Neoplasms

Digestive System Diseases

All Conditions

Rare Diseases

Esophageal Neoplasms

Esophageal Cancer

All Drugs and Chemicals

Antineoplastic Agents

Antibodies

Antibodies, Monoclonal

Paclitaxel

Carboplatin

Albumin-Bound Paclitaxel

Immunoglobulins

Tubulin Modulators

Antimitotic Agents

Participants will receive standard of care chemoradiation, consisting of:

* External beam radiation in daily fractions (28 fractions) from Weeks 1-6, administered once per day up to 5 days/week.
* Carboplatin (area under the carboplatin plasma concentration versus time curve = 2) and paclitaxel (50 mg/m\^2) chemotherapy intravenously (IV) over 1 hour, once weekly, from Weeks 1-5.

The participants also will receive concurrent 0.3 mg/kg APX005M IV over 1 hour, once weekly, on Weeks 1, 2, 4, and 6 (2-3 days after chemoradiation).

Surgical resection of the tumor will be planned from Week 10 up to approximately Week 17, as indicated in the protocol amendment under which each participant is enrolled.

APX005M

Radiation therapy, total dose 5040cGy in 180cGy fractions

Radiation Therapy

Surgical removal of the tumor will occur between weeks 10-17

Surgical resection of tumor

This pilot phase II trial studies the therapeutic effects and side effects of CD40 agonistic monoclonal antibody APX005M when combined with chemotherapy and radiation therapy, and to see how well they work to reduce or remove esophageal or gastroesophageal (GE) cancers when given before surgery in treating patients with esophageal cancer or GE cancer than can be removed by surgery. APX005M is intended to stimulate the body's own immune system so that the immune cells can more effectively invade and destroy the tumor, adding to the benefits of the chemotherapy and radiation therapy. Drugs used in chemotherapy, such as carboplatin and paclitaxel, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Radiation therapy uses high energy x-rays to kill tumor cells and shrink tumors. Giving APX005M, chemotherapy, and radiation therapy before surgery may make the tumor smaller and reduce the amount of normal tissue that needs to be removed.

Primary Objective:

To assess the efficacy of this novel combination, as measured by the pathologic complete response (pCR) rate.

Secondary Objectives:

1. To further characterize the safety and feasibility of combining APX005M with SOC chemoradiation (external beam radiation in daily fractions, with concurrent weekly low-dose carboplatin/paclitaxel) in the neoadjuvant setting for patients with resectable esophageal and GE junction cancers.
2. To assess the efficacy of combining APX005M with SOC chemoradiation as measured by rates of R0 resection (microscopically negative margins, i.e., no tumor remains following surgery); and radiographic/metabolic response to neoadjuvant treatment on CT-PET.

Exploratory Objectives:

1. To identify possible predictive molecular or immune-based efficacy biomarkers for this novel combination.
2. To characterize and assess overall survival.

APX005M With Concurrent Chemoradiation for Resectable Esophageal and Gastroesophageal Junction Cancers

A Phase 2 Study of APX005M in Combination With Concurrent Chemoradiation as Neoadjuvant Therapy for Resectable Esophageal and Gastroesophageal Junction Cancers

The pCR was defined as post-neoadjuvant pathologic tumour, node, metastasis (ypTNM) (after chemoRT; after surgery) with T0, N0 stages. pCR rate was defined as the percentage of participants who achieved a pCR at surgery, as assessed by the Investigator.

* T0: No evidence of primary tumor.
* N0: Cancer has not spread to nearby lymph nodes.

An exact Clopper-Pearson lower 95% confidence limit was used to test the null hypothesis that the pCR rate is ≤30%.

The pCR was defined as ypTNM (after chemoRT; after surgery) with T0, N0 stages. pCR rate was defined as the percentage of participants who achieved a pCR at surgery, as assessed by the Investigator.

An exact Clopper-Pearson lower 95% confidence limit was used to test the null hypothesis that the pCR rate is ≤30%.

