Antineoplastic agents are a class of drugs designed to combat cancer by inhibiting the growth and proliferation of neoplastic cells (cancer cells). They are also commonly referred to as Anticancer drugs or Chemotherapy.

The action of antineoplastic agents can be broadly categorized into two main mechanisms: affecting cell survival (cytotoxicity) and enhancing the immune system’s ability to fight abnormal cells (immunotherapy/targeted therapy).

• Before 1940: No effective treatment available for systemic cancers.
• Before 1955: Surgery was the primary and only definitive treatment.
• 1955–1965: Radiotherapy became widely established.
• After 1965: The advent and widespread use of systemic Chemotherapy.
• Modern Era: Introduction of Immunotherapy and Gene Therapy, revolutionizing targeted cancer treatment.

Cell Cycle Phase	Cell Cycle Specific (CCS) Drugs	Cell Cycle Non-Specific (CCNS) Drugs
G1 - S Phase	Etoposide	These agents affect cells across all phases: ➔ Platinum compounds (Cisplatin, Carboplatin) ➔ Alkylating agents (Cyclophosphamide, Busulfan, Nitrosoureas) ➔ Antibiotics (Anthracyclines, Dactinomycin, Mitomycin) ➔ Camptothecins
S Phase	Antimetabolites (Methotrexate, 5-FU, Cytarabine, 6-MP)
G2 - M Phase	Bleomycin, Etoposide
M Phase (Mitosis)	Vinca alkaloids, Taxanes, Ixabepilone, Estramustine

• Cure or induce prolonged "remission": Macroscopic and microscopic features of the cancer disappear entirely. Highly achievable in: Acute Lymphoblastic Leukaemia (ALL), Wilm's tumor, Ewing's sarcoma, Hodgkin's lymphoma (in children), testicular teratoma, and choriocarcinoma.
• Palliation: Aimed at the shrinkage of an evident tumor, alleviation of symptoms, and prolongation of life rather than absolute cure. Targeted for: Breast cancer, ovarian cancer, endometrial carcinoma, CLL, CML, Small cell lung cancer (SCLC), and Non-Hodgkin lymphoma.
• Insensitive Tumors: These are less sensitive to chemotherapy, but life may still be prolonged. Includes: Cancer of the esophagus, cancer of the stomach, squamous cell carcinoma of the lung, melanoma, pancreatic cancer, myeloma, and colorectal cancer.
• Adjuvant Therapy: Used routinely now for "mopping up" residual cancer cells, including micrometastases, after surgery or radiation. Mainly utilized in solid tumors.

• It is analogous to Bacterial chemotherapy but with critical differences:
  • Selectivity of drugs is highly limited (they attack normal host cells as well).
  • No or less defense mechanism (the host immune system does not recognize cancer as readily as bacteria; cytokines are used as adjuvants now to boost this).
• The goal is to kill all malignant cells to stop progeny.
• Tumors contain subpopulations of cells that differ in their rate of proliferation and susceptibility to chemotherapy.
• Total Tumor Cell Kill via COMBINATION CHEMOTHERAPY: Formerly, single drugs were used; now, 2-5 drugs are used in intermittent pulses.

• Utilizes drugs which are effective when used alone.
• Combines drugs with different mechanisms of action.
• Combines drugs with differing toxicities (and different mechanisms of toxicities) to prevent overlapping fatal side effects (e.g., combining bone marrow-sparing Bleomycin with a myelosuppressive agent).
• Utilizes synergistic biochemical interactions.
• Applies an optimal schedule determined by trial and error, relying heavily on cell cycle specificity.

• Intrinsic Resistance: Tumors naturally possess primary resistance without prior exposure. Examples: Malignant melanoma, renal cell cancer, and brain cancer.
• Acquired Resistance: Develops after initial exposure.
  • Single drug resistance: Change in the genetic apparatus, amplification, or increased expression of one or more specific genes targeted by the drug.
  • Multidrug resistance (MDR): Resistance to a wide variety of drugs after exposure to a single variety. Often due to increased expression of a normal gene (the MDR1 gene) which codes for a cell surface glycoprotein (P-glycoprotein) involved in active drug efflux (pumping the drug out of the cell).

