Hematology Oncology

Front 1

What is the staging for colorectal cancer?

Back 1

1:ITumor does not invade the full thickness of bowel wall (T1, T2); lymph nodes not involved (N0)90%-95%

IITumor invades full thickness of the bowel and may invade into pericolonic or perirectal fat (T3, T4); lymph nodes not involved (N0)70%-85%

III One or more lymph nodes involved with cancer (N1, N2); any T stage25%-70%

IVMetastatic tumor spread to distant site (M1); any T stage; any N stage0%-10%

Front 2

What is the treatment by stage I/II?

Back 2

I - surgery, no addition treatment

II - no clear survival advantage for adjuvant chemo, subsequently surgery alone is acceptable standard practice for most patients

Exception: pateitns with high risk features for recurrence (T4 disease, inadequate LN sampling), lymphovascular invasion, poorly differentiated histology or clinical perforation/obstruction

Front 3

What is the preferred surgery in rectal cancer?

Back 3

Patients with rectal tumors that are not full thickness and do not have lymph node involvement (stage I) on pretreatment imaging usually undergo surgery, with a total mesorectal excision being the preferred procedure. The mesorectum is a fatty sheath covering the rectum that contains the regional lymph nodes. A total mesorectal excision entails a sharp dissection of the pelvis outside of the mesorectum to allow removal of the mesorectum fully intact en bloc with the rectum.

if pathology confirms stage I cancer, no further therapy is needed

In patients with tumors that are too distal to permit an adequate margin of resection without resection of the anal sphincter muscles, an abdominal-peritoneal resection is likely to be required, which results in a permanent colostomy.

Front 4

How are full thickness rectal tumors (T3-T4) or clearly enlarged LNs on preop imaging treated?

Back 4

Patients who have full-thickness rectal tumors (T3-T4) or clearly enlarged lymph nodes on preoperative imaging require combined-modality therapy with neoadjuvant radiation and chemotherapy and adjuvant chemotherapy alone. More recently, an accepted alternative has been chemotherapy first, followed by chemoradiotherapy, and then surgery, with no postoperative treatment (“total neoadjuvant therapy”).

Front 5

What are the adjuvant chemotherapy regimens in colon cancer?

Back 5

5-FU

Reduced folate leucovorin: when used w/ 5-FU causes 5-FU to bind more tightly to its target enzyme

Capecitabine: oral prodrug converted to 5-FU in the body - requires extensive adherence

FOLFOX: leucovorin, 5-FU, oxaliplatin

CPOX: capecitabine plus oxaliplatin

These regimens have been shown to be modestly but statistically significantly more effective than the same regimens without oxaliplatin in patients with stage III (but not stage II) disease - those w/ stage II and high risk features can still receive 5-FU + leucovorin or capecitabine

Front 6

What is the adjuvant therpay for rectal cancer?

Back 6

Because of the difficulty getting adequate tumor free margins, patients with locally advanced T3/T4 rectal cancer should get neoadjuvant chemotradiotherapy

For chemo: 5Fu and capcetabine

Addition of oxaliplatin has not been promising

FOLFOX or CAPOX is typically used after neoadjuvant chemoradiotherapy and surgery for 4 months to complete a total of 6 months of therapy

- An acceptable alternative if 4 month FOLFOX/CAPOX as initial treatment followed by chemoradiation and then surgery

Front 7

What is the treatment of metastatic colon cancer?

Back 7

Good prognostic factors: long disease free interval, limited number of mets, mets confined to a single organ

- patients w/ limited number of liver only lesions have long term disease free survival rates of 25-50%

Treatment s chemo: FOLFOX

FOLFIRI (instead of oxaliplatin, use irinotecan)

Bevacizumab can be added to chemotherapy regimens

All patients should undergo tumor genotyping to identify mtuations in the K-ras and N-ras genes - anti EGFR receptor antibodies are inactive in 50% of tumors that harbor mutations

- RASH corrlates w/ response

Front 8

What is the post-operative surveillance in patients w/ colorectal cancer?

Back 8

Postoperative surveillance of patients with colorectal cancer includes CT scans of the chest, abdomen, and pelvis annually for at least the first 3 years postoperatively and colonoscopy 1 year after resection, 3 years later, and then every 5 years with the goal of identifying surgically curable recurrence.

Front 9

What is the treatment of anal cancer?

Back 9

anal cancer is often curable with radiation therapy and concurrent chemotherapy with mitomycin plus 5-FU.

Anal tumors may continue to regress for at least 6 months up to 1 year after completion of chemoradiation therapy. Should not dictate treatment failure just before there is unequivocal growth or mets

. Salvage surgery is performed in patients with local tumor growth after radiation plus chemotherapy; however, this procedure necessarily removes the sphincter muscle, thus requiring a permanent colostomy.

Front 10

What is the staging of pancreatic cancer? Which tumors are resectable?

Back 10

Resectable tumors:

Stage IA: Resectable tumors are confined to the pancreas or just beyond it that correspond to stage IA (tumor limited to the pancreas and ≤2 cm in diameter),

Stage IB: tumor limited to the pancreas but >2 cm in diameter

Stage IIA (tumor extension beyond the pancreas but without involvement of the celiac axis) without involved lymph nodes or evidence of metastatic disease.

Borderline resectable pancreatic cancer is that which extends to nearby blood vessels but that may be removed completely with surgery, such as some stage III tumors (involving the celiac axis or superior mesenteric artery with or without involved lymphadenopathy) without evidence of metastatic disease.

Front 11

What tumors cannot be resected?