The pCR was defined as ypTNM (after chemoRT; after surgery) with T0, N0 stages. pCR rate was defined as the percentage of participants who achieved a pCR at surgery, as assessed by the Investigator. Steroids use: Yes was defined as participants with any steroid (ATC2 class corticosteroids for systemic use) from within 30 days of the first dose of sotigalimab to up to 7 days after the first dose and participants not fulfilling previous requirements are defined as Steroids use: No.

An exact Clopper-Pearson lower 95% confidence limit was used to test the null hypothesis that the pCR rate is ≤30%.

The pCR was defined as ypTNM (after chemoRT; after surgery) with T0, N0 stages. pCR rate was defined as the percentage of participants who achieved a pCR at surgery, as assessed by the Investigator.

The subgroup of participants who had surgery before or at 16/17 weeks were defined as start of study treatment to surgery date from the surgical resection form, less than or equal to 17 weeks (119 days = 17 weeks \* 7 days) or participants who were scheduled to have surgery but had their procedure aborted due to progressive disease at the time of the procedure or immediately before and did not have surgery because of metastasis. The subgroup of participants who had surgery after Week 17 were defined as start of study treatment to surgery date from the surgical resection form, greater than 17 weeks.

An exact Clopper-Pearson lower 95% confidence limit was used to test the null hypothesis that the pCR rate is ≤30%.

R0 was defined as the absence of gross and microscopic tumor involvement in the surgical margins i.e., no tumor remains following surgery. Rate of R0 resection was defined as the percentage of participants who achieved R0 following surgical resection.

Pathologic staging was assessed via ypTNM (after chemoRT and surgery):

* Tumor Stage (TX, T0, T1, T1a, T1b, T2, T3, T4, T4a, T4b) refers to the size and/or extent of the main tumor. The higher the number after the T, the larger the tumor or the more it had grown into the wall of the esophagus.
* Node Stage (NX, N0, N1, N2, N3) refers to the number and location of lymph nodes that cancer has spread to. The higher the number after the N, the more lymph nodes that contained cancer cells.
* Metastasis Stage (M0, M1) refers to whether the cancer had not spread (M0) or spread (M1) to other parts of the body.
* Stage group (0, I, IA, IB, II, IIA, IIB, III, IIIA, IIIB, IV, IVA, IVB) are based on the TNM stages detailed above. The higher the number, the more advanced the cancer was.

For each category, a lower stage/group represents a better outcome.

Response was adjudicated by the investigator; based on combination of change in wall thickening; size of regional lymph nodes; and metabolic activity of involved areas.

As the population does not typically have measurable disease by Response Evaluation Criteria in Solid Tumors (RECIST), radiographic/metabolic response was described in qualitative terms (responding/ stable, unchanged/ progressing/ not evaluable).

Response was adjudicated by the investigator; based on combination of change in wall thickening; size of regional lymph nodes; and metabolic activity of involved areas.

As the population does not typically have measurable disease by RECIST, radiographic/metabolic response was described in qualitative terms (responding/ stable, unchanged/ progressing/ not evaluable).

TEAEs were defined as adverse events which started on or after the first infusion of study treatment (Carboplatin/Paclitaxel/Sotigalimab/Radiotherapy) until 100 days after receiving the last dose of study treatment, death, or initiation of new anticancer therapy, whichever occurs first. Laboratory values that were considered clinically significant were reported as adverse events.

Apexigen America, Inc.

All-cause mortality was collected for all participants enrolled/randomized in the study. Adverse events were collected for all participants in the Safety Population who received at least one dose of sotigalimab and scheduled SOC of chemoradiation therapy. Adverse events are presented regardless of causal relationship to any of the study treatments.

Participants received SOC chemoRT, consisting of:

* External beam radiation in daily fractions (28 fractions) from Weeks 1-6, administered once per day up to 5 days/week.
* Carboplatin (AUC = 2) and paclitaxel (50 mg/m\^2) chemotherapy IV over 1 hour, once weekly, from Weeks 1-5.

