Off-target effects of chemotherapy need further elucidation in order to allow a rationale-based, rather than empirical, selection of combinatorial regimens. Adjuvant chemotherapy regimens using cytotoxic drugs with immunomodulatory properties, possibly in combination with immunotherapy approaches, should be evaluated as strategies for tertiary prevention of cancer. Conventional anticancer chemotherapy is generally thought to act through selective killing of tumor cells or by irreversibly arresting their growth.
However, this concept neglects the possible contribution of the host to the therapeutic process of chemotherapy. Accumulating evidence indicates that several chemotherapeutic drugs are more efficient against tumors that are implanted in immunocompetent, with respect to immunodeficient, hosts.
Conventional chemotherapy can stimulate the immune system in two ways. Some agents elicit cellular rearrangements that render dying tumor cells visible to the immune system. Other drugs induce a transient lymphodepletion, subvert immunosuppressive mechanisms, or exert direct or indirect stimulatory effects on immune effectors. All these observations open to the intriguing possibility that immunomodulatory chemotherapeutic agents may be good candidates for combination with immune-based therapeutic approaches.
This review will provide an overview on the immune-based mechanisms exploited by some cytotoxic drugs Figure 1 , with the final aim of identifying prerequisites for optimal combination with immunotherapy strategies for the development of more effective, rationale-driven treatments against cancer. Immunomodulation by conventional cytotoxic drugs. Conventional antineoplastic drugs can activate anticancer immune responses through different mechanisms: i the inhibition of tumor-induced-suppressive mechanisms, ii the direct stimulation of T and B cell responses, iii the enhancement of tumor immunovisibility by cytotoxic cell subsets or phagocytes.
Low-dose CTX and gemcitabine deplete regulatory T-cells or myeloid suppressor cells and facilitate tumor attack by effectors. Paclitaxel, cisplatin and doxorubicin induce the upregulation of mannosephosphate receptors on the surface of tumor cells, rendering them permeable to granzyme B. Targeted therapies act by blocking biochemical pathways or mutant proteins essentially required for tumor cell growth and survival.
Most targeted therapies induce dramatic tumor regressions, although long-term clinical benefit is hampered by the occurrence of drug-resistant variants. Similar to conventional chemotherapeutic agents, some targeted agents display immunomodulatory properties. Several direct effects of cytotoxic drugs have been described for macrophages, dendritic cells DCs and natural killer NK cells. Earlier studies on NK-cell function in cancer patients undergoing cytotoxic chemotherapy have shown variable effects, especially in correlation with the clinical outcome.
Effects of chemotherapy on macrophages have also been documented. Macrophages can differentiate from blood monocytes into two distinct subtypes, namely classically activated M1 and alternatively activated M2 macrophages endowed with effector or suppressive functions, respectively. For example, low-dose CTX can promote the skewing of M2 macrophages into M1 in vivo, thus enhancing the production of oxygen radicals, IL-6 and IL, and potentiating innate responses.
F10 melanoma, combined treatment with vincristine, CTX and doxorubicin resulted in substantial enrichment of a TAM subpopulation that can be M1-polarized upon concomitant immunotherapy. Conversely, paclitaxel-induced influx of TAMs was detrimental to chemotherapy response in mouse mammary carcinoma and breast cancer patients.
Chemotherapy has influence on bone marrow BM hematopoiesis, affecting myeloid cell mobilization differentially. A single injection of low-dose CTX was shown to spare DC precursors in the BM, promoting their expansion and differentiation in the peripheral lymphoid organs. The platinum-based compound cisplatin was also reported to modulate the percentages of myeloid cells by increasing DCs and eliminating myeloid-derived suppressor cells MDSCs , thus favoring immune effector responses in melanoma-bearing mice.
Induction of immunogenic tumor cell death and stimulation of DC cross-presentation by CTX in vitro and in vivo. Modified from Schiavoni et al Direct immunostimulatory effects of cytotoxic drugs on DC activities were also reported. An unbiased functional screen of 54 chemotherapeutic agents unveiled striking diversity of the tested drugs on the maturation, survival and growth of DCs. Cytotoxic chemotherapy can affect DC activities also through indirect mechanisms.