Chemotherapy is harmful to normal tissues because it has a steep dose-response curve and a low therapeutic index. It is particularly harmful to rapidly multiplying normal tissues (GI mucosa, Bone Marrow, Reticuloendothelial [RE] system, gonads, and hair cells). Effects occur in a dose-dependent manner.

• Bone Marrow Depression (BMD): Leukopenia, thrombocytopenia, anemia. This is the primary dose-limiting toxicity for most treatments.
• Buccal Mucosa Erosion: High epithelial turnover leads to stomatitis, severe mucositis, and bleeding gums.
• Gastrointestinal (GIT): Diarrhea, shedding of mucosa, hemorrhage. Nausea and vomiting are severe due to direct stimulation of the Chemoreceptor Trigger Zone (CTZ).
• Skin: Alopecia (hair loss).
• Gonads: Oligospermia, impotence, amenorrhoea, and permanent infertility.
• Lymphoreticular System: Lymphocytopenia and inhibition of lymphocyte function, leading to a loss of host defense mechanisms and extreme susceptibility to infections.
• Other systemic: Carcinogenicity (secondary tumors), Teratogenicity, and Hyperuricemia (due to rapid tumor cell lysis releasing purines).

Drug	Distinctive Toxicity
Cyclophosphamide	Alopecia, Hemorrhagic cystitis, SIADH (Syndrome of Inappropriate Antidiuretic Hormone).
Ifosfamide	Hemorrhagic cystitis, SIADH.
Busulfan	Pulmonary fibrosis ("Busulfan lung"), Hyperpigmentation, Adrenal insufficiency, Tonic-clonic seizures.
Procarbazine	Secondary leukemias, Disulfiram-like reaction (with alcohol), behavioral changes, CNS depression.
Cisplatin	Severe Emesis, Nephrotoxicity, Peripheral sensory neuropathy, Ototoxicity (deafness).

Toxicities are countered via intermittent therapy (giving normal cells time to recover) and specific pharmacological rescue agents:

Drug (Rescue/Preventive Agent)	Mechanism of Action	Indications / Used For
Allopurinol	Inhibits xanthine oxidase.	Prevents hyperuricemia from massive tumor lysis syndrome.
Rasburicase	Recombinant urate oxidase (converts uric acid to soluble allantoin).	Prevents hyperuricemia from rapid tumor lysis.
Mesna (Sodium-2-mercaptoethane sulfonate)	Neutralizing agent (binds toxic metabolite acrolein).	Prevents hemorrhagic cystitis due to Ifosfamide and high-dose Cyclophosphamide.
Leucovorin (Folinic Acid)	Repletes Tetrahydrofolic acid directly.	"Leucovorin Rescue" after high-dose Methotrexate to save bone marrow and GIT mucosa.
Amifostine	Scavenges free radicals.	Prevents radiation-induced xerostomia and Cisplatin-induced nephrotoxicity.
Dexrazoxane	Iron chelator.	Prevents cardiotoxicity due to Anthracyclines (Doxorubicin, Daunorubicin).
Palifermin	Keratinocyte growth factor.	Prevents severe mucositis following heavy chemotherapy.
Pilocarpine	Cholinergic agonist.	Treats radiation-induced xerostomia (dry mouth).
Pamidronate / Zoledronate	Bisphosphonates.	Treats hypercalcemia of malignancy and bone metastases.
Epoetin alpha / Darbepoetin	Recombinant Erythropoietin.	Treats chemotherapy-induced anemia.
Filgrastim / Peg-filgrastim	G-CSF (Granulocyte Colony-Stimulating Factor).	Febrile neutropenia prophylaxis; speeds recovery of granulocytopenia.
Sargramostim	GM-CSF (Granulocyte-Macrophage CSF).	Myeloid reconstitution.
Oprelvekin	IL-11 (Interleukin-11).	Treats severe chemotherapy-induced thrombocytopenia.
Ondansetron / Granisetron / Palonosetron	5-HT3 antagonists.	Prevents acute nausea and vomiting.
Aprepitant	NK-1 (Neurokinin-1) receptor antagonist.	Prevents Cisplatin-induced delayed vomiting.

