HAT-Pi chemotherapy arrests uncontrolled replication and metastatic migration of neoplastic cells by inhibiting enzymatic activity of poly (ADP-ribose) polymerase 1 (PARP 1) through administration of one or more halogenated analogs of thymidine (HAT). A full HAT-Pi treatment regimen, involving repeated HAT-Pi courses over extended periods (24 weeks), may lead to tumor regression through HAT-Pi-induced neoplastic cell death and disintegration. Pain related to neoplastic disease may be reduced during HAT-Pi treatment and for extended periods thereafter. Myelosuppression is a potentially life-threatening but manageable HAT-Pi toxicity and other HAT-Pi side-effects may be tolerated by most patients. Acquired patient resistance to HAT-Pi has not been observed. HAT-Pi is potentially teratogenic and is restricted to post-reproductive adults with advanced neoplastic disease. Modified HAT-Pi treatment regimens may allow for broader application to treat additional individuals and/or conditions.