Pioneering studies showed that 5-FU and doxorubicin induced in vitro cancer expression of heat shock proteins HSPs that promote the engulfment of cell debris by human DCs and the subsequent cross-presentation of tumor antigens to T-cells. Subsequent work from L. Treatment of cancer patients with intensive chemotherapy results in profound depletion of all lymphocytic populations, especially of B cells.
The effects of CTX on humoral responses appear controversial. In some reports, CTX, even at low-dose regimens, exerted suppressive effects on humoral responses while boosting cellular responses, suggesting that B cells are particularly sensitive to CTX-induced cytotoxic effects.
Numerous evidence indicate the benefits of chemotherapy on T-cell-mediated immune responses. Mice vaccinated with doxorubicin- or cisplatin-treated ovarian cancer cells have enhanced antitumor immunity, and prolonged survival largely dependent on CD4 T-cell-mediated immune responses. A single CTX injection potently enhances the antitumor response of tumor-bearing mice following adoptive transfer of tumor-reactive T-cells.
Evidence for the positive impact of chemotherapy on antitumor immune responses also arises from pilot clinical trials with cancer vaccines. Gene expression analysis of peripheral blood mononuclear cells PBMCs from melanoma patients treated with dacarbazine and a peptide-based vaccine revealed, by 1 day after chemotherapy, increased expression of immunoregulatory factors that can account for the enhancement of tumor antigen-specific CD8 T-cell responses observed in those patients, compared with patients treated with vaccine alone.
Th17 cells are a T-cell subset having important roles in inflammatory and autoimmune diseases. Besides the active stimulation of effector cells, immunopotentiation by cytotoxic chemotherapy can also be achieved through the inhibition of tumor-induced immune suppression. Several subsets of immunoregulatory cells have been identified so far in cancer patients. Different strategies to achieve therapeutic depletion of suppressive cell subsets have been described so far.
Early reports have supported the concept that CTX induces the development of natural suppressor cells. Suppressor cells adopt various means to inhibit the antitumor activity of effector lymphocytes. Some studies suggest that several enzymes, such as arginase I, indoleamine 2, 3-dioxygenase IDO and iNOS, as well as surface molecules, such as latency-associated peptide and CD, are related to immune suppression and tumor progression.
A serial analysis of blood samples from advanced non-small cell lung cancer patients treated with platinum-based compounds revealed decreased iNOS, IDO and CD expression after chemotherapy. TCD is the main goal of chemotherapy. Cytotoxic drugs kill tumor cells in different ways and modulate the host immune system accordingly, with consequences that are only now beginning to be elucidated.
In addition, there is now evidence that the nature of the immune infiltrate, which often outnumbers neoplastic cells, is relevant for cancer prognosis. Under defined circumstances, chemotherapy-induced TCD can set the stage for an effective antitumor immune response. Some chemotherapeutics, including anthracyclines, oxaliplatin and CTX, are unique in their capacity to induce an immunogenic type of TCD, 21 , 97 thereby converting dying tumor cells into adjuvanted-endogenous vaccines.
The rational base of vaccination is that tumor antigens must be captured by activated DCs, which would activate CD4 and CD8 T-cell-mediated adaptive immune responses. In an immunogenic type of TCD, antigen is provided by the dying tumor cells in the context of an immunostimulatory environment for DCs. The molecular mechanisms that distinguish immunogenic from non-immunogenic cell death have been elucidated and rely on at least three independent events: i early surface exposure of calreticulin ecto-CRT on stressed cells, ii subsequent secretion of ATP and iii release of high-mobility group box-1 HMGB1 and HSPs by dying tumor cells.
Recently, ATP was shown to also mediate the recruitment and differentiation of myeloid DC to the tumor site following anthracycline treatment in mice. Seldom, non-apoptotic death pathways are also induced by chemotherapy with mechanisms that are now beginning to be explained.
Some alkylating agents nitrogen mustard and N-methyl-N-nitro-N-nitrosoguanidine induce necrosis, an unregulated process rising from acute cellular stress or massive cell injury.
A number of antineoplastic therapies were shown to induce autophagy in human cancer cells. Myelosuppression, which develops after cytotoxic chemotherapy, represents the major toxic side effect of cancer treatment, thus limiting its use. As the BM contains the most mitotically active cells in the organism, it becomes a preferential target for chemotherapy-induced cytotoxicity.