The participants also received concurrent 0.3 mg/kg sotigalimab IV over 1 hour, once weekly, on Weeks 1, 2, 4, and 6 (2-3 days after chemoRT).

Surgical resection of the tumor was planned to be performed from Week 10 up to approximately Week 17, as indicated in the protocol amendment under which each participant was enrolled.

Sotigalimab With SOC ChemoRT

Age, Continuous

Sex: Female, Male

Ethnicity (NIH/OMB)

Race/Ethnicity, Customized

Tumor Histology

Non-gastroesophageal (GE) Junction tumor location includes upper, middle, and lower thirds of the esophagus.

Tumor Location

Safety Population: All participants who received at least one dose of sotigalimab and scheduled SOC of chemoradiation therapy.

Pyxis Oncology Clinical Operations

Efficacy Population: All participants who were eligible, received neoadjuvant sotigalimab and chemoRT followed by surgery, or had their planned surgery aborted due to the discovery of progressive disease.

Pathologic Complete Response (pCR) Rate (%) Overall

Squamous Cell Carcinoma

Adenocarcinoma

pCR Rate (%) by Baseline Histologic Subgroup

GE Junction

Non-GE Junction

pCR Rate (%) by Baseline Tumor Location Subgroup

Steroid Use: Yes

Steroid Use: No

pCR Rate (%) by Steroid Use Subgroup

Surgery Before or at Week 16-17

Surgery After Week 17

pCR Rate (%) by Surgery Subgroup

Rate (%) of R0 Resection Overall

Rate (%) of R0 Resection by Baseline Histologic Subgroup

Tumor Stage: Missing

Tumor Stage: T0

Tumor Stage: T1a

Tumor Stage: T2

Tumor Stage: T3

Node Stage: Missing

Node Stage: N0

Node Stage: N1

Node Stage: N2

Node Stage: N3

Metastasis Stage: Missing

Metastasis Stage: M0

Stage Group: Missing

Stage Group: I

Stage Group: IA

Stage Group: II

Stage Group: III

Stage Group: IIIA

Stage Group: IIIB

Stage Group: IVA

Pathologic Stage at Time of Surgery

At Time of Surgery

Postoperative Follow-up/Month 3

Postoperative Follow-up/Month 6

End of Study Visit

Efficacy Population: All participants who were eligible, received neoadjuvant sotigalimab and chemoRT followed by surgery, or had their planned surgery aborted due to the discovery of progressive disease. Participants with data available at each time point are presented. Participants included at End of Study Visit discontinued prior to completion of Postoperative Follow-up/Month 6.

Radiographic/Metabolic Response to Neoadjuvant Treatment on Computed Tomography (CT)/CT-Positron Emission Tomography (PET) (CT-PET) Overall

Squamous Cell Carcinoma: At Time of Surgery

Squamous Cell Carcinoma: Postoperative Follow-up/Month 3

Squamous Cell Carcinoma: Postoperative Follow-up/Month 6

Squamous Cell Carcinoma: End of Study Visit

Adenocarcinoma: At Time of Surgery

Adenocarcinoma: Postoperative Follow-up/Month 3

Adenocarcinoma: Postoperative Follow-up/Month 6

Adenocarcinoma: End of Study Visit

Radiographic/Metabolic Response to Neoadjuvant Treatment on CT-PET by Baseline Histologic Subgroup

GE Junction: At Time of Surgery

GE Junction: Postoperative Follow-up/Month 3

GE Junction: Postoperative Follow-up/Month 6

GE Junction: End of Study Visit

Non-GE Junction: At Time of Surgery

Non-GE Junction: Postoperative Follow-up/Month 3

Non-GE Junction: Postoperative Follow-up/Month 6

Non-GE Junction: End of Study Visit

Radiographic/Metabolic Response to Neoadjuvant Treatment on CT-PET by Baseline Tumor Location Subgroup

Number of Participants With Treatment-emergent Adverse Events (TEAEs)

Participants received SOC chemoRT, consisting of:

* External beam radiation in daily fractions (28 fractions) from Weeks 1-6, administered once per day up to 5 days/week.
* Carboplatin (area under the carboplatin plasma concentration versus time curve \[AUC\] = 2) and paclitaxel (50 mg/m\^2) chemotherapy intravenously (IV) over 1 hour, once weekly, from Weeks 1-5.

