Patients known to have BRCA/ gene mutations (testing for gene mutations is not required) Patients must have HER- amplification as determined by central testing (+ or + by immunohistochemistry and HER- gene amplification by in situ hybridization with a ratio of HER- gene signals to centromere signals >= .) For Part C dose confirmation: All participants must have histological evidence of advanced or metastatic breast cancer and prescreened mutations, amplification, or gene/protein expression alterations related to Notch pathway. Has received previous treatment with another agent targeting the lymphocyte-activation gene (LAG-) receptor. Has a tumor that contains a nonsynonymous mutation, insertion, or deletion in the TP gene determined previously or at screening. All patients must have at least two of the following diagnostic criteria for NF, and/or a pathogenic NF gene mutation demonstrated in peripheral blood-derived DNA: HER-positive (immunohistochemistry score +) or ERBB- amplification (ratio ERBB/centromeres >= . or mean gene copy number >= ) on primary tumor or of metastatic or unresectable loco-regional biopsy. Have received prior gene therapy or therapy with cytolytic virus of any type Patients who have received prior surgery, gene therapy, or combination chemotherapy will be permitted if it has been at least days since the last treatment CD gene count > /ul STRATUM A: Participants with a pathogenic somatic or known germline retinoblastoma (RB) gene mutation STRATUM B: Participants with a pathogenic somatic or known germline retinoblastoma (RB) gene mutation STRATUM C: Participants with a pathogenic somatic or known germline retinoblastoma (RB) gene mutation Patients must have documented IDH-R gene-mutated disease as evaluated by the site Subjects must have an IDH gene mutation (IDH-R or R) as determined by local laboratory result Previous treatment with investigational gene or chimeric antigen receptor therapy; Must be willing to participate in Gene Therapy Long Term Followup Protocol (-C-), which will follow patients for up to years per Food and Drug Administration (FDA) requirements Previous treatment with investigational gene or chimeric antigen receptor therapy. DNA damage repair deficiency as assessed centrally by a gene mutation biomarker panel (testing of de novo or archiaval tumor tissue (via central laboratory) or prior historical testing (with Sponsor approval) using the Foundation Medicine, FoundationOne NGS gene panel test. Documented HER overexpression or gene-amplified tumor by a validated approved method Prior treatment with gene modified T cells Subjects must have one of the following: a. somatic mutations in human epidermal growth factor receptor (EGFR, HER, HER, and HER); b. EGFR gene amplification (patients with + results on immunohistochemistry testing for EGFR may be allowed to enroll if gene amplification results are unavailable); c. HER gene amplification (patients with + results on immunohistochemistry testing for HER- may be allowed to enroll if gene amplification results are unavailable). Patients who have been treated on other protocols of genetically-modified T cells at the NIH only are potentially eligible under these conditions:\r\n* At least months have elapsed since the last genetically-modified T-cell therapy that the patient received and there is no evidence of replication-competent retroviruses (evidence must be provided from prior NIH gene-therapy protocol principal investigator) and persisting genetically-modified T cells are not detectable in the patients blood (evidence must be provided by prior NIH gene-therapy protocol principal investigator) Part B: Relapsed or refractory primary CNS tumors with molecular alterations, including gene fusions, documented by a CLIA-approved lab prior to enrollment; Received any previous gene therapy using an integrating vector within months Have received prior gene therapy or gene-modified cellular immunotherapy Patients who have been treated on other protocols of genetically-modified T cells at the NIH only are potentially eligible under these conditions:\r\n* At least months have elapsed since the last genetically-modified T-cell therapy that the patient received and there is no evidence of replication-competent retroviruses (evidence must be provided from prior NIH gene-therapy protocol principal investigator) and persisting genetically-modified T cells are not detectable in the patients