::- 1966 – doxycycline
  
  BULLET::::- 1967 – carbenicillin
  
  BULLET::::- 1967 – rifampicin
  
  BULLET::::- 1967 – nalidixic acid, the first quinolone
  
  BULLET::::- 1968 – clindamycin, the second lincosamide
  
  BULLET::::- 1970 – cefalexin
  
  BULLET::::- 1971 – cefazolin
  
  BULLET::::- 1971 – pivampicillin
  
  BULLET::::- 1971 – tinidazole
  
  BULLET::::- 1972 – amoxicillin
  
  BULLET::::- 1972 – cefradine
   The amplification of the cell surface receptor MET often drives resistance to anti-EGFR therapies in colorectal cancer.
  
  Section::::Clinical significance.:Role in autism.
   In adult patients with Acute Respiratory infections, a 2017 systematic review found that PCT-guided therapy reduced mortality, reduced antibiotic use(2.4 less days of antibiotics) and led to decreased adverse drug effects across a variety of clinical settings(ED, ICU, primary care clinic).
  
  Procalcitonin-guided treatment limits antibiotic exposure with no increased mortality in patients with acute exacerbation of chronic obstructive pulmonary disease.
   Cancer drugs and therapies commonly used today are evolutionary inert and represent a strong selection force, which leads to drug resistance. A possible way to avoid that is to use a treatment agent that would co-evolve alongside cancer cells.
  
  Section::::Harnessing evolution in therapeutics.:Anoxic bacteria.
   Drug interactions with anthracyclines can be complex and might be due to the effect, side effects, or metabolism of the anthracycline. Drugs which inhibit Cytochrome P450 or other oxidases may reduce clearance of anthracyclines, prolonging their circulating half-life which can increase cardiotoxicity and other side effects. As they act as antibiotics anthracyclines can reduce the effectiveness of live culture treatments such as Bacillus Calmette-Guerin therapy for bladder cancer. As they act as myelosuppressors anthracyclines can reduce the effectiveness of vaccines by inhibiting the immune system.
   When anticancer drugs such as doxorubicin accumulate in microvesicles, the drug's cellular levels decrease. This can ultimately contribute to the process of drug resistance. Similar processes have been demonstrated in microvesicles released from cisplatin-insensitive cancer cells. Vesicles from these tumors contained nearly three times more cisplatin than those released from cisplatin-sensitive cells. For example, tumor cells can accumulate drugs into microvesicles. Subsequently, the drug-containing microvesicles are released from the cell into the extracellular environment, thereby mediating resistance to chemotherapeutic agents and resulting in significantly increased tumor growth, survival, and metastasis.
  
  Section::::Relevance in disease.:Cancer.:Interference with antitumor immunity.
   4.At the end of the treatment bacterium should be easily eliminated from the host
  
  5.It should not be causing severe immune response
  
  6.It should be able to cause tumor cells death through competition for nutrients. 
  
  In the process of the treatment, cancer cells are most likely to evolve some form of resistance to the bacterial treatment. However, being a living organism, bacteria would coevolve with tumor cells, potentially eliminating the possibility of resistance.
  
  Section::::Harnessing evolution in therapeutics.:Anoxic bacteria.:Possible limitations.
   "Streptomyces" research is expected to provide new antibiotics, including treatment against MRSA and infections resistant to commonly used medication. Efforts of John Innes Centre and universities in the UK, supported by BBSRC, resulted in the creation of spin-out companies, for example Novacta Biosystems, which has designed the type-b lantibiotic-based compound NVB302 (in phase 1) to treat "Clostridium difficile" infections.
   Aerosolization of antibiotics is necessary because infections of the lung are especially troublesome, which is why direct targeting of the infection is needed. Broad spectrum antibiotics can have detrimental side effects when their action is also taken against necessary non-pathogenic bacteria residing in the human microbiome. Aerosolization is effective in bypassing the microbiome that exists in the gastrointestinal tract by directing the antibiotic directly to the lungs. This process is undertaken after the production of the antibiotic itself.
   The European Society of Cardiology recently released a PCT-guided algorithm for administering antibiotics in patients with dyspnea and suspected acute heart failure. The guidelines use a cut off point of .2 ng/mL and above as the point at which to give antibiotics. This coincides with a 2017 review of literature which concluded that PCT can help reduce antibiotic overuse in patients presenting with acute heart failure. In regards to mortality, a meta analysis of over 5000 patients with heart failure concluded that elevated PCT was reliable in predicting short term mortality.
  
  Section::::Medical uses.:Meningitis.
   In the 1980s the antibiotic class of cephalosporins was introduced, further increasing bacterial resistance. During this decade infection control programs began to be established in hospitals, which systematically recorded and investigated hospital-acquired infections. Evidence-based treatment guidelines and regulation of antibiotic use surfaced. Australian researchers published the first medical guideline outcomes research.
   Additionally, calicheamicin is able to cleave DNA at low concentrations, proving to be up to 1000 times more effective than adriamycin at combating certain types of tumors. In all cases, cells lack the ability to repair double-stranded DNA breaks, making these compounds especially effective for treating tumor cells.
   Antibiotics may be given as a preventive measure and this is usually limited to at-risk populations such as those with a weakened immune system (particularly in HIV cases to prevent pneumonia), those taking immunosuppressive drugs, cancer patients, and those having surgery. Their use in surgical procedures is to help prevent infection of incisions. They have an important role in dental antibiotic prophylaxis where their use may prevent bacteremia and consequent infective endocarditis. Antibiotics are also used to prevent infection in cases of neutropenia particularly cancer-related.
  
  Section::::Medical uses.:Administration.
   Antibiotics have no effect on viral infections such as the common cold. They are also ineffective against sore throats, which are usually viral and self-resolving. Most cases of bronchitis (90–95%) are viral as well, passing after a few weeks—the use of antibiotics against bronchitis is superfluous and can put the patient at risk of suffering adverse reactions. If you take an antibiotic when you have a viral infection, the antibiotic attacks bacteria in your body, bacteria that are either beneficial or at least not causing disease. This misdirected treatment can then promote antibiotic-resistant properties in harmless bacteria that can be shared with other bacteria, or create an opportunity for potentially harmful bacteria to replace the harmless ones.
  
raw_presuppositions: Antibiotics aren't meant for treating cancer.
raw_corrections: Certain antibiotics can be used to treat cancer.