The participants also received concurrent 0.3 mg/kg sotigalimab IV over 1 hour, once weekly, on Weeks 1, 2, 4, and 6 (2-3 days after chemoRT).

Surgical resection of the tumor was planned to be performed from Week 10 up to approximately Week 17, as indicated in the protocol amendment under which each participant was enrolled.

Overall Study

Stomach Neoplasms

Gastrointestinal Neoplasms

Digestive System Neoplasms

Gastrointestinal Diseases

Stomach Diseases

Head and Neck Neoplasms

Esophageal Diseases

Stomach Cancer

Irinotecan

Docetaxel

Cisplatin

Topoisomerase I Inhibitors

Enzyme Inhibitors

Given once weekly for 2 weeks followed by a one week rest period (1 cycle is 3 weeks) Participants may continue on treatment unless there is disease progression or intolerable toxicities.

Taxotere

Peter C. Enzinger, MD

This is a phase II study of taxotere, cisplatin and irinotecan (CPT-11) used in combination to treat metastatic esophageal and gastric cancer in an effort to see what effects (good and bad) the combination may have on the patients cancer.

* Taxotere, cisplatin and irinotecan will be administered to the patient once weekly for 2 weeks followed by a one week rest period (1 cycle is 3 weeks).
* Patients will also receive corticosteroids, intravenous hydration and anti-emetic therapy prior to each treatment.
* A physical exam and bloodwork will be done each week of the treatment and every 2 cycles, reassessment of the tumor by the same imaging method to determine the baseline size will be conducted.
* Patients will remain on the study unless disease progression or intolerable toxicity occur.

Taxotere, Cisplatin and Irinotecan (CPT-11) for Esophagogastric Cancer

A Phase II Trial of Taxotere, Cisplatin, and Irinotecan in Advanced Esophageal and Gastric Cancer

Massachusetts General Hospital

Beth Israel Deaconess Medical Center

Brigham and Women's Hospital

Aventis Pharmaceuticals

Dana-Farber Cancer Institute

Amino Acids

Capecitabine

Lapatinib

Antimetabolites

Tyrosine Kinase Inhibitors

Protein Kinase Inhibitors

Tyrosine

oral lapatinib (1250mg) administered as a monotherapy run-in followed by its combination with capecitabine

Lapatinib and Capecitabine

GSK Clinical Trials

The study will determine if changes in expression of markers involved in the 5-FU pathways are associated with response to treatment with the combination of lapatinib and capecitabine independent of tumor erbB2 status.

Study For Patients With Untreated Gastric Cancer Who Will Receive Capecitabine And Lapatinib

An Exploratory, Phase II Trial to Determine the Association of Lapatinib Induced Fluoropyrimidine Gene Changes With Efficacy Parameters of Lapatinib and Capecitabine in First Line Gastric Cancer

Participants were analyzed for intratumoral expression levels of genes involved in the 5-fluorouracil (FU) pathway and lapatinib-targeted genes. Change in biomarker expression levels was calculated as the levels measured after the lapatinib Run-in Period (Baseline) of the study minus the levels measured at the start of monotherapy (Day -7). EGFR, epidermal growth factor receptor; HER, human epidermal growth factor receptor. Data are presented as ratios of the normalized gene expression of the target gene to that of beta actin.

