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LE4 College aantekeningen Oncology (NWI-BM015C) - Chemotherapy and Receptor Mediated Therapy

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December 14, 2023
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LE 4 – Chemotherapy and
receptor-mediated therapy
November 17th, 2023

Introduction
Cancer treatment
 Local treatment: surgery, radiotherapy
 Systemic treatment: distant metastasis

HIPEC – Hyperthermic intraperitoneal chemotherapy. It is a two-step procedure that certain cancers
in the abdomen. Cancerous tumors are surgically removed, and then heated chemotherapy drugs are
applied directly inside the abdomen to eliminate the remaining cancerous cells.

Therapeutic options
 Chemotherapy
 Targeted therapy
 Hormonal therapy
 Immunotherapy




Goals of treatment
Curati on
 Systemic treatment as single treatment
 In combination with local treatment:
o Neoadjuvant: treatment administered before primary cancer treatment to enhance
the outcome of the primary treatment.
o Adjuvant: treatment given after the main treatment to reduce the chance of cancer
coming back by destroying and remaining cancer cells.
o Concomitant: Given at the same time during cancer therapy.

Palliati on
 Relief of complaints
 Prolonged survival

, Chemotherapy
Mechanisms of acti on
Chemotherapy causes DNA damage in dividing cells:
 Inhibition of DNA synthesis
 inhibition of DNA repair
 Inhibition of DNA transcription
 inhibition of the mitotic process

DNA damage to all dividing cells, also normal cells  side effects. Cancer cells are fast dividing cells
and thus are sensitive to chemotherapy. Different agents intervene at different steps in the cell cycle.

Principles of chemotherapy
 Growth speed: initially exponential
 Growth fraction = % of cells that divide actively.
o Decreases when tumor is growing
o Lower blood flown in larger tumors

Thus, smaller tumors are more sensitive/vulnerable for chemotherapy than larger tumors.

Goldie-Coldman hypothesis
 Cancer cells are genetically instable; during growth: more mutations
 Because of mutations less sensitive for chemotherapy (=resistance)
 Larger tumors contain more resistant cells
 Thus, combine different chemotherapy agents

Cell-kill hypothesis
 Multiple cycles
 Eventually resistance
o Intrinsic (cellular)
o Adaptation (post Tx detoxification pathways)
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