Do esophageal cancer survivors have an increased risk of a “second primary cancer?” Yes. Why? After researching this question it seems to me that oncologists don’t really know. Certainly, there is an increased risk if you undergo cancer-causing therapy such as radiation and many forms of chemotherapy.
One of the many chemotherapy regimens I underwent was Cytoxan chemotherapy and therefore have an increased risk of bladder cancer. I underwent local radiation to my C5 which caused dysphagia which then caused GERD which increases my risk of esophageal cancer. I underwent local palliative radiation and therefore am at increased risk of certain cancers.
My point is that in addition to studying multiple myeloma, my primary cancer, I study all those secondary cancers that I have an increased risk of. Or I should say that I research/look for evidence-based, non-toxic therapies shown to reduce my risk of
But there are specific cancers, such as esophageal cancer, that have an increased risk of head and neck cancers and lung cancers.
My solution? I live my life as if I am at risk for both a relapse of my first cancer, multiple myeloma, as well as a second “primary” tumor. I don’t like it but I cannot change this fact.
I take a number of anti-oxidant, anti-angiogenic supplements. All have evidence-based research showing anti-cancer properties- curcumin, green tea extract, silibinin, etc.
For more information about preventing a second primary cancer that YOU may be concerned about, scroll down the page, post a question or a comment and I will reply ASAP.
“A term used to describe a new primary cancer that occurs in a person who has had cancer in the past. Second primary cancers may occur months or years after the original (primary) cancer was diagnosed and treated. Certain types of cancer treatment, such as chemotherapy and radiation therapy, may increase the risk of a second primary cancer…”
Background: The objective of this study is to assess the risk of second primary cancers following a first primary esophageal cancer as well as the risk of esophageal cancer as a second primary, following first primary cancers of other sites.
Results: During the study period, 959 cases of second primary cancers occurred after an initial esophageal cancer, resulting in a SIR of 1.15 (95% confidence interval, 1.08-1.22). Second primary stomach cancers were associated with first primary esophageal adenocarcinomas (SIR, 2.13; 95% confidence interval, 1.26-3.37) and second primary cancers of the oral cavity and pharynx (6.68; 5.33-8.26), stomach (1.53; 1.14-2.01), larynx (3.24; 1.88-5.18), lung (1.55; 1.28-1.87), kidney (1.88; 1.18-2.85), and thyroid (2.92; 1.18-6.02) were associated with first primary squamous cell carcinomas of the esophagus. An excess of esophageal cancer as a second primary were observed following first primary cancers of the aerodigestive tract, female breast, cervix, testis, bladder, Hodgkin’s lymphoma, and non–Hodgkin lymphoma.
CONCLUSION: We observed associations of esophageal cancer with second primary head and neck cancers and lung cancer regardless of years of follow-up, which may suggest that common risk factors play a role in multiple tumor development.
“Background/Aims: Unexpected diagnosis of synchronous second primary cancers (SPC) complicates physicians’ decision-making because clinical details of squamous esophageal cancer (EC) patients with SPC have been limited. We evaluated clinical features and treatment outcomes of patients with synchronous SPC detected during the initial staging of squamous EC.
Methods:We identified a total of 317 consecutive patients diagnosed with squamous EC. Relevant clinical and cancer-specific information were reviewed retrospectively.
Results: EC patients with synchronous SPC were identified in 21 patients (6.6%). There were significant differences in median age (70 years vs. 63 years, p = 0.01), serum albumin level (3.3 g/dL vs. 3.9 g/dL, p < 0.01) and body mass index (20.4 kg/m2 vs. 22.8 kg/m2, p = 0.01) between EC patients with and without SPC.
Head and neck, lung and gastric cancers accounted for 18.2%, 22.7%, and 18.2% of SPC, respectively. Positron emission tomography-computed tomography (PET-CT) detected four cases (18.2%) of SPC that were missed on CT. Management plans were altered in 13 of 21 patients (61.9%) with detected SPC. Curative esophagectomy was attempted in 28.6% of EC patients with SPC (vs. 59.1% of patients without SPC; p = 0.006). EC patients with SPC had significantly lower 5-year survival than patients without SPC (10.6% vs. 36.7%, p = 0.008).
Conclusions: Synchronous SPC were found in 6.6% of squamous EC patients, and PET-CT contributed substantially to the detection of synchronous SPC. EC patients with SPC had poor survival due to challenges of providing stage-appropriate treatment.