Response is defined as documented evidence of complete response (CR) or partial response (PR). The investigator evaluated response based on Response Evaluation Criteria in Solid Tumors (RECIST) criteria. Complete response is defined as the disappearance of all target lesions (TLs) and non-TLs and the appearance of no new lesions (NLs). Partial response for TLs is defined as \>= a 30% decrease in the sum of the longest diameter (LD) of TLs, taking as a reference the Baseline sum LD. For non-TLs it is defined as the persistence of 1 or more non-TL and no new TLs or non-TLs.

5-month (mo.) PFS was defined as the percentage of par. who were alive/progression free for 5 months from the time of initial treatment. PFS is defined as the time from the initial treatment until the first observation of disease progression (DP)/death due to any cause; the percentage of par. whose follow-up ended or was ongoing was reported. DP is defined as symptomatic progression or the appearance of \>=1 NL and/or unequivocal progression of existing non-TLs, and a \>=20% increase in the sum of the LD of TLs, taking as a reference the smallest sum LD recorded since treatment started.

PFS is defined as the time from the initial treatment until the first observation of disease progression or death due to any cause. The date of documented disease progression was defined as the earliest date of radiographic disease assessment progression or symptomatic progression, whichever came first. For participants who did not die/progress, survival was censored at the time of the last assessment (or contact).

Overall survival is defined as the time from the initial treatment until death due to any cause. A death occurring during the study is defined as a death occurring during treatment or within 30 days of the last administration of study medication.

Time to progression is defined as the time from the initial treatment (first dose) until the first documented radiological symptomatic sign of disease progression. Time to progression data are presented as cumulative incidence estimate, which is defined as the time from the initial treatment until crude hazard probability of the occurrence of a particular event is reached to a particular point. All factors that hinder the observation of the event are defined as competing risks.

Time to progression is defined as the time from the initial treatment (first dose) until the first documented radiological symptomatic sign of disease progression. Time to progression data are presented as cumulative incidence estimate, which is defined as the time from the initial treatment until crude hazard probability of occurrence of a particular event is reached to a particular point. All factors that hinder the observation of the event are defined as competing risks.

Time to response is defined as the time from the initial treatment until the first documented evidence of CR (disappearance of all TLs and non-TLs and the appearance of no new lesions) or PR (\>= a 30% decrease in the sum of the longest diameter of TLs, taking as reference the Baseline sum longest diameter) (whichever status was recorded first). Time to response data are presented as cumulative incidence estimate, which is defined as the time from the initial treatment until crude hazard probability of the occurrence of a particular event is reached to a particular point.

Duration of response is defined as the time from the first documented evidence of tumor response (CR or PR) until the first documented sign of disease progression or death due to any cause, whichever came first.

Best overall response was evaluated by the investigator based on RECIST criteria: CR; PR; Stable Disease (SD), defined as no sufficient shrinkage to qualify for PR, no sufficient increase to qualify for progressive disease (PD), taking as reference the smallest sum LD since the treatment started; PD, defined as at least a 20% increase in the sum of the LD of target lesions, taking as a reference the smallest sum LD recorded since the treatment started or the appearance of \>= 1 new lesions; Unknown, defined as participants who do not have CR, PR, SD, or PD.