However, it is now becoming clearer that not all side effects of cytotoxic chemotherapy are necessarily harmful. Genome-wide expression analysis of different tissue samples from CTX-treated tumor-bearing animals revealed the occurrence of an immunogenic apoptosis not only in tumor cells but also in BM and spleen cells, which paralleled with activation of bystander inflammatory responses. Moreover, the drug type and dosage crucially dictate the outcome of drug-induced cytotoxicity.
For example, it has been reported that CTX and 5-FU are less damaging for most primitive cells than other cytotoxic drugs. Other non-immune targets of cytotoxic chemotherapy are the endothelial cells. Indeed, the collateral damage inflicted upon dividing endothelial cells within the tumor bed indirectly helps tumor destruction.
The observations reported above have several implications for planning future clinical trials combining chemotherapy with immunotherapy. First, cytotoxic agents that elicit immunogenic TCD, which converts the tumor itself into an endogenous vaccine and provides adequate DC stimulation, through release of danger signals, are ideal candidates for combination with adoptive immunotherapy strategies aimed at eliminating immune suppressor cells. For example, combining standard chemotherapy with ipilimumab, a human anti-CTLA-4 monoclonal antibody that blocks the CTLA-4 inhibitory signal on T-cells, proved extremely effective in a phase-III clinical trial on advanced melanoma patients, , as well as in a phase-II clinical trial on lung cancer patients.
As type I IFN enhances the cross-presentation of tumor-derived antigens by DCs and synergizes with CTX when injected intratumorally, 21 these cytokines are attractive candidates to be combined with chemotherapy.
Third, the selective depletion of inhibitory subsets by some anticancer drugs for example, CTX or gemcitabine or regimens for example, metronomic provides the optimal setting for combination, with active vaccination strategies aimed at expanding the already existing tumor-reactive immune responses.
Data obtained in both animal models and humans suggest that immunotherapy should immediately follow chemotherapy 1—2 days interval to achieve the best synergism between the two treatments.
It is now becoming evident that standard chemotherapy agents can deeply have an impact on both tumor and host immune system. Although to our knowledge no systematic analysis has been carried out to evaluate differences in the immune-based effects of conventional chemotherapeutic agents depending on cancer histology or stage, it is now clear that the existence of tumor—host interplay dictates the magnitude, quality and efficacy of most anticancer strategies.
Advances in tumor immunology have now undisclosed some key mechanisms that represent the basis of therapeutic synergy or of antagonism with other treatments. The ensemble of results discussed herein contributes to pave the way towards mechanism-based, rather than empirical, rationales for combination of specific chemotherapeutic agents with selective immunotherapeutic interventions, opening novel horizons for more effective management of cancer patients.
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For example, you might get a dose of chemotherapy on the first day and then have 3 weeks of recovery time before repeating the treatment.
Each 3-week period is called a treatment cycle. Several cycles make up a course of chemotherapy. A course usually lasts 3 months or more. Some cancers are treated with less recovery time between cycles. This is called a dose-dense schedule. It can make chemotherapy more effective against some cancers.
But it also increases the risk of side effects. Talk with your health care team about the best schedule for you. Intravenous IV chemotherapy. Many drugs require injection directly into a vein. This is called intravenous or IV chemotherapy. Treatment takes a few minutes to a few hours. Some IV drugs work better if you get them over a few days or weeks.
You take them through a small pump you wear or carry. This is called continuous infusion chemotherapy. Oral chemotherapy. You can take some drugs by mouth. They can be in a pill, capsule, or liquid. This means that you may be able to pick up your medication at the pharmacy and take it at home. Oral treatments for cancer are now more common. Some of these drugs are given daily, and others are given less often. For example, a drug may be given daily for 4 weeks followed by a 2-week break.
Injected chemotherapy. This is when you receive chemotherapy as a shot. The shot may be given in a muscle or injected under the skin. You may receive these shots in the arm, leg, or abdomen. Abdomen is the medical word for your belly. Chemotherapy into an artery.
