I Wish I Knew Earlier
- Mar 21, 2024
- 5 min read
Updated: Aug 10
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: Taxans (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
...tamab: Bispecific T-cell engager (BiTE)
...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: PI3K inhibitors
...sidenib: IDH inhibitor
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 has 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 solid tumors:
Complete response (CR):
Disappearance of all target lesions
Partial response (PR):
≥30% decrease in the sum of diameters of target lesions
Progressive disease (PD):
≥20% increase in the sum of diameters, with an absolute increase ≥5 mm
Appearance of new lesions.
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 (nmCRPC) and metastatic (mCRPC) 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 conventional morphologic examination (light microscopy).
After a patient achieves complete remission by standard criteria (no detectable disease by microscopy), more sensitive lab techniques (multiparameter flow cytometry, molecular methods such as PCR and NGS) can identify very low levels of leukemic cells that persisted.
MRD positivity is generally associated with higher relapse risk and adverse outcomes.
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 if HCC is suspected
Systemic therapy in HCC:
Generally recommended for Child-Pugh A; selected Child-Pugh B (particularly B7) patients may also be considered.
It is not usually recommended for Child-Pugh class >B7 or C.
Lesson Number 8
Basics of Radiation Therapy (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.
In lymphoma, NCCN uses involved-site radiotherapy (ISRT) to limit radiation exposure to uninvolved tissues, 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 usually treated with 24–30 Gy, while DLBCL may require 30–36 Gy for consolidation after chemotherapy.
RT broadly divides into three delivery categories:
External beam radiation therapy (EBRT):
Radiation is generated outside the body and directed toward the tumor.
Techniques:
3D conformal RT (3D-CRT):
Beams are shaped to conform to the tumor.
IMRT (intensity-modulated RT):
An advanced form of conformal RT in which radiation intensity varies across the beams → improves dose conformity and helps spare nearby normal structures.
Stereotactic radiation:
Stereotactic body RT (SBRT) is a very precise EBRT delivering relatively high doses per fraction to a small, well-defined target for extracranial tumors.
Proton therapy:
Uses protons rather than photons, allowing different dose deposition that can reduce radiation beyond the target.
Brachytherapy:
A radioactive source is placed inside or immediately adjacent to the tumor, producing a high local radiation dose with rapid dose falloff.
Common oncology applications include prostate and gynecologic cancers.
Systemic radiopharmaceuticals:
A radioactive compound is administered systemically, and the molecule preferentially delivers radiation to cells/tissues expressing or accumulating its target.
Examples:
¹⁷⁷Lu-DOTATATE → somatostatin-receptor–positive neuroendocrine tumors
¹⁷⁷Lu-PSMA → PSMA-expressing prostate cancer
Radioiodine → differentiated thyroid cancer
Lesson Number 9
Anticoagulation use in renal and hepatic dysfunction:
Direct oral anticoagulants (DOAC):
Mixed renal and hepatic clearance
Renal clearance: Dabigatran (80%) > Edoxaban (50%) > Rivaroxaban (35%) > Apixaban (27%)
Indirect inhibitors:
Renal clearance increases as the molecule gets smaller:
UFH → least renal dependence
LMWH → mostly renal
Fondaparinux → almost completely renal
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)