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Anthracyclines: Myelosuppression (esp neutropenia ) Nausea, vomiting Total alopecia Mucositis Red-colored urine Cardiomyopathy (mostly with Doxorubicin, risk increases with cumulative dose) Secondary malignancies (AML, MDS) Topoisomerase I inhibitors: Irinotecan: Severe diarrhea , nausea, vomiting Neutropenia Top otecan: Myelosuppression Less GI toxicity Interstitial lung disease (rare but serious) Topoisomerase II inhibitors:  Doxorubicin: Discussed in Anthracyclines section Etoposide: Myelosuppression (esp neutropenia and thrombocytopenia) Nausea, vomiting Secondary leukemias (with long-term use) Hypersensitivity reactions (anaphylaxis, rash, urticaria) Embryo-fetal toxicity, Infertility Alkylating agents: Myelosuppression (neutropenia, anemia, thrombocytopenia) Nausea and vomiting Mucositis Alopecia Gonadal dysfunction (infertility, premature menopause, ovarian/testicular failure) Hemorrhagic cystitis (esp with cyclophosphamide and ifosfamide) Secondary malignancies (leukemia and myelodysplasia) Organ-specific toxicities (cardiac, renal and hepatic toxicities) Pulmonary fibrosis (with Busulfan, Melphalan and Carmustine) Taxens: Peripheral neuropathy (esp Paclitaxel) Hypersensitivity reactions (esp Paclitaxel) Myelosuppression (severe neutropenia in Docetaxel) Fluid retention (esp Docetaxel) Organ-specific toxicities Erythropoiesis Stimulating Agents (ESA): Allergic reactions Hypertension Seizures Thrombosis Decreased overall survival in cancer patients Neutralizing antibodies can lead to pure red cell aplasia Granulocyte Colony-Stimulating Factor (G-CSF): Allergic reactions Bone pain (treat with NSAID and/or antihistamines) ARDS Splenic Rupture Sickle Cell Crises Sweet syndrome, cutaneous vasculitis MDS/AML (0.4% absolute risk) Granulocyte-macrophage colony-stimulating factor (GM-CSF): Allergic reaction Edema/ capillary leak syndrome Pleural/pericardial effusion Supraventricular tachycardia Thrombomimetics (TPO): Headache, Arthralgia/myalgia, GI symptoms, thromboembolism (venous and arterial) + Eltrombopag (Promacta): Menorrhagia Hepatic toxicity (rare) Avatrombopag (Doptelet): Fever Headache Peripheral edema Romiplostim (Nplate): Bone marrow reticulin ( myelofibrosis ) Increase in blasts (in patients with MDS) IN PROGRESS..!

Here are some points that can make your Hem/Onc life easier- The earlier you learn them, the better. Lesson Number 1 Below is a list of anticancer agents for which the category and mechanism of action can be recognized by their names: Chemotherapy: ... rubicin : Anthracycline ...tecan : Topoisomerase I inhibitors ...mustine : Alkylating agents ...carbazine : Alkylating agents ...taxel : Taxens (Microtubule-targeting agent) Vin...stine: Vinca alkaloids ( Microtubule-targeting agent) ...platin: Platinum compounds ...trexed : Antifolates ( Antimetabolites) ...citabine: Pyrimidine analogues ( Antimetabolites) Immunotherapy: ...limab: PD-1 inhibitor ...limumab: CTLA-4 inhibitors ... alidomide: Immunomodulators ... cabtagene ...leucel: CAR T-cell therapy Targeted therapy: ...rafenib: BRAF inhibitors ... metinib: MEK inhibitors ...rolimus : mTOR inhibitor ...tinib : TK inhibitor ... brutinib: BTK inhibitor ... rasib: KRAS inhibitors ...trectinib : NTRK inhibitors ... zomib: Proteasome inhibitors ...lisib: PI3Kδ inhibitors Antibody-drug conjugate (ADC): ... Vedotin ... Ozogamicin Lesson Number 2 Antibody-drug conjugate ( ADC): ADCs are composed of three main components: Monoclonal antibody targeting a tumor-associated antigen Cytotoxic payload Chemical linker Antibody binds to a specific antigen on the cancer cell surface → ADC is internalized → release the cytotoxic drug in cancer cells → targeted cell death Bispecific antibody (BsAb): Engineered Ab that have two distinct binding domains → recognize and bind two different antigens or two different epitopes (most commonly a tumor antigen and CD3 on T cells) → redirect immune cells toward malignant cells → facilitating targeted cytotoxicity The most clinically relevant BsAB in hematology are those that engage a tumor-associated antigen (CD19, CD20, BCMA, GPRC5D) and a T cells (CD3). Lesson Number 3 Route of administration: All TKI agents are administered orally. All immunotherapy medications are administered IV, except for immunomodulatory agents (lenalidomide, thalidomide, pomalidomide) which are given orally. Lesson Number 4 Assessment of treatment efficacy in hematology/oncology: Complete response (CR): Disappearance of all evidence of disease. In lymphomas (Lugano criteria): No abnormal FDG uptake on PET (Deauville score 1-3), regression of all lesions to normal size, and no new lesions. In acute leukemias: No circulating blasts, no extramedullary disease, trilineage hematopoiesis in BM with <5% blasts, and recovery of blood counts (ANC ≥1000, platelets ≥100k) Partial response (PR) : Significant but incomplete reduction in disease burden. In lymphomas: ≥50% decrease in the sum of the product of diameters of target lesions, with no new lesions and reduced FDG uptake compared to baseline (Deauville score 4-5 with decreased avidity). In leukemias: PR is less commonly used, but may refer to a substantial reduction in blast percentage or disease burden without meeting all CR criteria. Progressive disease (PD) : Worsening or growth of disease. In lymphomas: >50% increase in the size of existing lesions, appearance