Classification is based on chemical structure, biochemical mechanism of action (blocking nucleic acid synthesis, interfering with DNA structure, blocking RNA/protein synthesis, influencing hormones), and cell cycle phase specificity.

• Mechanism of Action: They act by binding irreversibly to nucleic acids (DNA). Nitrogen mustards inhibit cell reproduction by adding an alkyl group. Bifunctional alkylating agents cause intrastrand linking and cross-linking of the DNA double helix (sugar-phosphate backbone).
• After alkylation, DNA is unable to replicate and cannot synthesize proteins or essential cell metabolites. Consequently, cell reproduction is inhibited, metabolic functions fail, and the cell eventually dies.

1. Nitrogen Mustards: Mechlorethamine, Cyclophosphamide, Ifosfamide, Melphalan, Chlorambucil.
   • Mechlorethamine: The first alkylating agent employed clinically. Bifunctional (crosslinks DNA). Extremely unstable and is inactivated within a few minutes following administration, thus given IV. Used in MOPP regimen for Hodgkin's disease. Highly vesicant (severe local toxicity on extravasation). ADRs: Severe vomiting, myelosuppression.
   • Cyclophosphamide: A prodrug transformed into active aldophosphamide and phosphoramide mustard in the liver. Given orally or IV. Used for ALL, NHL, Polycythemia Vera, Hodgkin's lymphoma, breast and ovary cancers. Causes hemorrhagic cystitis (due to acrolein).
   • Ifosfamide: Has a longer half-life, used mainly for testicular tumors. Also causes hemorrhagic cystitis.
   • Chlorambucil: Orally active against lymphoid tissues. Preferred for CLL, Polycythemia Vera, and NHL.
   • Melphalan: Oral agent used for Multiple Myeloma.
2. Alkyl Sulfonates:
   • Busulfan: Orally active. Great effect for Chronic Granulocytic/Myelogenous Leukemia (CML). Delayed toxicities: Pulmonary infiltrates/fibrosis ("Busulfan lung"), tonic-clonic seizures in epileptics, skin pigmentation, adrenal insufficiency.
3. Nitrosoureas:
   • Carmustine (BCNU) & Lomustine (CCNU): Bifunctional; active against broad spectrums of neoplastic disease. They inhibit synthesis of both DNA and RNA, as well as proteins. These drugs are highly lipophilic, easily crossing the blood-brain-barrier (BBB), making them excellent for primary and metastatic brain tumors. Also used for Hodgkin's, melanoma, and GI adenocarcinomas.
   • Major Toxicity: Highly mutagenic/carcinogenic. Delayed bone marrow depression (prolonged leukopenia/thrombocytopenia), and pulmonary fibrosis.
4. Platinum Coordination Compounds:
   • Cisplatin: Forms crosslinks within DNA strands. Very powerful IV agent against Testicular cancer, ovary, bladder, head, and neck carcinomas. Toxicity is severe: Renal tubular damage (minimized via massive hydration + amifostine), Ototoxicity, peripheral neuropathy, and VERY SEVERE vomiting (treated with Ondansetron/Aprepitant).
   • Carboplatin: A derivative of cisplatin with significantly less nephrotoxicity, neurotoxicity, and ototoxicity (but higher myelosuppression).

These are structural analogues of essential metabolites that interfere with DNA/RNA synthesis (block nucleic acid biosynthesis). Myelosuppression is the primary dose-limiting toxicity.