Toxicity was measured in grades (AE severity) per National Cancer Institute Common Toxicity Criteria for Adverse Event (NCI CTCAE) version (v) 3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For albumin (per blood samples): G 1 (\<lower limit of normal \[LLN\] to 3 grams per deciliter \[g/dL\]), mild; G 2 (\<3 to 2 g/dL), moderate; G 3 (\<2 g/dL), severe; G 4 (value not available), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For ALP: G 1 (upper limit of normal \[ULN\] to 2.5x ULN), mild; G 2 (\>2.5 to 5.0x ULN), moderate; G 3 (\>5.0 to 20.0x ULN), severe; G 4 (\>20.0x ULN), life threatening/disabling; G 5 (value not available), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of AST. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For AST: G 1 (\>ULN to 2.5x ULN), mild; G 2 (\>2.5 to 5.0x ULN), moderate; G 3 (\>5.0 to 20.0x ULN), severe; G 4 (\>20.0x ULN), life threatening/disabling; G 5 (value not available), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of ALT. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For ALT: G 1 (\>ULN to 2.5x ULN), mild; G 2 (\>2.5 to 5.0x ULN), moderate; G 3 (\>5.0 to 20.0x ULN), severe; G 4 (\>20.0x ULN), life threatening/disabling; G 5 (value not available), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of total bilirubin. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For total bilirubin: G 1 (\>ULN to 1.5x ULN), mild; G 2 (\>1.5 to 3.0x ULN), moderate; G 3 (\>3.0 to 10.0x ULN), severe; G 4 (\>10.0x ULN), life threatening/disabling; G 5 (value not available), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for calcium evaluation. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For calcium (low and high, respectively): G 1 (\<LLN to 8.0 mg/dL; \>ULN to 11.5x ULN), mild; G 2 (\<8.0 to 7.0 mg/dL; \>11.5 to 12.5 ULN), moderate; G 3 (\<7.0 to 6.0 mg/dL; \>12.5 to 13.5 mg/dL), severe; G 4 (\<6 mg/dL; \>13.5 mg/dL), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of creatinine. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For creatinine: G 1 (\>ULN to 1.5x ULN), mild; G 2 (\>1.5 to 3.0x ULN), moderate; G 3 (\>3.0 to 6.0x ULN), severe; G 4 (\>6.0x ULN), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of glucose. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For glucose (high and low, respectively): G 1 (\>ULN to 160 mg/dL; \<LLN to 55 mg/dL), mild; G 2 (\>160 to 250 mg/dL; \<55 to 40 mg/dL), moderate; G 3 (\>250 to 500 mg/dL; \<40 to 30 mg/dL), severe; G 4 (\>500 mg/dL; \<30 mg/dL), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For potassium (high and low \[per blood samples\], respectively): G 1 (\>ULN to 5.5 millimoles per liter \[mmol/L\]; \<LLN to 3.0 mmol/L), mild; G 2 (\>5.5 to 6.0 mmol/L; value not available), moderate; G 3 (\>6.0 to 7.0 mmol/L; \<3.0 to 2.5 mmol/L), severe; G 4 (\>7.0 mmol/L; \<2.5 mmol/L), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for magnesium evaluation. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For magnesium (high and low, respectively): G 1 (\>ULN to 3.0 mg/dL; \<LLN to 1.2 mg/dL), mild; G 2 (value not available; \<1.2 to 0.9 mg/dL), moderate; G 3 (\>3.0 to 8.0 mg/dL; \<0.9 to 0.7 mg/dL), severe; G 4 (\>8.0 mg/dL; \<0.7 mg/dL), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for sodium evaluation. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of each AE severity. For sodium (high and low, respectively): G 1 (\>ULN to 150 mmol/L; \<LLN to 130 mmol/L), mild; G 2 (\>150 to 155 mmol/L; value not available), moderate; G 3 (\>155 to 160 mmol/L; \<130 to 120 mmol/L), severe; G 4 (\>160 mmol/L; \<120 mmol/L), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of hemoglobin. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For hemoglobin: G 1 (\<LLN to 10 g/dL), mild; G 2 (\<10.0 to 8.0 g/dL), moderate; G 3 (\<8.0 to 6.5 g/dL), severe; G 4 (\<6.5 g/dL), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of lymphocytes. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For lymphocytes: G 1, mild; G 2, moderate; G 3, severe; G 4, life threatening/disabling; G 5, death related to AE; ranges were provided by local laboratories. Change from Baseline was measured as any grade increase (AGI), increase to G 3 (ItoG3), and increase to G 4 (ItoG4). Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of total neutrophils. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For neutrophils: G 1 (\<LLN to 1500/millimeters cubed \[mm\^3\] of blood plasma \[bp\]), mild; G 2 (\<1500 to 1000/mm\^3 of bp), moderate; G 3 (\<1000 to 500/mm\^3 of bp), severe; G 4 (\<500/mm\^3 of bp), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of platelet count. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For platelet count: G 1 (\<LLN to 75000/mm\^3 of blood plasma \[bp\]), mild; G 2 (\<75000 to 50000/mm\^3 of bp), moderate; G 3 (\<50000 to 25000/mm\^3 of bp), severe; G 4 (\<25000/mm\^3 of bp), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