An artery is a blood vessel that carries blood from your heart to another part of your body. Sometimes chemotherapy is injected into an artery that goes directly to the cancer. This is called intra-arterial or IA chemotherapy. Chemotherapy into the peritoneum or abdomen. For some cancers, medication might be placed directly in your abdomen. This type of treatment works for cancers involving the peritoneum.
The peritoneum covers the surface of the inside of the abdomen and surrounds the intestines, liver, and stomach. Once a candidate target has been identified, the next step is to develop a therapy that affects the target in a way that interferes with its ability to promote cancer cell growth or survival.
For example, a targeted therapy could reduce the activity of the target or prevent it from binding to a receptor that it normally activates, among other possible mechanisms. Most targeted therapies are either small molecules or monoclonal antibodies. Small-molecule compounds are typically developed for targets that are located inside the cell because such agents are able to enter cells relatively easily.
Monoclonal antibodies are relatively large and generally cannot enter cells, so they are used only for targets that are outside cells or on the cell surface. Candidate small molecules are usually identified in what are known as "high-throughput screens," in which the effects of thousands of test compounds on a specific target protein are examined. Compounds that affect the target sometimes called " lead compounds " are then chemically modified to produce numerous closely related versions of the lead compound.
These related compounds are then tested to determine which are most effective and have the fewest effects on nontarget molecules. Monoclonal antibodies are developed by injecting animals usually mice with purified target proteins, causing the animals to make many different types of antibodies against the target. These antibodies are then tested to find the ones that bind best to the target without binding to nontarget proteins.
Before monoclonal antibodies are used in humans, they are " humanized " by replacing as much of the mouse antibody molecule as possible with corresponding portions of human antibodies. Humanizing is necessary to prevent the human immune system from recognizing the monoclonal antibody as " foreign " and destroying it before it has a chance to bind to its target protein. Humanization is not an issue for small-molecule compounds because they are not typically recognized by the body as foreign.
Many different targeted therapies have been approved for use in cancer treatment. These therapies include hormone therapies , signal transduction inhibitors , gene expression modulators, apoptosis inducers, angiogenesis inhibitors , immunotherapies , and toxin delivery molecules.
Cancer vaccines and gene therapy are sometimes considered targeted therapies because they interfere with the growth of specific cancer cells. For some types of cancer, most patients with that cancer will have an appropriate target for a particular targeted therapy and, thus, will be candidates to be treated with that therapy. The use of a targeted therapy may be restricted to patients whose tumor has a specific gene mutation that codes for the target; patients who do not have the mutation would not be candidates because the therapy would have nothing to target.
Sometimes, a patient is a candidate for a targeted therapy only if he or she meets specific criteria for example, their cancer did not respond to other therapies, has spread, or is inoperable. These criteria are set by the FDA when it approves a specific targeted therapy. Targeted therapies do have some limitations. One is that cancer cells can become resistant to them. For this reason, targeted therapies may work best in combination. For example, a recent study found that using two therapies that target different parts of the cell signaling pathway that is altered in melanoma by the BRAF VE mutation slowed the development of resistance and disease progression to a greater extent than using just one targeted therapy 1.
Another approach is to use a targeted therapy in combination with one or more traditional chemotherapy drugs.
One example is Ras, a signaling protein that is mutated in as many as one-quarter of all cancers and in the majority of certain cancer types, such as pancreatic cancer. To date, it has not been possible to develop inhibitors of Ras signaling with existing drug development technologies. However, promising new approaches are offering hope that this limitation can soon be overcome.
Scientists had expected that targeted cancer therapies would be less toxic than traditional chemotherapy drugs because cancer cells are more dependent on the targets than are normal cells. However, targeted cancer therapies can have substantial side effects. The most common side effects seen with targeted therapies are diarrhea and liver problems, such as hepatitis and elevated liver enzymes.
Other side effects seen with targeted therapies include:. Certain side effects of some targeted therapies have been linked to better patient outcomes. For example, patients who develop acneiform rash skin eruptions that resemble acne while being treated with the signal transduction inhibitors erlotinib Tarceva or gefitinib Iressa , both of which target the epidermal growth factor receptor , have tended to respond better to these drugs than patients who do not develop the rash 2.