• Methotrexate (MTX): Structure is similar to folic acid. It actively transports into mammalian cells and competitively inhibits dihydrofolate reductase (DHFR), the enzyme that normally converts dietary folate to the tetrahydrofolate required for thymidine and purine synthesis.
• Kinetics & Indications: Orally, IM, IV, and intrathecally (for CSF entry). Used for ALL, Breast cancer, Tumors of head/neck, Meningeal metastases. It was the first demonstration of curative chemotherapy for Choriocarcinoma.
• Leucovorin (Folinic acid) Rescue: Administered as part of high-dose MTX therapy. Leucovorin is directly converted to tetrahydrofolic acid (producing DNA/cellular protein) in spite of the presence of MTX, rescuing bone marrow and GIT mucosal cells from lethal toxicity.

• 5-Fluorouracil (5-FU): Analogue of thymine. Converted to 5-fluoro-2-deoxy-uridine monophosphate (5-FdUMP), which irreversibly inhibits thymidylate synthase. This blocks the conversion of deoxyuridylic acid to deoxythymidylic acid, causing failure of DNA synthesis. Used for solid tumors (breast, colorectal, gastric, head/neck). Toxicity: Hand and foot syndrome, severe oral/GI ulceration.
• Cytarabine: Inhibits DNA polymerase. Used IV for Acute Myeloid Leukemia (AML). Delayed toxicity includes cerebellar ataxia (neurotoxicity).

• 6-Mercaptopurine (6-MP) & 6-Thioguanine (6-TG): Inhibit purine ring biosynthesis and nucleotide interconversions. 6-MP is used for childhood ALL maintenance and remission, and in combination with MTX for choriocarcinoma.
• Important Interaction: 6-MP is metabolized by xanthine oxidase (which is inhibited by Allopurinol). If a patient is taking Allopurinol for hyperuricemia, the dose of 6-MP must be adjusted to ½ or ¼ to prevent fatal bone marrow toxicity. Well tolerated long term but causes mild hepatotoxicity.

• Hydroxyurea: Inhibits ribonucleotide reductase. Used orally for CML, AML (blast crisis), and Polycythemia vera.

• Anthracyclines (Doxorubicin, Daunorubicin): Insert themselves into DNA causing breaks. They activate Topoisomerase II, causing DNA strand breaks, and generate excess free radicals (superoxide) causing DNA damage.
  • Unique Toxicity: Known to irreversibly damage cardiac cells (Cardiomyopathy). Prevented with Dexrazoxane.
  • Uses: Doxorubicin (Breast, ovary, lung, prostate, ALL, sarcomas, neuroblastoma). Daunorubicin (ALL, AML).
  • Resistance: Develops due to increased efflux of drug via P-glycoprotein.
• Bleomycin: Used for Carcinoma testis, malignant effusions, Hodgkin's. Toxicity: Pulmonary fibrosis, stomatitis, oedema of hands. Causes minimal myelosuppression (alopecia common).
• Dactinomycin (Actinomycin D): Used for Wilm’s tumour.
• Mitomycin C: Carcinoma stomach. Causes severe thrombocytopenia and leukopenia.
• Streptozotocin: Targeted for Insulinoma (pancreatic islet cell tumors). Toxicity: Renal damage, hypoglycemia, nephrogenic diabetes insipidus.

• Vinca Alkaloids (Vincristine, Vinblastine, Vinorelbine): Bind tubulin, destroy the spindle apparatus to produce mitotic arrest (M phase).
  • Vincristine: ALL, NHL. Toxicity: Peripheral neuritis, alopecia, BMD.
  • Vinblastine: Hodgkin's Disease. Toxicity: Loss of reflexes, BMD.
  • Vinorelbine: Carcinoma lung. Toxicity: Paresthesia, hyporeflexia, fatigue.
• Taxanes (Paclitaxel, Docetaxel): Stabilize microtubules, preventing disassembly.
  • Paclitaxel: Carcinoma breast, ovary. Toxicity: Peripheral neuritis, BMD.
  • Docetaxel: Advanced breast cancer. Toxicity: Fluid retention, neurotoxicity, neutropenia.

