Table 3.

List of various treatment modalities for cancer.

No.	Cancer Therapy	Details	Reference
1.	Radiotherapy		[175]
	Radiotherapy individualization based on hypoxia markers	Elevates the oxygen in the blood by breathing in high oxygen levels before and during the irradiation to destroy hypoxic cells using bioreductive compounds or to radiosensitize hypoxic cells using oxygen mimicking drugs.
	Radiotherapy individualization based on FDG-PET	Fludeoxyglucose (18F-FDG) intensity on a positron emission tomography (PET) image represents the level of glucose uptake by active malignant cells.
	Markers of DNA repair	One of the best biomarkers for tumor radioresponse of DNA double-strand breaks is gH2AX, a histone protein, which is found after the induction of double-strand breaks.
	Cancer-stem-cell markers	CD44 is considered as one of the best cancer stem cell markers. A significant correlation of CD44 mRNA expression as well as CD44 immunohistochemical score with local tumor control after radiotherapy was shown in a hypothesis-driven approach.
	Radiotherapy individualization based on EGFR status	The application of anti-EGFR antibody cetuximab showed locoregional tumor control compared to radiotherapy alone.
2.	Gene Therapy		[176]
	Oncolytic Virotherapy	It uses replication-competent viruses, which are able to proliferate selectively at tumor cells. It can directly lyse cancer cells, and it also can introduce wild-type p53 tumor suppressor genes into the cells lacking the tumor suppressor gene.
	Gendicine (Recombinant Human P53 Adenovirus (Ad5RSV-P53))	Gendicine is a non-replicative vector, where the E1 gene is replaced with the p53 cDNA gene. The expression of p53 in tumor cells stimulates the anticancer effect by triggering the apoptotic pathway and inhibiting damaged DNA repair.
	Oncolytic recombinant ad5 (rAd5-H101)	It was proven to treat refractory nasopharyngeal cancer. Oncorine is an ad5 virus with a deletion in the E1B 55K gene. Host cell p53 gene inactivation is essential for wild-type to block the activation of the apoptotic pathway.
	Imlygic (Talimogene Laherparepvec)	It was proven that administration of Imlygic causes the apoptosis of cancer cells, improves antigen presentation and increases antitumor response.
	Rexin-G (Mx-dnG1)	Rexin-G synthesizes cytocidal dnG1 proteins suppress the cell cycle in the G1 phase, leading to the apoptotic pathway of cancer cells.
3.	Thermotherapy		[177]
	Thermal Ablation Options	It causes destruction and the eradication of the tumor by overheating using temperatures from 55 °C to 100 °C as an external excitation. It can cure many types of cancer such as kidney, liver, lung, rectum, and prostate.
	Radio Frequency Ablation (RFA)	It uses a high-frequency heating source from 375 to 500 KHz to kill the targeted cells. It has shown a positive result against different kinds of cancers, including breast, liver, and brain.
	Micro Wave Ablation (MWA)	It uses an electro-magnetic (EM) signal to heat the selected area and stimulate a direct hyperthermic injury. The frequency range begins from 915 MHz to 2.45 GHz.
	High Intensity Focused Ultra Sound (HIFU)	It sends an ultra sound (US) beam focused on overheating a targeted tissue in order to cause coagulation necrosis. It is highly precise in killing tumors and cures some of the related health issues.
	LASER Ablation	A LASER (Light Amplification by Stimulated Emission of Radiation) is a monochromatic directed and focused beam of light. It has been used to kill different tumors, especially brain tumors.
	Cryoablation	Cryotherapy uses a low temperature of −30 to −40 °C to create a freezing zone and generate the destruction of a targeted region. The probe tip is alimented by a source of nitrogen or argon to cool the tissue to −100 °C.
4.	Chemotherapy		[177]
	Dacarbazine, temozolomide Ethyleneimines: thiotepa, mechlorethamine, chlorambucil, cyclophosphamide streptozocin, carmustine, busulfan	Damage DNA at different phases of the cell cycle. GO phase (resting phase), G1 phase, S phase, G2 phase and M phase. Breast cancer, ovarian cancer, lymphoma, Hodgkin’ disease, multiple, myeloma, sarcoma, lung cancer.
	Daunorubin, Doxorubixin Epirubicin, Actinomycin-D Bleomycin, Mitomycin-C	Interfere with enzymes involved in DNA replication in all phases of the cell cycle. Leukaemia, breast, cancer, ovarian cancer, intestinal tracts and other various types of cancers.
	5-fluorouracil (5-FU) 6-mercaptopurine (6-MP) Capecitabine, Cladribine Cloafarabine, Cytarabine Floxuridine, Fludarabine Gemicitabine, Hydroxyurea Methotrexate, Pemetrexed Pentostatin, Thioguanine	Interfere the DNA and RNA formation of cells. Breast cancer, ovarian cancer, intestinal tracts, and other various types of cancers.
	Topotecan, Irinotecan Etoposide, teniposide	Interfere with topoisomerase such as topoisomerase inhibitor I and II and inhibit the splits of DNA strands during replication. Lung cancer, colon, ovarian, and other gastrointestinal cancers.
	Paclitaxel, Docetaxel Ixabepilone, vinblastine Estraustine and Vinblastine	Stop cell mitosis or inhibit enzymes associated with protein synthesis required for DNA replication. Breast cancer, lung cancer, lymphomas, colon, other leukaemias.
	Bortezomib, Carfilzomib, ixazomib	Inhibit the proteasome and the downstream events that lead to selective cell death. Multiple myeloma and mantle cell lymphoma cancers.
	L-asparaginase	Reduces the level of L asparagine from plasma. As a result, RNA and DNA synthesis are inhibited. Acute lymphocytic leukaemia (ALL).
5.	Targeted Therapy		[178]
	Monoclonal antibodies EGFR inhibitors: Erlotinib (Tarceva), Afatinib (Gilotrif), Gefitinib (Iressa), Osimertinib (Tagrisso), Dacomitinib (Vizimpro	EGFR inhibitors work by attaching to the EGFR cell surface receptor to block the action of EGF.
	HER2 inhibitors: Herceptin, Herceptin Hylecta, Margenza, Perjeta	HER2 inhibitors work by attaching to HER2 cell surface receptor to block the action.
	SMALL MOLECULES Tyrosine Kinase Inhibitors: Imatinib, gefitinib, erlotinib, sorafenib, sunitinib, dasatinib	Tyrosine kinase inhibitors work by blocking the action of receptor tyrosine. Kinases enzymes help to send growth signals in cancer cells.
	Mammalian target of rapamycin inhibitors (mTOR): everolimus, temsirolimus, sirolimus	mTOR regulates growth factors that stimulate cell growth. The mTOR inhibitors block the activity of mTOR.
	Poly adenosine diphosphate-ribose polymerase inhibitors (PARP): Olaparib, niraparib, rucaparib, talazoparib.	PARP protein helps to repair damaged DNA in cancer cells. PARP inhibitors act by stopping PARP proteins from repairing DNA in cancer cells.
	Vascular Endothelial Growth Factor Inhibitor (VEGF): Bevacizumab, Sorafenib, Sunitinib, Nilotinib, Pazopanib, Dasatinib	VEGF forms new blood vessels in cancer cells which helps cell growth. VEGF inhibitors attach to VEGF and inhibit them from growing.