Similarly, patients who develop high blood pressure while being treated with the angiogenesis inhibitor bevacizumab generally have had better outcomes 3. The few targeted therapies that are approved for use in children can have different side effects in children than in adults, including immunosuppression and impaired sperm production 4. The FDA has approved targeted therapies for the treatment of some patients with the following types of cancer some targeted therapies have been approved to treat more than one type of cancer :.
Bladder cancer: Atezolizumab Tecentriq , nivolumab Opdivo , avelumab Bavencio , pembrolizumab Keytruda , erdafitinib Balversa , enfortumab vedotin-ejfv Padcev , sacituzumab govitecan-hziy Trodelvy.
Brain cancer: Bevacizumab Avastin , everolimus Afinitor , belzutifan Welireg. Breast cancer: Everolimus Afinitor , tamoxifen Nolvadex , toremifene Fareston , trastuzumab Herceptin , fulvestrant Faslodex , anastrozole Arimidex , exemestane Aromasin , lapatinib Tykerb , letrozole Femara , pertuzumab Perjeta , ado-trastuzumab emtansine Kadcyla , palbociclib Ibrance , ribociclib Kisqali , neratinib maleate Nerlynx , abemaciclib Verzenio , olaparib Lynparza , talazoparib tosylate Talzenna , alpelisib Piqray , fam-trastuzumab deruxtecan-nxki Enhertu , tucatinib Tukysa , sacituzumab govitecan-hziy Trodelvy , pertuzumab, trastuzumab, and hyaluronidase-zzxf Phesgo , pembrolizumab Keytruda , margetuximab-cmkb Margenza.
Cervical cancer: Bevacizumab Avastin , pembrolizumab Keytruda. Colorectal cancer: Cetuximab Erbitux , panitumumab Vectibix , bevacizumab Avastin , ziv-aflibercept Zaltrap , regorafenib Stivarga , ramucirumab Cyramza , nivolumab Opdivo , ipilimumab Yervoy , encorafenib Braftovi , pembrolizumab Keytruda.
Dermatofibrosarcoma protuberans: Imatinib mesylate Gleevec. Endometrial cancer: Pembrolizumab Keytruda , lenvatinib mesylate Lenvima , dostarlimab-gxly Jemperli. Esophageal cancer : Trastuzumab Herceptin , ramucirumab Cyramza , pembrolizumab Keytruda , nivolumab Opdivo , fam-trastuzumab deruxtecan-nxki Enhertu. Head and neck cancer: Cetuximab Erbitux , pembrolizumab Keytruda , nivolumab Opdivo. Gastrointestinal stromal tumor: Imatinib mesylate Gleevec , sunitinib Sutent , regorafenib Stivarga , avapritinib Ayvakit , ripretinib Qinlock.
Giant cell tumor: Denosumab Xgeva , pexidartinib hydrochloride Turalio. Kidney cancer: Bevacizumab Avastin , sorafenib Nexavar , sunitinib Sutent , pazopanib Votrient , temsirolimus Torisel , everolimus Afinitor , axitinib Inlyta , nivolumab Opdivo , cabozantinib Cabometyx , lenvatinib mesylate Lenvima , ipilimumab Yervoy , pembrolizumab Keytruda , avelumab Bavencio , tivozanib hydrochloride Fotivda , belzutifan Welireg.
Leukemia: Tretinoin Vesanoid , imatinib mesylate Gleevec , dasatinib Sprycel , nilotinib Tasigna , bosutinib Bosulif , rituximab Rituxan , alemtuzumab Campath , ofatumumab Arzerra , obinutuzumab Gazyva , ibrutinib Imbruvica , idelalisib Zydelig , blinatumomab Blincyto , venetoclax Venclexta , ponatinib hydrochloride Iclusig , midostaurin Rydapt , enasidenib mesylate Idhifa , inotuzumab ozogamicin Besponsa , tisagenlecleucel Kymriah , gemtuzumab ozogamicin Mylotarg , rituximab and hyaluronidase human Rituxan Hycela , ivosidenib Tibsovo , duvelisib Copiktra , moxetumomab pasudotox-tdfk Lumoxiti , glasdegib maleate Daurismo , gilteritinib Xospata , tagraxofusp-erzs Elzonris , acalabrutinib Calquence , avapritinib Ayvakit , brexucabtagene autoleucel Tecartus.