• Etoposide: A podophyllotoxin (toxin found in the mandrake root). Inhibits the enzyme Topoisomerase II, causing breaks in DNA inside cancer cells, preventing them from dividing. Useful for Testicular cancer and Small Cell Lung Cancer (SCLC). Side effects: Vomiting, alopecia, bone marrow suppression.
• Camptothecin Analogues (Irinotecan, Topotecan): Inhibit Topoisomerase I.

• L-Asparaginase: Depletes the amino acid asparagine, inhibiting protein synthesis. Used IV for ALL in children. Toxicity: Hepatotoxicity, mental depression, pancreatitis.
• Mitotane: Used for Adrenocortical carcinoma. Toxicity: Adrenal insufficiency, lethargy, diarrhea.

Influence hormone homeostasis in hormone-sensitive tumors.

Agent	Cancers Where Preferred	Delayed Toxicity / Comments
Corticosteroids (Hydrocortisone, Prednisone)	ALL, CLL, NHL, Hodgkin's, Multiple myeloma	Fluid retention, hypertension, diabetes mellitus, susceptibility to infection, moon face.
Androgens (Testosterone)	Premenopausal breast cancer (estrogen receptor positive)	Fluid retention, masculinization.
Oestrogens (Diethylstilboestrol, Ethinyloestradiol)	Carcinoma prostate, Postmenopausal breast cancer (ER negative)	Feminization in males, fluid retention.
Progestins (Hydroxyprogesterone, Medroxyprogesterone)	Carcinoma endometrium	None significant.
Antiandrogens (Flutamide, Bicalutamide)	Carcinoma prostate	None significant.
Antiestrogens (Tamoxifen - SERM)	Carcinoma breast (early stage, metastatic after surgery)	Risk of endometrial proliferation/cancer.
GnRH Agonists (Goserelin, Leuprolide)	Carcinoma prostate	Medical castration effect.
Aromatase Inhibitors (Letrozole, Anastrozole, Aminoglutethimide)	Metastatic breast cancer (postmenopausal)	Osteoporosis.
Peptide Hormone Inhibitors (Octreotide)	Carcinoid tumour	Controls severe carcinoid syndrome symptoms.

Drug	Inhibits TK activated by:	Indication
Axitinib / Pazopanib	VEGFR - 1,2,3 / abl-bcr	Advanced renal cell carcinoma
Imatinib	Abl-bcr (Philadelphia chromosome), c-KIT	CML, GIST (Gastrointestinal Stromal Tumor)
Bosutinib / Dasatinib / Nilotinib	Abl-bcr, src, VEGFR	CML (often for Imatinib-resistant cases)
Crizotinib	c-MET, ALK	Non-small cell lung carcinoma (ALK-positive)
Cabozantinib / Vandetanib	c-MET, VEGFR-2, EGFR	Medullary carcinoma thyroid
Erlotinib / Gefitinib	EGFR, abl-bcr, PDGF	Non-small cell lung carcinoma, Pancreatic carcinoma
Lapatinib	HER-2/neu, erb-B2, abl-bcr	Breast carcinoma (HER2 positive)
Regorafenib	VDGFR2, TIE2	Colorectal carcinoma, GIST
Ruxolitinib / Tofacitinib	JAK 1,2	Myelofibrosis / Rheumatoid arthritis
Sorafenib / Sunitinib	VEGFR, PDGFR, RAF, c-KIT, RET	Renal cell carcinoma, Hepatocellular carcinoma, Pancreatic neuroendocrine, GIST
Vemurafenib	BRAF	Malignant melanoma (BRAF V600E positive)