blood (evidence must be provided by prior NIH gene-therapy protocol principal investigator) Subjects with a malignancy that contains a non-synonymous mutation, insertion, or deletion in the TP gene determined previously or at screening Subjects must not have received prior gene therapy or gene-modified cellular immunotherapy; subject may have received, however, non-gene-modified autologous T-cells in association with an anti-myeloma vaccine (e.g., human telomerase reverse transcriptase [hTERT] or melanoma-associated antigen [MAGEA]) or vaccination against infectious agents (e.g., influenza or pneumococcus) as was performed on our previous studies Patients who have received a vaccine for HIV- or any prior gene modified cell product, at any time Is willing to undergo malignancy genotyping for TP gene mutation, insertion, or deletion at screening. Has a malignancy that contains a non synonymous mutation, insertion, or deletion in the TP gene determined previously or at screening. Prior gene therapy Previous treatment with gene therapy Patient must have confirmed HER overexpression or gene-amplified tumor Prior gene therapy. Favorable biomarker profile defined by either wild type p gene sequence or less than % p positive tumor cells by immunohistochemistry Has received previous treatment with another agent targeting the Lymphocyte-activation gene (LAG-) receptor Prior gene transfer therapy or prior therapy with a cytolytic virus of any type Receipt of a vaccine for HIV- or any prior gene modified cell product, at any time Patients with wild type BRAF gene molecular results on ECD affected tissue Test result showing genetic change in MET tumor gene Subjects must have documented IDH R gene-mutated advanced hematologic malignancy based on local or central evaluation. Patient must have histologically or cytologically confirmed solid tumor, including glioma, with documented IDH and/or IDH gene-mutation. Patients in the dose escalation phase must have disease that has recurred or progressed following standard therapy and/or therapy with an inhibitor of mutant IDH and/or IDH, or that has not responded to this therapy. Patients in the expansion phase may have previously untreated disease Prior treatment with gene therapy product Treatment with any prior gene therapy product Documented HER overexpression or gene-amplified tumor by a validated approved method Treatment with any prior gene therapy product HER- positive BC as defined by an immunohistochemistry score of or gene amplified by in-situ hybridization as defined by a ratio of greater than or equal to (>=) . for the number of HER gene copies to the number of chromosome copies Diagnosis of one of the following: Part Only: NUT Midline Carcinoma based on ectopic expression of NUT protein as determined by IHC and/or detection of NUT gene translocation as determined by FISH. Subjects may be treatment nave or have had prior therapy; SCLC, CRC, NB, TNBC, ER positive BC, CRPC, NSCLC and any other solid tumor which has been confirmed by clinical testing to be MYCN amplified (defined as a MYCN gene copy number gain of >=). Subjects should have tumor progression after receiving at least one prior standard/approved chemotherapy, or where there is no approved therapy, or where standard therapy is refused. Part only: NUT Midline Carcinoma as diagnosed by the Central Laboratory. Subjects may be treatment nave or have had prior therapy. SCLC, CRPC, TNBC and ER+BC . Prior therapy with gene modified cells Patients must have a tumor protein (p) mutation which is defined as cytoplasmic positivity by immunohistochemistry and/or next gene mutation sequencing Prior gene therapy treatments or prior therapy with cytolytic virus of any type Patient must agree to testing of GBM tumor promoter methylation status of the MGMT gene and tumor (IDH) gene mutation status. Tissue may be tested at study entry, if not done previously, or data may be obtained from last known test result for MGMT and IDH. IDH status may be assessed at study entry, but MGMT status is required prior to randomization. HER/neu gene amplification by fluorescence, chromogenic, or silver in situ hybridization [FISH, CISH or SISH;>= HER/neu gene copies per nucleus or a FISH, CISH, or SISH test ratio (HER gene copies to chromosome signals) of >=. OR HER/chromosome ratio <=. with average HER copy number >= signals/cell nucleus] Subjects must have histologically-confirmed diagnosis