Liver and bile duct cancer: Sorafenib Nexavar , regorafenib Stivarga , nivolumab Opdivo , lenvatinib mesylate Lenvima , pembrolizumab Keytruda , cabozantinib Cabometyx , ramucirumab Cyramza , ipilimumab Yervoy , pemigatinib Pemazyre , atezolizumab Tecentriq , bevacizumab Avastin , infigratinib phosphate Truseltiq , ivosidenib Tibsovo.
Lymphoma: Ibritumomab tiuxetan Zevalin , denileukin diftitox Ontak , brentuximab vedotin Adcetris , rituximab Rituxan , vorinostat Zolinza , romidepsin Istodax , bexarotene Targretin , bortezomib Velcade , pralatrexate Folotyn , ibrutinib Imbruvica , siltuximab Sylvant , idelalisib Zydelig , belinostat Beleodaq , obinutuzumab Gazyva , nivolumab Opdivo , pembrolizumab Keytruda , rituximab and hyaluronidase human Rituxan Hycela , copanlisib hydrochloride Aliqopa , axicabtagene ciloleucel Yescarta , acalabrutinib Calquence , tisagenlecleucel Kymriah , venetoclax Venclexta , mogamulizumab-kpkc Poteligeo , duvelisib Copiktra , polatuzumab vedotin-piiq Polivy , zanubrutinib Brukinsa , tazemetostat hydrobromide Tazverik , selinexor Xpovio , tafasitamab-cxix Monjuvi , brexucabtagene autoleucel Tecartus , crizotinib Xalkori , umbralisib tosylate Ukoniq , lisocabtagene maraleucel Breyanzi , loncastuximab tesirine-lpyl Zynlonta.
Malignant mesothelioma: Ipilimumab Yervoy , nivolumab Opdivo. Microsatellite instability-high or mismatch repair-deficient solid tumors : Pembrolizumab Keytruda , dostarlimab-gxly Jemperli. Multiple myeloma: Bortezomib Velcade , carfilzomib Kyprolis , panobinostat Farydak , daratumumab Darzalex , ixazomib citrate Ninlaro , elotuzumab Empliciti , selinexor Xpovio , isatuximab-irfc Sarclisa , daratumumab and hyaluronidase-fihj Darzalex Faspro , belantamab mafodotin-blmf Blenrep , idecabtagene vicleucel Abecma.
Neuroblastoma: Dinutuximab Unituxin , naxitamab-gqgk Danyelza. Pancreatic cancer: Erlotinib Tarceva , everolimus Afinitor , sunitinib Sutent , olaparib Lynparza , belzutifan Welireg. Plexiform neurofibroma: Selumetinib sulfate Koselugo. Prostate cancer: Cabazitaxel Jevtana , enzalutamide Xtandi , abiraterone acetate Zytiga , radium dichloride Xofigo , apalutamide Erleada , darolutamide Nubeqa , r ucaparib camsylate Rubraca , olaparib Lynparza. Skin cancer: Vismodegib Erivedge , sonidegib Odomzo , ipilimumab Yervoy , vemurafenib Zelboraf , trametinib Mekinist , dabrafenib Tafinlar , pembrolizumab Keytruda , nivolumab Opdivo , cobimetinib Cotellic , alitretinoin Panretin , avelumab Bavencio , encorafenib Braftovi , binimetinib Mektovi , cemiplimab-rwlc Libtayo , atezolizumab Tecentriq.
Soft tissue sarcoma: Pazopanib Votrient , alitretinoin Panretin , tazemetostat hydrobromide Tazverik. Stomach gastric cancer: Pembrolizumab Keytruda , trastuzumab Herceptin , ramucirumab Cyramza , fam-trastuzumab deruxtecan-nxki Enhertu , nivolumab Opdivo. Systemic mastocytosis: Imatinib mesylate Gleevec , midostaurin Rydapt , avapritinib Ayvakit. Thyroid cancer: Cabozantinib Cometriq , vandetanib Caprelsa , sorafenib Nexavar , lenvatinib mesylate Lenvima , trametinib Mekinist , dabrafenib Tafinlar , selpercatinib Retevmo , pralsetinib Gavreto.
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