Monoclonal Antibody	Targeted Against	Indication	Comments / Toxicities
Rituximab	CD-20	Non-Hodgkin lymphoma, CLL	Infusion reactions common.
Alemtuzumab	CD-52	Low grade lymphomas and CLL	Profound immunosuppression.
Trastuzumab	HER 2/neu	Breast Carcinoma (metastatic)	Can cause severe cardiotoxicity / cardiac failure.
Cetuximab / Panitumumab	EGFR	EGFR-positive metastatic colorectal carcinoma	Causes rash, Hypomagnesemia, and Interstitial lung disease.
Bevacizumab	VEGF (Vascular Endothelial Growth Factor)	Metastatic colorectal carcinoma	Combined with 5-FU. Inhibits angiogenesis.
Gemtuzumab	CD-33	CD-33 Positive AML	Linked to calicheamicin (antibody-drug conjugate).
Tositumomab (I-131) / Ibritumomab (Y-90)	CD-20	Relapsed lymphomas	Conjugated with radioisotopes for targeted radiation.
Denileukin diftitox	IL-2 receptor	Recurrent cutaneous T-cell lymphoma	Recombinant IL-2 plus diphtheria toxin.

Modern oncology relies heavily on standardized, combination protocols based on extensive clinical trials.

Diagnosis	Treatment of Choice (Regimen)
Acute Lymphocytic Leukaemia (ALL)	Induction: Vincristine + Prednisolone + Daunorubicin + Asparaginase + Intrathecal Methotrexate. Maintenance: Methotrexate + 6-Mercaptopurine + Cyclophosphamide. Consolidation: Hyper-CVAD alternated with Cytarabine+Methotrexate.
Acute Myeloid Leukaemia (AML)	Cytarabine + Daunorubicin/Idarubicin.
Chronic Myelogenous Leukaemia (CML)	Imatinib (Busulfan or Interferon as alternatives). Bone marrow transplant in selected patients.
Chronic Lymphocytic Leukaemia (CLL)	FCR (Fludarabine, Cyclophosphamide, Rituximab) or Fludarabine/Chlorambucil+Prednisone alone.
Hairy cell leukemia	Cladribine.
Hodgkin's disease	Stage I/II: Radiotherapy. Stage III/IV: ABVD (Doxorubicin [Adriamycin], Bleomycin, Vinblastine, Dacarbazine).
Non-Hodgkin lymphoma	CHOP-R (Cyclophosphamide, Doxorubicin, Vincristine, Prednisolone + Rituximab).
Multiple Myeloma	Bortezomib + Dexamethasone + Lenalidomide (or Melphalan + Prednisone).
Waldenstrom macroglobulinemia	FCR (Fludarabine, Cyclophosphamide, Rituximab).
Polycythemia vera	Hydroxyurea (or Busulfan/Chlorambucil).
Choriocarcinoma	Methotrexate + folic acid OR Cisplatin + Etoposide.
Carcinoma testis	Bleomycin + Cisplatin + Etoposide (BEP regimen).
Wilm's tumour	Surgery + radiotherapy followed by Vincristine + Dactinomycin.
Non-small cell lung cancer	Cisplatin + Vinorelbine ± Bevacizumab.
Small cell lung cancer	Cisplatin + Etoposide.
Mesothelioma	Cisplatin + Pemetrexed.
Head and neck cancer	Cisplatin + 5-FU.
Carcinoma breast stage 1	Tamoxifen after breast surgery.
Carcinoma breast stage II to IV	Cyclophosphamide + Methotrexate + 5-FU (CMF) OR Trastuzumab + Prednisone + Antiestrogen.
Carcinoma ovary	Cisplatin/Carboplatin + Paclitaxel + Interferon.
Carcinoma prostate	GnRH agonist OR Oestrogen + Androgen antagonist (Flutamide).
Melanoma	Dacarbazine, Cisplatin, Interferon.
Carcinoma adrenal gland	Mitotane.
Carcinoid tumour	Doxorubicin + Cyclophosphamide OR 5-FU + Octreotide.