Blood samples were collected for the evaluation of WBC count. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For WBCs: G 1 (\<LLN to 3000/mm\^3 of blood plasma \[bp\]), mild; G 2 (\<3000 to 2000/mm\^3 of bp), moderate; G 3 (\<2000 to 1000/mm\^3 of bp), severe; G 4 (\<1000/mm\^3 of bp), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment.

GlaxoSmithKline

Lapatinib tablets were administered orally at a dose of 1250 mg OD and capecitabine tablets were administered orally at a dose of 1000 milligrams per meters squared (mg/m\^2) twice daily (BID) for the first 14 days of each subsequent 21-day cycle. The capecitabine dose schedule was an intermittent regimen consisting of 2 weeks of treatment followed by 1 week of rest (drug-free period). Capecitabine and lapatinib were taken at two different times of the day.

Lapatinib + Capecitabine

Baseline data were collected in members of the Intent-to-Treat Population, comprised of all participants who entered the study and received at least one dose of lapatinib.

White - White/Caucasian/European Heritage

Asian - East Asian Heritage

American Indian or Alaskan Native

Asian - South East Asian Heritage

GSK Response Center

Thymidylate synthase (TS), n=34

Deoxypyridinoline (DPD), n=26

EGFR/HER1, n=32

HER2, n=28

HER3, n=33

Lapatinib 250 milligram (mg) tablets administered at a dose of 1250 mg once daily (OD) for 7 days

Intent-to-Treat (ITT) Population: all participants who entered the study and received at least one dose of lapatinib. Only those participants contributing viable samples were analyzed. Different participants contributed samples for different biomarkers.

Change From Start of Run-in Period in Biomarker Expression Levels at Day 0

Response Rate (Measured as the Percentage of Participants With Response [Complete Response or Partial Response])

ITT Population. PFS was censored for participants who did not have an event before data cut off. The last available assessment prior to the data cut off was used for censored participants.

Percentage of Participants (Par.) With 5-month Progression-free Survival (PFS)

ITT Population. OS was censored for participants who did not have an event before data cut off. The last available assessment prior to the data cut off was used for censored participants.

Overall Survival (OS)

ITT Population. Time to progression was censored for participants who did not have an event before data cut off. The last available assessment prior to the data cut off was used for censored participants.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
APX005M With Concurrent Chemoradiation for Resectable Esophageal and Gastroesophageal Junction Cancers	NCT03165994	Esophageal Canc... GastroEsophagea...	APX005M Radiation Thera... Paclitaxel Carboplatin Surgical resect...	18 Years -	Apexigen America, Inc.
Taxotere, Cisplatin and Irinotecan (CPT-11) for Esophagogastric Cancer	NCT00165464	Esophageal Canc... Gastric Cancer GE Junction Can...	Taxotere Cisplatin Irinotecan	18 Years -	Dana-Farber Cancer Institute
Study For Patients With Untreated Gastric Cancer Who Will Receive Capecitabine And Lapatinib	NCT00526669	Neoplasms, Gast...	Lapatinib and C...	18 Years -	GlaxoSmithKline

Spots Global Cancer Trial Database for ge junction

Every month we try and update this database with for ge junction cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Spots Global Cancer Trial Database for ge junction

Every month we try and update this database with for ge junction cancer trials from around the world to help patients and their families find trials that might be right for them. We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Every month we try and update this database with for ge junction cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.