of IDH gene-mutated cholangiocarcinoma Stage II, III, or IV (intra-hepatic, extra-hepatic and perihilar) that is not eligible for curative resection, transplantation, or ablative therapies. Tumors of mixed histology are not allowed. Dose Expansion: Chondrosarcoma a. Subjects must have IDH gene-mutated chondrosarcoma that is either locally advanced or metastatic and not amenable to complete surgical excision. IDH gene-mutated solid tumors refractory to conventional therapy or the subject does not tolerate the conventional therapy Subjects must have documented IDH gene-mutated disease based on local test evaluation. (Centralized testing will be performed retrospectively.) Prior treatment with any gene therapy product Subjects must have documented IDH gene-mutated disease: Over-expression by immunohistochemistry (IHC) with score of + (in > % of invasive tumor cells) AND/OR HER gene amplification (average of > HER gene copies per nucleus or a FISH ratio [HER gene copies to chromosome signals] of >= .), according to guidelines and in keeping with past eligibility for ratio of >= . rather than the ratio of > . required by new guidelines mutations of amplifications involving the c-Met gene but not the ALK gene Patient must have either mutation or amplification of c-KIT gene tested by commercially available molecular or gene sequencing techniques Prior treatment with any gene therapy product Prior therapy with IL- or prior gene therapy. AKT INHIBITOR MK ARM: Patients must have one of the following as determined by analysis of the primary tumor or a metastatic site in a CLIA certified laboratory:\r\n* Phosphatidylinositol-,-bisphosphate -kinase, catalytic subunit alpha (PIKCA) mutation or\r\n* PIKCA gene amplification by fluorescent in situ hybridization (FISH) (gene to chromosome ration > ) or\r\n* V-akt murine thymoma viral oncogene homolog (AKT) mutation or\r\n* Phosphatase and tensin homolog (PTEN) mutation LAPATINIB DITOSYLATE ARM: Patients must have one of the following as determined by analysis of the primary tumor or a metastatic site in a CLIA certified laboratory:\r\n* Human epidermal growth factor receptor (ERBB) mutation or\r\n* ERBB gene amplification by FISH (gene to chromosome ration > ) SUNITINIB MALATE ARM: Patients must have one of the following as determined by analysis of the primary tumor or a metastatic site in a CLIA certified laboratory:\r\n* Platelet derived growth factor receptor alpha (PDGFR-A) mutation or\r\n* PDGFR-A gene amplification by FISH (gene to chromosome ratio > ) or\r\n* V-kit Hardy-Zuckerman feline sarcoma viral oncogene homolog (KIT) mutation Patient has participated or is currently participating in any bone marrow derived autologous and allogeneic stem cell or gene therapy study. HER/neu gene amplification by fluorescence, chromogenic or silver in situ hybridization [FISH, CISH or SISH; > HER/neu gene copies per nucleus or a FISH, CISH or SISH HER gene copies to chromosome signal ratio of ?.] Documented IDH gene-mutated disease based on local site testing Test results showing genetic change in tumor gene for CREBBP and/or EP Prior receipt of gene therapy. ER+/HER+ breast, ovarian, cervical, endometrial cancer, or other solid cancers, resistance to standard therapies with a PIKCA gene mutation (Part C), AKT gene mutation (Part D) or a dysregulatory aberration on the PIK/AKT pathway (Part D), advanced or metastatic ER+ positive breast cancer that has an AKT gene mutation (Part E) or advanced or metastatic ER+ positive breast cancer that has a PTEN gene mutation (Part F). Have documented IDH RH gene mutation by local testing and known pq or ATRX mutation status by local testing. Prior therapy with IL- or prior gene therapy Subjects have had their PIKCA gene mutation status assessed prior to enrolling into the study Hematologic malignancy associated with a poor prognosis or other diagnosis for which hematopoietic cell therapy (allogeneic or autologous, including gene therapy) is indicated DONOR: Autologous or allogeneic gene modified cells allowed Any previous gene therapy using an integrating vector. Prior treatment with any prior gene therapy product Evidence for clonal T-cell receptor gene rearrangement (obtained within year prior to study drug administration). CTCL-Specific: Documentation of a TP gene mutation by next generation sequencing (NGS) based on central or local evaluation Confirmed HER overexpression or gene-amplified tumor