• Contraindications Check: Assess for drug allergies, severe hepatorenal impairment, pre-existing bone marrow suppression, and verify pregnancy/lactation status (ensure barrier contraception is utilized by women of childbearing age).
• Baseline Physical Assessment: Check orientation, reflexes, vital signs, bowel sounds, and oral mucosa to establish baseline data before therapy begins.
• Laboratory Monitoring:
  • CBC with differential: Crucial to identify bone marrow suppression (leukopenia, neutropenia, thrombocytopenia, anemia). Calculates the Absolute Neutrophil Count (ANC).
  • Renal/Hepatic panels (BUN, Creatinine, AST, ALT, Bilirubin): To determine the need for dose adjustments and identify toxicities.
  • Uric Acid: Monitor for Tumor Lysis Syndrome (prophylactic Allopurinol or Rasburicase may be needed).

No.	Nursing Diagnosis	Interventions & Rationale
1	Risk for Infection related to chemotherapy-induced leukopenia and immunosuppression.	Institute strict neutropenic precautions: Hand hygiene, avoid fresh flowers/plants, and raw unpeeled fruits/vegetables to prevent exposure to environmental pathogens. Monitor temperature daily: A fever >38°C (100.4°F) in a neutropenic patient is a medical emergency requiring immediate broad-spectrum antibiotics. Administer Colony-Stimulating Factors (e.g., Filgrastim/Peg-filgrastim) as ordered: Stimulates the bone marrow to accelerate neutrophil recovery.
2	Imbalanced Nutrition: Less than body requirements related to severe nausea, vomiting (CTZ stimulation), and stomatitis/mucositis.	Administer antiemetics prophylactically: Give agents like Ondansetron (5-HT3 antagonists) 30-60 minutes before chemotherapy administration. For delayed emesis (like with Cisplatin), administer Aprepitant. Provide frequent, small, high-calorie, bland meals: Easier to digest and less likely to trigger nausea than large, spicy, or hot meals. Implement meticulous oral hygiene: Use soft-bristled toothbrushes and non-alcoholic mouthwashes (or administer Palifermin) to soothe stomatitis and prevent bleeding gums or candidiasis.
3	Risk for Bleeding related to chemotherapy-induced thrombocytopenia.	Implement bleeding precautions: Avoid IM injections, use electric razors, and prevent hard nose-blowing to avoid inducing uncontrollable hemorrhage. Monitor for petechiae, ecchymosis, or melena: Early clinical indicators of dangerously low platelet counts. Administer Platelet/Granulocyte transfusions or Oprelvekin (IL-11): As indicated to manage severe thrombocytopenia.
4	Disturbed Body Image related to alopecia and physical changes from targeted therapies (e.g., severe acneiform rash).	Educate prior to hair loss: Inform the patient that hair loss is usually temporary and will regrow after therapy cessation. Suggest exploring wigs, hats, or scarves beforehand. Provide emotional support: Validate their feelings regarding their changing appearance; refer to oncological support groups if appropriate.
5	Risk for Impaired Tissue Integrity (Vesicant Toxicity) related to extravasation of alkylating agents or antibiotics (e.g., Mechlorethamine, Doxorubicin, Vincristine).	Ensure patent IV access via central line or port: Peripheral lines are highly risky for vesicants. Check for blood return prior to administration. Monitor IV site continuously during infusion: If swelling, pain, or redness occurs, stop the infusion immediately, aspirate residual drug, and follow hospital extravasation protocols.

• Presentation Slides: Treatment options of cancer / Anticancer drugs (Slides 57 pages detailing Cell Cycle, Alkylating Agents, Antimetabolites, Antibiotics, Targeted Therapies, Toxicities, and Therapy of Choice).
• Brunton, L. L., Hilal-Dandan, R., & Knollmann, B. C. (2017). Goodman & Gilman's The Pharmacological Basis of Therapeutics (13th ed.). McGraw-Hill Education.
• Katzung, B. G. (2017). Basic & Clinical Pharmacology (14th ed.). McGraw-Hill Education.
• Nursing considerations adapted from Oncology Nursing Society (ONS) guidelines for safe handling and administration of chemotherapy.