Back 11

Unresectable cancers cannot be removed entirely by surgery and may include locally advanced disease that has not yet spread to distant organs but still cannot be completely surgically removed (stage IIB [localized tumor or with extension beyond the pancreas but with associated involved lymph nodes] and most stage III cancers).Metastatic cancer has spread to distant organs and might involve surgery to ameliorate symptoms, but surgery cannot excise the tumor completely or cure the cancer.

Front 12

What is the treatment of resectable tumors?

Back 12

Postoperative adjuvant therapy with chemotherapy, local radiation, or the combination is also controversial.

For patients with locally unresectable disease, neoadjuvant chemoradiation remains controversial.

Front 13

What is the treatment of metastatic pancreatic cancer?

Back 13

For decades, gemcitabine alone was considered an appropriate standard treatment for metastatic pancreatic cancer. More recently, a combination regimen of oxaliplatin, irinotecan, 5-FU, and leucovorin (FOLFIRINOX), has been shown to provide better outcomes; however, this regimen has substantial toxicity and is only a reasonable option in patients who are both medically well (have an excellent performance status) and who are highly motivated. A more recent trial has shown that the addition of liposomally encapsulated paclitaxel (nab-paclitaxel) to gemcitabine also improves outcome modestly, albeit with some increased toxicity.

Front 14

What is the staging of gastroesophageal cancer?

Back 14

n simple terms, stage I disease is a superficial lesion that has not spread and does not penetrate the full thickness of the esophagus or stomach wall, whereas stage II disease is a full-thickness lesion. Stage III disease is defined by spread to locoregional lymph nodes, and stage IV disease is defined by the presence of distant metastatic disease. Virtually all gastric and gastroesophageal junction cancers are adenocarcinomas, as are approximately 95% of esophageal cancers. About 5% of esophageal cancers are of squamous cell histology, although currently, patients with adenocarcinomas and squamous cell carcinoma receive the same treatments.

Front 15

What is the treatment for nonmetastatic disease?

Back 15

Although only 30% to 40% of patients have potentially resectable disease at presentation, patients with local and locoregional disease (AJCC stages I, II, and III) are typically treated surgically. Unfortunately, recurrence rates are high and cure rates with surgical resection remain low.

Because of the low cure rates for locoregional therapy for esophageal cancer, chemotherapy has been added to many treatment regimens, and many patients are currently treated with combination chemoradiation therapy following surgery for resectable disease. However, the optimal treatment regimen and the overall effectiveness of different treatment approaches have not yet been established.

Front 16

What is the treatment of metastatic disease?

Back 16

Treatment of metastatic (stage IV) gastroesophageal cancer remains unsatisfactory and palliative. Numerous agents have shown modest activity, and combination cisplatin-based regimens are typically used owing to the insufficient activity of single agents.

Front 17

What is a molecular target in gastric cancers of the GE junction?

Back 17

Up to 20% of gastric cancers and 30% of gastroesophageal junction adenocarcinomas recently have been found to overexpress the HER2 growth factor receptor, which is a target for the anti-HER2monoclonal antibody trastuzumab. Therefore, evaluation of all metastatic gastroesophageal carcinomas for HER2 is performed, and trastuzumab is added to chemotherapy regimens in patients whose tumors express HER2.

Front 18

What is the treatment of neuroendocrine tumors?

Back 18

Most neuroendocrine tumors are hormonally nonfunctioning, but about 25% that manifest are hormone producing.Because well-differentiated neuroendocrine tumors are so indolent, patients often can be effectively managed with expectant observation and serial imaging using triple-phase contrast-enhanced CT scanning or MRI with gadolinium.In pancreatic neuroendocrine tumors, the small-molecule inhibitors sunitinib and everolimus and combination capecitabine and temozolomide are active.

riple-phase contrast-enhanced CT scanning or MRI with gadolinium are the preferred imaging modalities. Indium 111 pentetreotide scanning can be used to establish the presence of somatostatin receptors, which are commonly expressed on these tumors. Tumors that have demonstrated somatostatin receptors and are hormonally symptomatic or show clear growth under observation may be treated with the somatostatin analogues octreotide or lanreotide. Mechanical interventions, such as hepatic arterial embolization, radiofrequency ablation, or surgical debulking, may be used to reduce symptomatic tumor bulk in the liver or to decrease hormone production.

Front 19

How are GIST tumors treated?

Back 19

Patients with localized gastrointestinal stromal tumors are managed with surgical resection.Following surgery, patients with localized gastrointestinal stromal tumors and tumors with favorable risk factors require no further treatment, whereas those with higher-risk tumors are treated with an extended course of imatinib.Patients with metastatic gastrointestinal stromal tumors are treated with lifelong imatinib until disease progresses or treatment toxicity is no longer tolerable.

or patients undergoing a potentially curative resection of a localized GIST, tumors with favorable risk factors require no further treatment, whereas patients with higher-risk tumors are treated with an extended course of the small-molecule receptor tyrosine kinase inhibitor imatinib, which blocks c-kit tyrosine kinase phosphorylation. I

. In such patients, recurrence-free survival and overall survival are superior in patients who receive 3 years of imatinib therapy versus 1 year of therapy.

Front 20

What is the pathophysiology of GIST?

Back 20

GISTs are the most common tumor of mesenchymal origin, or sarcoma, of the gastrointestinal tract, representing 1% to 3% of all gastrointestinal tumors, and are derived from the precursors of the intestinal cells of Cajal. Almost all GISTs have an activating mutation in the c-kit proto-oncogene, leading to constitutive activation of the KIT receptor tyrosine kinase. CD-117, the immunohistochemical marker for the KIT protein, is the hallmark of most GISTs. GISTs may also present with mutations in the platelet-derived growth factor-α receptor.