of new lesions, or increased FDG uptake (Deauville score 5). In leukemias: Increase of at least 25% in the absolute number of circulating or BM blasts, or development of new extramedullary disease. Lesson Number 5 Castrate-sensitive prostate cancer (CSPC): Also termed "hormone-sensitive" or "androgen-sensitive" prostate cancer. Responds to androgen deprivation therapy (ADT), with tumor growth suppressed when serum testosterone is reduced to castrate levels (typically <50). Castrate-resistant prostate cancer (CRPC): Prostate cancer that progresses clinically, radiographically, or biochemically (rising PSA) despite ongoing ADT and maintenance of castrate levels of serum testosterone (<50). This resistance can occur in both non-metastatic (M0 CRPC) and metastatic (M1 CRPC) disease. Confirm castrate testosterone levels before diagnosing CRPC, and continue ADT even after resistance develops. Lesson Number 6 Measurable Residual Disease (MRD): Residual malignant cells that persist after treatment but are undetectable by standard microscopy.  After a patient achieves complete remission by standard criteria (no detectable disease by microscopy), more sensitive lab techniques (multiparameter flow cytometry, real-time quantitative PCR, NGS) can identify very low levels of leukemic cells that persisted. Patients who are MRD-positive after induction or consolidation therapy have a significantly higher risk of relapse and worse overall survival compared to those who are MRD-negative (regardless of their initial risk category or disease subtype). MRD positivity at key time points (end of induction, end of consolidation) identifies patients at higher risk for relapse and may prompt consideration of therapy intensification or allo-HSCT. Lesson Number 7 Liver biopsy: Liver mass + Cirrhosis: biopsy is generally not indicated for a patient with cirrhosis who has a liver mass if the lesion meets established imaging criteria for HCC on CT or MRI. In this setting, imaging features (arterial phase hyperenhancement, washout, capsule appearance) has high specificity, and biopsy is not routinely required. Consider biopsy if: Imaging is inconclusive Lesion does not meet criteria for definite HCC (LI-RADS 5) Suspicion for a non-HCC malignancy (cholangiocarcinoma) Atypical risk factors (cirrhosis due to congenital or vascular causes) Tumor markers suggest alternative diagnoses Liver mass, No cirrhosis: Biopsy is recommended to confirm malignancy and guide management Systemic therapy in HCC: Generally indicated for patients with HCC and Child-Pugh class A or ≤B7 , while it is not recommended for Child-Pugh class >B7 or C. Lesson Number 8 Basics of radiotherapy (RT): RT application ranges from definitive therapy in localized disease, to consolidation after chemotherapy, palliation of symptoms, and as part of conditioning regimens for HSCT. NCCN emphasize the use of involved-site radiotherapy (ISRT) to limit exposure to adjacent uninvolved organs, thereby reducing long-term complications such as hypothyroidism, cardiac toxicity, and secondary malignancies. Treatment planning requires CT-based simulation and often incorporates PET and MRI for precise target delineation. NCCN provides specific dose and fractionation recommendations based on histology, disease stage, and treatment intent. For example, follicular lymphoma is typically treated with 24–30 Gy, while DLBCL may require 30–36 Gy for consolidation after chemotherapy. Lesson Number 9 Anticoagulation use in renal and hepatic dysfunction: DOACs (apixaban, rivaroxaban, edoxaban, dabigatran): generally avoided in severe renal (CrCl <30 mL/min) or hepatic dysfunction (Child-Pugh B/C or significant LFT elevation). Apixaban may be used with caution in renal impairment but should be avoided in severe hepatic dysfunction. LMWHs (dalteparin, enoxaparin): preferred in patients with GI malignancy or if DOACs are contraindicated, but require caution and possible anti-Xa monitoring in renal dysfunction. DOACs (especially rivaroxaban and edoxaban) are associated with a higher risk of GI bleeding in patients with GI malignancy. Data  on hepatic dosing adjustments are limited. UFH: preferred in severe renal dysfunction or when rapid reversal is needed. Warfarin: consider if other agents are contraindicated, but requires close INR monitoring, especially in hepatic dysfunction. Lesson Number 10 You can stare at this table to strengthen your visual memory and learn about lymphomas! Black cells: Positive For example: CLL has CD5 + White cells: Negative For example: FL has CD5 – Gray cells: Weak/dim For example: CLL has weak/dim CD20 Black cells with white circles: Positive, occasionally negative For example: FL often has positive CD10, but can be negative as well. Lesson Number 11 Terminal deoxynucleotidyl transferase (TdT): Template-independent DNA polymerase expressed in immature lymphoid cells Normally present in precursor B and T lymphoblasts Hallmark of lymphoblastic neoplasms, including ALL and lymphoblastic lymphoma Occasionally seen in the blast phase of CML (when transformation is lymphoid rather than myeloid) Lesson Number 12 Key distinguishing features of leukemias: CLL:  CD5+ and CD23+ co-expression on B-cells (unique among leukemias). CML: BCR-ABL1 fusion; immunophenotype less diagnostic ALL:  TdT+, lymphoid markers CD10+ in B-ALL CD3+ in T-ALL AML:  TdT−, MPO+, myeloid markers (CD13, CD33, CD117) IN PROGRESS...!