A preparation of autologous T-lymphocytes that have been genetically modified to express a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-C*08:02-restricted oncogenic K-RAS (KRAS) substitution mutation G12D, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo and re-introduction into the patient, the autologous KRAS G12D-specific HLA-C*08:02-restricted TCR gene engineered T-lymphocytes NT-112 target and bind to KRAS G12D-expressing tumor cells, resulting in cytotoxic T-lymphocyte (CTL)-mediated killing of KRAS-G12D-expressing tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.